seniors

Estrogen & Hormone therapy

Estrogen's effect on the brain is a complex story, one which we are only beginning to understand. We know it's important for women, but we're not sure about the details. One of the problems is that it appears to interact with stress. There are two aspects to estrogen's effects on women: normal monthly fluctuations in estrogen levels, and menopause.

It's also important to distinguish post-menopause (once you have completely stopped menstruating) from perimenopause (the years of menstrual irregularity leading up to this).

In general, the last few years of research seem to be coming to the conclusion that any cognitive problems women experience as they approach menopause is limited, both in time and in task, and depends in part on other factors. For example, those who experience many hot flashes may have poorer verbal memory, but the main cause for this may be the poorer sleep quality; those who are distressed or experience mood changes may find their memory and concentration affected for that reason.  These findings suggest the best approach to dealing with cognitive problems in perimenopause is to tackle the physical and/or emotional causes.

Post-menopause is different. Post-menopause is all about low estrogen levels, and the importance of estrogen for brain function. Nevertheless, estrogen therapy for postmenopausal women has had inconsistent results; there has even been some research suggesting it may increase the risk of later dementia. There is also some suggestion that it may not help those women who have cognitively stimulating environments, or are highly educated. And other indications that timing might be critical -- the age at which you begin hormone therapy. At the moment, we simply have too little clear evidence to warrant recommending hormone therapy for cognitive reasons (particularly in light of the possible cancer risk), or to know when it might be effective.

Excitingly, however (because there is no downside!), there is some evidence that physical exercise can counter the cognitive decline postmenopausal women may experience. There's also a study suggesting that the effect of low estrogen after menopause is not to impair cognition but simply to change it -- however, because women aren't prepared for, or understand, these changes, they perceive it as impairment. That would suggest that what is needed is an education program in how the brain changes (but first we have to understand exactly how it does change!).

Older news items (pre-2010) brought over from the old website

How does estrogen affect cognition?

Estrogen levels affect hippocampal wiring

Many studies have established the role of estrogen in female cognition. A rat study has now revealed the reason. It appears that the "wiring" in the hippocampus expands and retracts in relation to the amount of estrogen present during the estrous/menstrual cycle. The findings also suggest that “the brain's capacity for growth is well beyond anything we considered in the past”.
Routtenberg, A. 2005. Presented at the Society for Neuroscience's 35th Annual Meeting in Washington, D.C.
http://www.eurekalert.org/pub_releases/2005-11/nu-bma111405.php

How estrogen affects the brain

A new study involved cultured rat neurons has revealed how estrogen affects learning and memory. It appears that, in females, estrogen can activate particular glutamate receptors within the hippocampus. Glutamate is the primary excitatory neurotransmitter in the brain, allowing for fast communication between neurons.
[271] Boulware, M. I., Weick J. P., Becklund B. R., Kuo S. P., Groth R. D., & Mermelstein P. G.
(2005).  Estradiol Activates Group I and II Metabotropic Glutamate Receptor Signaling, Leading to Opposing Influences on cAMP Response Element-Binding Protein.
J. Neurosci.. 25(20), 5066 - 5078.
http://www.eurekalert.org/pub_releases/2005-05/uom-uom051905.php

Estrogen effect on memory influenced by stress

The question of whether estrogen helps memory and cognition in women has proven surprisingly difficult to answer, with studies giving conflicting results. Now it seems the answer to that confusion is: it depends. And one of the things it depends on may be the level of stress the woman is experiencing. A rat study has found that the performance of female rats in a water maze was affected by the interaction of hormone level (whether the rat was estrous or proestrous) with water temperature (a source of physical stress). Those rats with high hormone levels did better when the water was warm, while those with low hormone levels did better when the water was cold. The researchers suggest both timing and duration of stress might be factors in determining the effect of hormones on cognition.
[384] Rubinow, M. J., Arseneau L. M., Beverly L. J., & Juraska J. M.
(2004).  Effect of the Estrous Cycle on Water Maze Acquisition Depends on the Temperature of the Water..
Behavioral Neuroscience. 118(4), 863 - 868.
http://www.eurekalert.org/pub_releases/2004-08/uoia-sss082704.php

Estrogen combines with stress to impair memory

A rat study has found that male and female rats performed equally well on a task involving the prefrontal cortex when under no stress, and when highly stressed, both made significant memory errors. But importantly, after exposure to a moderate level of stress, females were impaired, but males were not. When investigated further, it was found that female rats only showed this sensitivity when they were in a high-estrogen phase of their estrus cycle. The estrogen effect was confirmed in a further study using female rats who had had their ovaries removed, thus enabling the researchers to compare the effects of estrogen versus a placebo. These results suggest that high levels of estrogen can act to enhance the stress response, causing greater stress-related cognitive impairments, while providing reassurance that estrogen appears to have no effect on cognitive performance under non-stressful conditions.
[746] Shansky, R. M., Glavis-Bloom C., Lerman D., McRae P., Benson C., Miller K., et al.
(2003).  Estrogen mediates sex differences in stress-induced prefrontal cortex dysfunction.
Mol Psychiatry. 9(5), 531 - 538.
http://www.eurekalert.org/pub_releases/2003-12/mp-epg112603.php

Why estrogen helps memory

Estrogen has been implicated as having a role in memory in a number of studies, although findings have been mixed as to the value of HRT for improving memory in post-menopausal women. A new study helps us understand why estrogen might be helpful. The study details how nerve cells in the hippocampus "grow in complexity" when exposed to estrogen, increasing connections among the nerve cells. It may be that, without estrogen, the connections that are there might not work as efficiently in storing and recalling certain types of memories. Previous studies have shown that the ability of women to remember word lists varies during their normal monthly cycle.
[1005] Akama, K. T., & McEwen B. S.
(2003).  Estrogen Stimulates Postsynaptic Density-95 Rapid Protein Synthesis via the Akt/Protein Kinase B Pathway.
J. Neurosci.. 23(6), 2333 - 2339.
[880] Znamensky, V., Akama K. T., McEwen B. S., & Milner T. A.
(2003).  Estrogen Levels Regulate the Subcellular Distribution of Phosphorylated Akt in Hippocampal CA1 Dendrites.
J. Neurosci.. 23(6), 2340 - 2347.
http://www.eurekalert.org/pub_releases/2003-03/ru-rwc031403.php

Estrogen may dictate the problem-solving strategy chosen

Several studies have suggested estrogen may be beneficial for cognitive functioning in women. New research using rats suggests estrogen may be very specific in what types of learning it helps - and what types it may impair. In rats, it appeared to enhance place-learning, at the expense of response learning. It is suggested that postmenopausal women may experience a shift into a problem-solving mode more common to men. "Women may actually get better at performing a task from a different approach, but they are not used to doing it that way, so they view the change as an impairment."
[831] Korol, D. L., & Kolo L. L.
(2002).  Estrogen-induced changes in place and response learning in young adult female rats..
Behavioral Neuroscience. 116(3), 411 - 420.
http://www.eurekalert.org/pub_releases/2002-05/uoia-emd051502.php

Are you likely to develop cognitive problems in menopause?

Menopause transition may cause trouble learning

A four-year study of over 2,300 women, aged 42 to 52, has found evidence suggesting that during the early and late perimenopause women do not learn as well as they do during other menopause transition stages. Processing speed improved with repeated testing during premenopause, early perimenopause (menstrual irregularity but no "gaps" of 3 months), and postmenopause (no period for 12 months), but scores during late perimenopause (no period for three to 11 months) did not show the same degree of improvement. Improvements in processing speed were considerably reduced in late perimenopause, and improvement in verbal memory performance was reduced during both early and late perimenopause (and indeed almost non-existent during late perimenopause). These findings are consistent with self-reported memory difficulties — 60% of women state that they have memory problems during the menopause transition. The good news is that the effect seems to be temporary. Interestingly, although taking estrogen or progesterone hormones before menopause helped verbal memory and processing speed, taking them after the final period had a negative effect. This is consistent with other research indicating that the timing of hormone therapy is crucial to its effects.
[554] Greendale, G. A., Huang M. - H., Wight R. G., Seeman T., Luetters C., Avis N. E., et al.
(2009).  Effects of the menopause transition and hormone use on cognitive performance in midlife women.
Neurology. 72(21), 1850 - 1857.
http://www.eurekalert.org/pub_releases/2009-05/aaon-mtm051909.php

Hot flashes underreported and linked to forgetfulness

In the first study to explore the relationship between objectively measured hot flashes in menopausal women and memory performance, it’s been found that women dramatically underreport the number of hot flashes they experience (by about 43%), and that, with a clear measure of hot flashes, an association between number of hot flashes and poor verbal memory is evident. There was no relationship between the number of hot flashes women thought they had and memory performance. The average number of objective hot flashes was 19.5 per day. Unsurprisingly, poor sleep also predicted poorer memory, but it was also affected by the number of hot flashes during the night when a woman was sleeping. The researchers recommend treating women for their vasomotor symptoms.
An extended interview as MP3 audio file is at https://blackboard.uic.edu/bbcswebdav/institution/web/news/podcasts/PdCs...
[1128] Maki, P. M., Drogos L. L., Rubin L. H., Banuvar S., Shulman L. P., & Geller S. E.
(2008).  Objective hot flashes are negatively related to verbal memory performance in midlife women.
Menopause (New York, N.Y.). 15(5), 848 - 856.
http://www.eurekalert.org/pub_releases/2008-06/uoia-hfu061608.php

Memory problems at menopause

Findings from a study of 24 women approaching menopause have confirmed an earlier study involving over 800 women that found such women are no more likely than anyone else to suffer from memory retrieval problems. However, they did find that the women who complained more about problems with forgetfulness had a harder time learning or "encoding" new information, although they didn’t have actually have an impaired ability to learn new information. Although a larger study is needed to explore this link in more detail, the researchers suggest that stress and emotional upheaval may be responsible for attention failures that mean information isn’t encoded. The researchers did find that most of the women in their study had some sort of mood distress, including symptoms of depression or anxiety (note that this was not a random group, but women who were worried about their memory).
The study was reported at the annual meeting of the International Neuropsychological Society in Boston.
http://www.eurekalert.org/pub_releases/2006-02/uorm-mpa020206.php

Since 1996, 803 African American and white women aged 40 to 55 have been tested annually for loss of brain function. Performance was compared annually for women in premenopausal, during menopause, and postmenopausal groups. Small but significant increases in performance were found over time during the premenopausal and perimenopausal phases, leading the authors to conclude that transition through menopause is not accompanied by a decline in working memory and perceptual speed.
[1201] Meyer, P. M., Powell L. H., Wilson R. S., Everson-Rose S. A., Kravitz H. M., Luborsky J. L., et al.
(2003).  A population-based longitudinal study of cognitive functioning in the menopausal transition.
Neurology. 61(6), 801 - 806.
http://www.eurekalert.org/pub_releases/2003-09/aa-nss091803.php

Does estrogen help cognition?

For:

Hormone replacement therapy may improve visual memory of postmenopausal women
A study of 10 postmenopausal women (aged 50-60) found that those taking combined estrogen-progestin hormone therapy for four weeks showed significantly increased activity in the prefrontal cortex when engaged in a visual matching task, compared with those on placebo.
[1409] Smith, Y. R., Love T., Persad C. C., Tkaczyk A., Nichols T. E., & Zubieta J-K.
(2006).  Impact of combined estradiol and norethindrone therapy on visuospatial working memory assessed by functional magnetic resonance imaging.
The Journal of Clinical Endocrinology and Metabolism. 91(11), 4476 - 4481.
http://www.eurekalert.org/pub_releases/2006-11/uomh-hrt111606.php

Estrogen improves verbal memory in postmenopausal women

A study involving 60 postmenopausal women aged 32.8 to 64.9, found those receiving daily estrogen treatment (conjugated equine estrogens — Premarin) showed improved oral reading and verbal memory performance, compared to those receiving a placebo. This is consistent with brain imaging date indicating estrogen produces brain activations in the inferior parietal lobule, a region sensitive to phonological demands and implicated in reading.
[374] Shaywitz, S. E., Naftolin F., Zelterman D., Marchione K. E., Holahan J. M., Palter S. F., et al.
(2003).  Better oral reading and short-term memory in midlife, postmenopausal women taking estrogen.
Menopause (New York, N.Y.). 10(5), 420 - 426.
http://www.eurekalert.org/pub_releases/2003-09/yu-eis092303.php

Hormone replacement therapy may have cognitive benefits for older women

A study of more than 2,000 women 65 or older, found that those who underwent hormone replacement therapy after menopause appeared to enjoy better mental functioning. Women 85 and older did especially well. The improvements were seen only in women free from dementia. However, the sample does not reflect the general population - most of the participants were Mormon, and the prohibition of alcohol and tobacco might be a significant factor.
[213] Carlson, M. C., Zandi P. P., Plassman B. L., Tschanz JA. T., Welsh-Bohmer K. A., Steffens D. C., et al.
(2001).  Hormone replacement therapy and reduced cognitive decline in older women: The Cache County Study.
Neurology. 57(12), 2210 - 2216.
http://tinyurl.com/i87m

The positive effects of estrogen on memory

Postmenopausal women who take estrogen and young college-aged women performed more consistently on memory tests compared with postmenopausal women not taking the hormone. Consistency differs from overall memory ability and is a relatively new area in research about the neuropsychology of aging. Consistency measures memory capability on multiple administrations of the same test or on several related tests in a short period of time.
The study involved 48 postmenopausal women (aged 60 - 80), and 16 younger women (18 - 30). The older women were divided into three groups: 16 non-hormone users, 16 estrogen-users and 16 estrogen and progesterone-users. Younger women and older women taking estrogen performed more consistently than the older women not taking the hormone, as well as having higher overall memory scores. Women taking a combination of estrogen and progesterone did not perform as consistently as the estrogen-only users. This finding suggests progesterone may block some of the beneficial effects of taking estrogen alone.
Wegesin, D.J., Friedman, D., Varughese, N. & Stern, Y. 2001. Effects of estrogen-use and aging on intraindividual variability in recognition memory. Paper presented to the annual Society for Neuroscience meeting in San Diego, US.
http://www.eurekalert.org/pub_releases/2001-11/cuco-ssp111501.php

Against:

Combined hormone therapy doesn't boost memory

A study of 180 recently menopausal women found no effect of hormone therapy (a combination of estrogen and progesterone) on cognitive function. Previous research has indicated a positive benefit of estrogen on cognition, so it is speculated that progestin may counteract these positive effects.

[917] Maki, P. M., Gast M. J., Vieweg A. J., Burriss S. W., & Yaffe K.
(2007).  Hormone therapy in menopausal women with cognitive complaints: A randomized, double-blind trial.
Neurology. 69(13), 1322 - 1330.

http://www.eurekalert.org/pub_releases/2007-09/aaon-hti091807.php

Removing ovaries before menopause increases risk of cognitive impairment

A very long-running study of some 1,500 women who underwent the removal of one or both ovaries for non-cancer-related reasons, has found that women who had one or both ovaries removed before menopause were nearly two times more likely to develop cognitive problems or dementia compared to women who did not have the surgery. In addition, those women who were younger when their ovaries were removed were more likely to develop dementia than women who were older when their ovaries were removed. This finding adds to other research suggesting that there may be a critical age window for the protective effect of estrogen on the brain in women.

[1291] Rocca, W. A., Bower J. H., Maraganore D. M., Ahlskog J. E., Grossardt B. R., de Andrade M., et al.
(2007).  Increased risk of cognitive impairment or dementia in women who underwent oophorectomy before menopause.
Neurology. 69(11), 1074 - 1083.

http://www.eurekalert.org/pub_releases/2007-08/aaon-rob082107.php

Estrogen-alone hormone therapy could increase risk of dementia in older women

A new report from the Women's Health Initiative Memory Study suggests that older women using estrogen-alone hormone therapy could be at a slightly greater risk of developing dementia, including Alzheimer's disease (AD), than women who do not use any menopausal hormone therapy. Among 10,000 women using conjugated equine estrogens, 37 could be expected to develop dementia, compared to 25 in 10,000 women using the placebo. Previous reports from the Study found a greater risk with hormone therapy involving both estrogen plus progestin: among 10,000 women over age 65 using estrogen plus progestin there might be 45 cases of dementia compared to 22 cases in 10,000 older women on placebo.
It was also reported that beginning estrogen-alone hormone therapy after age 65 can have a small negative effect on overall cognitive abilities and that this negative effect may be greater in women with existing cognitive problems.
[871] Lewis, C. E., Masaki K., Coker L. H., for the Women's Health Initiative Memory Study, Shumaker S. A., Legault C., et al.
(2004).  Conjugated Equine Estrogens and Incidence of Probable Dementia and Mild Cognitive Impairment in Postmenopausal Women: Women's Health Initiative Memory Study.
JAMA. 291(24), 2947 - 2958.
[1309] Hays, J., Johnson K. C., Coker L. H., Dailey M., Bowen D., Rapp S. R., et al.
(2003).  Effect of Estrogen Plus Progestin on Global Cognitive Function in Postmenopausal Women: The Women's Health Initiative Memory Study: A Randomized Controlled Trial.
JAMA. 289(20), 2663 - 2672.
http://www.eurekalert.org/pub_releases/2004-06/nioa-eht062204.php
http://www.eurekalert.org/pub_releases/2004-06/wfub-etd061704.php

For women over 65, Combined Hormone Therapy increases risk of dementia

Much to the researchers’ surprise and disappointment, a four-year experiment involving 4,532 women at 39 medical centers, has found that combined hormone therapy (involving both estrogen and progestin) doubles the risk of Alzheimer's disease and other types of dementia in women who began the treatment at age 65 or older, although the risk is still small : for every 10,000 women 65 and older who take hormones, 23 of the predicted 45 cases of dementia a year, will be attributable to the hormones. The study also found that the combined hormone therapy produced no improvement in general cognitive function, and in fact had adverse effects on cognition among some women. This supports an earlier study suggesting that, while estrogen is helpful to cognitive function in postmenopausal women, the benefits can be cancelled out by progestin / progesterone. The study also confirmed previous research showing that the combination therapy increased the risk of stroke - previous research has indicated that risk factors for stroke are also risk factors for cognitive decline.
[918] Jackson, R. D., Morley Kotchen J., Wassertheil-Smoller S., Wactawski-Wende J., Shumaker S. A., Legault C., et al.
(2003).  Estrogen Plus Progestin and the Incidence of Dementia and Mild Cognitive Impairment in Postmenopausal Women: The Women's Health Initiative Memory Study: A Randomized Controlled Trial.
JAMA. 289(20), 2651 - 2662.
[1309] Hays, J., Johnson K. C., Coker L. H., Dailey M., Bowen D., Rapp S. R., et al.
(2003).  Effect of Estrogen Plus Progestin on Global Cognitive Function in Postmenopausal Women: The Women's Health Initiative Memory Study: A Randomized Controlled Trial.
JAMA. 289(20), 2663 - 2672.
[1194] Rossouw, J. E., Aragaki A., Safford M., Stein E., Laowattana S., Mysiw J. W., et al.
(2003).  Effect of Estrogen Plus Progestin on Stroke in Postmenopausal Women: The Women's Health Initiative: A Randomized Trial.
JAMA. 289(20), 2673 - 2684.
http://www.eurekalert.org/pub_releases/2003-05/wfub-chr052203.php

When is estrogen therapy helpful?

Cognitive benefit of estrogen minimal for the highly educated?
A mouse study sheds light on the mixed results coming from investigations into the cognitive effects of hormone replacement therapy. The study found no beneficial effect of estrogen in female mice who were raised in a stimulating environment. On the other hand, mice raised in standard conditions showed significant spatial and object memory improvement when treated with a high dose of estrogen (following removal of their ovaries). Among mice not treated with estrogen, an enriched environment alone significantly improved spatial memory. These results might help to explain why studies of hormone replacement therapy do not show beneficial effects for all women. Most studies of HRT use very well-educated women.
[1229] GRESACK, J. E., & Frick K. M.
(2004).  ENVIRONMENTAL ENRICHMENT REDUCES THE MNEMONIC AND NEURAL BENEFITS OF ESTROGEN.
Neuroscience. 128(3), 459 - 471.
http://www.eurekalert.org/pub_releases/2004-10/yu-eos102204.php

New insights into hormone therapy highlight when estrogen best aids brain

Several studies have been exploring some of the many variables that may be important in determining the effect of hormone replacement therapy.
A mouse study compared the effects of receiving daily estrogen injections (“continuous treatment”) with the effects of receiving it every four days (“cyclical treatment”). The treatment lasted three months. Ovariectomized mice receiving the continuous treatment performed better on memory tasks than those receiving cyclical treatment.
Another mouse study compared the brains of ovariectomized mice treated with continuous estrogen for 47 days with those not so treated, and found that, after five days on estrogen, estrogen-treated mice produced more of the proteins important for neuron repair and neuronal function. However, with prolonged, continuous estrogen treatment, this effect diminished, and by day 47 the estrogen-treated mice were similar to the non-estrogen-treated mice in levels of the repair proteins. Mice that did not receive estrogen showed an elevation of a brain protein associated with the negative aspects of brain aging, while estrogen-treated mice did not.
A rat study examined the effects of progesterone (a component of many hormone therapies), and found that ovariectomized rats receiving progesterone exhibited deficiencies in learning and memory, supporting the hypothesis that progesterone negatively affects memory during aging. It’s suggested that the negative outcome of several studies evaluating combined estrogen/progesterone HT may be due, in part, to unfavorable effects of progesterone.
Other rat studies have found that two established protective actions of estrogen with relevance to Alzheimer's are negatively affected by the presence of progesterone.
Another study using neurons in culture demonstrated the importance of timing. Neurons exposed to estrogen prior to exposure to beta-amyloid (the protein implicated in Alzheimers) had a significantly greater rate of survival than those exposed to estrogen after being exposed to beta-amyloid. The results are consistent with clinical studies in which women who received estrogen hormone therapy at the time of menopause, before cognitive degeneration becomes apparent, have a lower risk of developing Alzheimer's disease than women who never receive any sort of HT, while for women in their 60s and 70s, hormone therapy may make things worse.
Papers presented at the 34th Society for Neuroscience annual meeting in San Diego in late October 2004.
http://www.eurekalert.org/pub_releases/2004-10/sfn-nii102604.php

Dangers of hormone therapy

Getting the benefits of estrogen without the downside

We know estrogen helps learning and memory, but estrogen therapy also increases cancer risk. That’s why the results of a mouse study are exciting. The study found that estrogen acts through calpain, a protein crucial to learning and memory, and like adrenalin (which acts like a hormone in most of the body but as a neurotransmitter in the brain), it does so as a neurotransmitter, modulating synaptic transmission. The findings suggest drugs that target calpain directly may provide the same cognitive benefits of estrogen therapy, without the medical risks.
[299] Zadran, S., Qin Q., Bi X., Zadran H., Kim Y., Foy M. R., et al.
(2009).  17-β-Estradiol increases neuronal excitability through MAP kinase-induced calpain activation.
Proceedings of the National Academy of Sciences. 106(51), 21936 - 21941.
http://www.eurekalert.org/pub_releases/2009-12/uosc-cot120809.php

Other aids to help memory in menopausal women

Less cognitive impairment seen in women taking raloxifene

Raloxifene modulates the activity of the hormone estrogen and is one of the most widely prescribed drugs for the treatment of osteoporosis. A 3-year worldwide clinical trial involving 7705 postmenopausal women with osteoporosis found that those taking 120mg of raloxifene had a 33% less chance of developing mild cognitive impairment. There was no cognitive benefit from a 60mg dose. Note that, of the 5386 women participating in the cognitive part of this trial, only 3.4% had mild cognitive impairment, and 1% had dementia.
[757] Yaffe, K., Krueger K., Cummings S. R., Blackwell T., Henderson V. W., Sarkar S., et al.
(2005).  Effect of Raloxifene on Prevention of Dementia and Cognitive Impairment in Older Women: The Multiple Outcomes of Raloxifene Evaluation (MORE) Randomized Trial.
Am J Psychiatry. 162(4), 683 - 690.
http://www.eurekalert.org/pub_releases/2005-04/uoc--lci040605.php

The estrogen drug raloxifene may help prevent cognitive decline in women over 70

The designer estrogen drug raloxifene has been prescribed to millions of postmenopausal women for osteoporosis, but its effects on the aging brain are unclear. A new study shows that although raloxifene does not affect the cognitive performance of most women, it may help prevent decline among women older than 70 and women whose cognitive performance is declining regardless of age.
Yaffe, K. et al. 2001. Cognitive Function in Postmenopausal Women Treated with Raloxifene. New England Journal of Medicine, 344, 1207-1213.Yaffe, K. et al. 2001. Cognitive Function in Postmenopausal Women Treated with Raloxifene. New England Journal of Medicine, 344, 1207-1213.
http://www.eurekalert.org/pub_releases/2001-04/UNKN-Derm-1704101.php

Fitness counteracts cognitive decline from hormone-replacement therapy

A study of 54 postmenopausal women (aged 58 to 80) suggests that being physically fit offsets cognitive declines attributed to long-term hormone-replacement therapy. It was found that gray matter in four regions (left and right prefrontal cortex, left parahippocampal gyrus and left subgenual cortex) was progressively reduced with longer hormone treatment, with the decline beginning after more than 10 years of treatment. Therapy shorter than 10 years was associated with increased tissue volume. Higher fitness scores were also associated with greater tissue volume. Those undergoing long-term hormone therapy had more modest declines in tissue loss if their fitness level was high. Higher fitness levels were also associated with greater prefrontal white matter regions and in the genu of the corpus callosum. The findings need to be replicated with a larger sample, but are in line with animal studies finding that estrogen and exercise have similar effects: both stimulate brain-derived neurotrophic factor.
[375] Erickson, K. I., Colcombe S. J., Elavsky S., McAuley E., Korol D. L., Scalf P. E., et al.
(2007).  Interactive effects of fitness and hormone treatment on brain health in postmenopausal women.
Neurobiology of Aging. 28(2), 179 - 185.
http://www.eurekalert.org/pub_releases/2006-01/uoia-fcc012406.php

tags development: 

tags lifestyle: 

tags problems: 

Post-surgery cognitive decline

Older news items (pre-2010) brought over from the old website

Cognitive decline after noncardiac surgery

Older surgical patients at greater risk for developing cognitive problems

There’s been quite a lot of research on the effects of cardiac surgery on cognitive function, but less is known about the effects of any surgery. Now a study of more than 1000 adult patients of different ages has tested memory and cognitive function before undergoing elective non-cardiac surgery, at the time of hospital discharge, and three months after surgery. It was found that many patients, regardless of age, experienced postoperative cognitive dysfunction (POCD) at the time they left the hospital (36.6% of young adults, 30.4% of the middle-aged, 41.4% of elderly). But three months later, those aged 60 and older were more than twice as likely to exhibit POCD (12.7% compared to less than 6% for both young and middle-aged). POCD was more common among those patients with lower educational level and a history of a stroke that had left no noticeable neurologic impairment. Those with POCD at both the time of hospital discharge and three months after surgery also were more likely to die within the first year after surgery. The reason for this is unclear, but it’s speculated that patients with prolonged cognitive dysfunction might be less able to take medicines correctly or may not recognize the need to seek medical care for symptoms of complications. [1]

Cognitive decline after heart bypass

More evidence bypass surgery not responsible for cognitive impairment

A 6-year study of 326 heart patients has found no differences in brain impairment between those who had on-pump coronary artery bypass surgery (152 patients), off-pump bypass surgery patients (75 patients), and those who had drugs and arterial stents to keep their blood vessels open instead of bypass surgery (99 patients). However, all of them were found to have experienced significant cognitive decline over the six-year study period on tests of verbal memory, visual memory, visuoconstruction, language, motor speed, psychomotor speed, attention, and executive function, when compared to 69 heart-healthy people who had no known risk factors for coronary artery disease. The findings provide more evidence that it is the disease and not the surgery that causes long-term cognitive problems. [2]

Long-term cognitive decline in bypass patients not due to surgery

Another study has come out supporting the view that coronary bypass patients have no greater risk of long-term cognitive decline than patients not undergoing surgery. The study involved 152 patients who had bypass surgery and 92 patients with coronary artery disease who did not have surgical intervention. Patients had memory and other cognitive tests at the beginning of the study period, and after 3, 12, 36 and 72 months. The results showed that there were no significant differences in cognitive scores between the two groups at the beginning of the study. Both groups showed modest decline in cognitive performance during the study period, but there were no significant differences in the degree of decline between the groups after six years. It was suggested that the decline in both groups was related to the presence of risk factors for vascular disease. [3]

Inflammatory system genes linked to cognitive decline after heart surgery

The finding that people with variants of two genes involved in the inflammatory system appear to be protected from suffering a decline in mental function following heart surgery raises the possibility that therapy involving drugs known to dampen the inflammatory response may be effective in preventing cognitive decline after heart surgery. The specific genes involved were those for C-reactive protein (which plays an important role in the body’s initial response to injury) and P-selectin (which helps recruit circulating white blood cells to the site of an injury). Patients with the variation of the C-reactive protein gene were 20.6% less likely to suffer mental decline, and patients with the P-selectin variant had a 15.2% risk reduction. The risk of cognitive decline for those with both gene variants was only 17% compared to 43% for patients who had neither variant. [4]

'Off-pump' CABG surgery appears to have no benefit on cognitive or cardiac outcomes at 5 years

A five-year study of 281 cardiac patients, half of whom received off-pump coronary artery bypass surgery and half on-pump surgery, has found that there was no difference in cognitive performance five years after surgery. The findings suggest that factors other than cardiopulmonary bypass may be responsible for cognitive decline, such as anesthesia and the generalized inflammatory response that is associated with major surgical procedures. [5]

Cognitive loss following coronary artery bypass surgery due to surgical technique?

A surgical strategy designed to minimize trauma to the body's largest artery – the aorta – during heart bypass surgery can significantly reduce cognitive loss that often follows the operation. The study found that at least 60% of patients showed neurological deficits following bypass surgery, but that at 6 months, 57% of patients who had traditional surgery still had deficits while only 32% of those who didn’t use the heart-lung machine during surgery, and 30% of those who had the new surgical technique still had deficits. Researchers conclude that surgical technique is the primary cause of cognitive decline following bypass surgery. [6]

Use of heart pump during bypass surgery not implicated in cognitive decline

A study involving 380 individuals has found that those patients undergoing coronary artery bypass grafting (CABG) surgery that used a cardiopulmonary heart pump had no significant differences in their mental functions compared to CABG patients whose surgery did not involve a heart pump. Patients with coronary heart disease all performed lower on cognitive tests than healthy controls, prior to surgery. By three months, both cardiac patients who had undergone surgery (with or without use of a heart pump) and those who had not, had improved cognitive function. [7]

Review finds bypass surgery free of long-term brain effects for most

A broad retrospective review of the effects of coronary artery bypass surgery on cognitive functions concludes that, although the research confirms the existence of mild deficits in the period up to three months after surgery, the procedure itself probably does not cause late or permanent neurological effects. Rather, they argue, the late cognitive declines seen in some long-term studies are for most people likely associated with progression of underlying conditions such as cerebrovascular disease. However, this is not true for all. The exceptions might include older patients and those with risk factors for cerebrovascular disease or a history of stroke. [8]

Elderly experience long-term cognitive decline after surgery

Researchers have found that two years after major non-cardiac surgery, 42% of elderly patients will have experienced a measurable cognitive decline. 59% of patients experienced cognitive decline immediately after surgery — these are the ones at greatest risk of long-term decline. Three months after surgery, 34% of patients had cognitive declines. The study involved 354 patients, with an average age of 69.5 years. [9]

Lower temperatures improve outcomes after bypass surgery

One of the possible adverse effects of cardiac bypass surgery is cognitive decline. Researchers have found that patients who were allowed an additional 10 to 12 minutes to return to normal body temperature after surgery scored almost one-third better on standard tests of cognition six weeks after surgery. (In order to protect the brain and other organs from damage while the heart is stopped during surgery, physicians cool a patient's blood as it passes through a heart-lung machine. However, toward the end of the operation, this blood needs to be rewarmed.) [10]

Cognitive decline after bypass surgery appears more transient than feared

Recent studies have found a high occurrence of cognitive problems in patients who undergo coronary artery bypass surgery, with such problems still found six weeks after surgery. In a new study comparing 140 patients who underwent bypass surgery and a second group of 92 coronary artery disease patients who did not have surgery, no differences in cognitive abilities were found when patients were re-tested at three and 12 months. This supports recent research suggesting that it is the disease itself that is the major problem, rather than the surgery. [11]

Lowered immunity puts older coronary bypass patients at higher risk for cognitive decline

Older patients with lowered immunity to certain common bacteria found in the gastrointestinal tract are more likely than younger patients to suffer cognitive decline after coronary artery bypass surgery. [12]

Cognitive impairment following bypass surgery may last longer than thought

More support for a link between cardiopulmonary bypass surgery and cognitive impairment comes from a new study. In particular, it seems, that attention may be most affected. The study also found evidence of longer-lasting cognitive decline than previously thought. Bypass patients also demonstrated poorer cognitive performance before the surgery, and it is now being suggested that it may be the disease itself that is the major problem, rather than the surgery itself. This is consistent with recent research connecting cardiovascular risk factors with risk factors for cognitive decline. [13]

Fever immediately after heart bypass surgery associated with cognitive decline

Elevated temperatures within 8-10 hours after surgery are often seen in patients who have undergone coronary bypass surgery. This has not however been regarded as anything other than a nuisance. Many bypass patients also suffer measurable cognitive decline. A new study reports on a relationship between these fevers and cognitive decline six weeks following surgery. Patients who suffered the highest post-operative temperatures also suffered the highest amount of cognitive decline. [14]

More on implications of having the Alzheimer's gene

Researchers have found an association between nerve cell changes associated with aging and the presence of a variation of the apolipoprotein gene known as apolipoprotein E4 (APOE4). This form is carried by approximately 25% of the population and has been linked to increased risk of Alzheimer's disease, cardiovascular disease and memory loss after head injury or bypass surgery. [15]

Frequency of cognitive decline after bypass surgery>

Heart bypasses are becoming increasingly common - in the U.S., more than half a million people undergo coronary-artery bypass grafting (CABG) each year. A common side-effect of the procedure is postoperative cognitive decline (frequency of occurrence estimates range from 33% to 82%, depending on the method of evaluation used). A recent study looked at the longer-term picture: in this study, cognitive decline was found in 53% of the patients at time of discharge; at 6 weeks, the rate was assessed at 36%; at 6 months, 24%. However, five years after the surgery the rate of cognitive decline was 42%. Older age, a lower level of education, a higher preoperative score for cognitive function, and the presence of cognitive decline at discharge were all predictors of cognitive decline at 5 years after CABG. Of these, the most significant predictor was a decline in cognition seen at discharge.
Note that there was no control group, so these results must be treated with caution. Note also that short-term declines in cognitive function are also reported in elderly subjects after non-cardiac surgery, and this can persist in a proportion of these patients - in fact, in 10% after 2 years. [16]

1.Monk, T.G. et al. 2008. Predictors of Cognitive Dysfunction after Major Noncardiac Surgery. Anesthesiology, 108(1), 18-30.
Price, C.C.; Garvan, C.W. & Monk, T.G. 2008. Type and Severity of Cognitive Decline in Older Adults after Noncardiac Surgery. Anesthesiology, 108(1), 8-17. Press release

2.Selnes, O.A. et al. 2009. Do Management Strategies for Coronary Artery Disease Influence 6-Year Cognitive Outcomes? Annals of Thoracic Surgery, 88, 445-454. Press release

3.Selnes, O.A. et al. 2008. Cognition 6 Years After Surgical or Medical Therapy for Coronary Artery Disease. Annals of Neurology, 63, 581-590. Press release Press release

4.Mathew, J.P. et al. 2007. Genetic Variants in P-Selectin and C-Reactive Protein Influence Susceptibility to Cognitive Decline After Cardiac Surgery. Journal of the American College of Cardiology, 49, 1934 - 1942. Press release

5.van Dijk, D. et al. 2007. Cognitive and Cardiac Outcomes 5 Years After Off-Pump vs On-Pump Coronary Artery Bypass Graft Surgery. JAMA, 297, 701-708. Press release

6.Hammon, J.W., Stump, D.A., Butterworth, J.F., Moody, D.M., Rorie, K., Deal, D.D., Kincaid, E.H., Oaks, T.E. & Kon, N.D. 2006. Single crossclamp improves 6-month cognitive outcome in high-risk coronary bypass patients: The effect of reduced aortic manipulation.The Journal of Thoracic and Cardiovascular Surgery, 131 (1), 114-121. Press release

7.McKhann, G.M., Grega, M.A., Borowicz, L.M.Jr, Bailey, M.M., Barry, S.J.E., Zeger, S.L., Baumgartner, W.A. & Selnes, O.A. 2005. Is there cognitive decline 1 year after CABG?: Comparison with surgical and nonsurgical controls. Neurology, 65, 991-999. Press release

8.Selnes, O.A. & McKhann, G.M. 2005. Neurocognitive Complications after Coronary Artery Bypass Surgery. Annals of Neurology, Published Online: April 25, 2005 (DOI: 10.1002/ana.20481) Press release

9.Monk, T. et al. 2004. Paper presented October 26 at the annual scientific sessions of the American Society of Anesthesiologists in Las Vegas. Press release

10.Grocott, H. et al. 2004. Paper presented April 26 at the annual scientific sessions of the Society of Cardiovascular Anesthesiologists. Press release

11.Selnes, O.A., Grega, M.A., Borowicz, L.M. Jr , Royall, R.M., McKhann, G.M. & Baumgartner, W.A. 2003. Cognitive changes with coronary artery disease: a prospective study of coronary artery bypass graft patients and nonsurgical controls. The Annals of Thoracic Surgery, 75 (5), 1377-1386. Press release

12.Mathew, J.P., Grocott, H.P., Phillips-Bute, B., Stafford-Smith, M., Laskowitz, D.T., Rossignol, D., Blumenthal, J.A. & Newman, M.F. 2003. Lower Endotoxin Immunity Predicts Increased Cognitive Dysfunction in Elderly Patients After Cardiac Surgery. Stroke, 34, 508. Press release

13.Keith, J.R., Puente, A.E., Malcolmson, K.L., Tartt, S., Coleman, A.E. & Marks, H.F. Jr. 2002. Assessing Postoperative Cognitive Change After Cardiopulmonary Bypass Surgery. Neuropsychology, 16(3), 411-21. Press release

14.Grocott, H.P., Mackensen, G.B., Grogore, A.M., Mathew, J., Reves, J.G., Phillips-Bute, B., Smith, P.K. & Newman, M.F. 2002. Postoperative Hyperthermia Is Associated With Cognitive Dysfunction After Coronary Artery Bypass Graft Surgery. Stroke, 33, 537-541. Press release

15.Doraiswamy, P.M. et al. 2002. Paper presented February 25 at the 15th annual meeting of the American Association for Geriatric Psychiatry in Orlando, Fla. Press release

16.Newman, M. F., Kirchner, J. L., Phillips-Bute, B., Gaver, V., Grocott, H., Jones, R. H., Mark, D. B., et al. (2001). Longitudinal Assessment of Neurocognitive Function after Coronary-Artery Bypass Surgery. N Engl J Med, 344(6), 395-402. Press release

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Long-term meditation fights age-related cognitive decline

August, 2011

Another study adds to the weight of evidence that meditating has cognitive benefits. The latest finding points to brain-wide improvements in connectivity.

Following on from research showing that long-term meditation is associated with gray matter increases across the brain, an imaging study involving 27 long-term meditators (average age 52) and 27 controls (matched by age and sex) has revealed pronounced differences in white-matter connectivity between their brains.

The differences reflect white-matter tracts in the meditators’ brains being more numerous, more dense, more myelinated, or more coherent in orientation (unfortunately the technology does not yet allow us to disentangle these) — thus, better able to quickly relay electrical signals.

While the differences were evident among major pathways throughout the brain, the greatest differences were seen within the temporal part of the superior longitudinal fasciculus (bundles of neurons connecting the front and the back of the cerebrum) in the left hemisphere; the corticospinal tract (a collection of axons that travel between the cerebral cortex of the brain and the spinal cord), and the uncinate fasciculus (connecting parts of the limbic system, such as the hippocampus and amygdala, with the frontal cortex) in both hemispheres.

These findings are consistent with the regions in which gray matter increases have been found. For example, the tSLF connects with the caudal area of the temporal lobe, the inferior temporal gyrus, and the superior temporal gyrus; the UNC connects the orbitofrontal cortex with the amygdala and hippocampal gyrus

It’s possible, of course, that those who are drawn to meditation, or who are likely to engage in it long term, have fundamentally different brains from other people. However, it is more likely (and more consistent with research showing the short-term effects of meditation) that the practice of meditation changes the brain.

The precise mechanism whereby meditation might have these effects can only be speculated. However, more broadly, we can say that meditation might induce physical changes in the brain, or it might be protecting against age-related reduction. Most likely of all, perhaps, both processes might be going on, perhaps in different regions or networks.

Regardless of the mechanism, the evidence that meditation has cognitive benefits is steadily accumulating.

The number of years the meditators had practiced ranged from 5 to 46. They reported a number of different meditation styles, including Shamatha, Vipassana and Zazen.

Reference: 

[2343] Luders, E., Clark K., Narr K. L., & Toga A. W.
(2011).  Enhanced brain connectivity in long-term meditation practitioners.
NeuroImage. 57(4), 1308 - 1316.

Source: 

http://medicalxpress.com/news/2011-07-meditation-push-up-brain.html

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Moderate to intense exercise may protect the brain in old age

August, 2011
  • Moderate but not light exercise was found to help protect the brain from brain infarcts in some older adults, but not all.

Another study showing the value of exercise for preserving your mental faculties in old age. This time it has to do with the development of small brain lesions or infarcts called "silent strokes." Don’t let the words “small” and “silent” fool you — these lesions have been linked to memory problems and even dementia, as well as stroke, an increased risk of falls and impaired mobility.

The study involved 1,238 people taken from the Northern Manhattan Study, a long-running study looking at stroke and vascular problems in a diverse community. Their brains were scanned some six years after completing an exercise questionnaire, when they were an average of 70 years old. The scans found that 16% of the participants had these small brain lesions.

Those who had reported engaging in moderate to intense exercise were 40% less likely to have these infarcts compared to people who did no regular exercise. Depressingly, there was no significant difference between those who engaged in light exercise and those who didn’t exercise (which is not to say that light exercise doesn’t help in other regards! a number of studies have pointed to the value of regular brisk walking for fighting cognitive decline). This is consistent with earlier findings that only the higher levels of activity consistently protect against stroke.

The results remained the same after other vascular risk factors such as high blood pressure, high cholesterol and smoking, were accounted for. Of the participants, 43% reported no regular exercise; 36% engaged in regular light exercise (e.g., golf, walking, bowling or dancing); 21% engaged in regular moderate to intense exercise (e.g., hiking, tennis, swimming, biking, jogging or racquetball).

However, there was no association with white matter lesions, which have also been associated with an increased risk of stroke and dementia.

Moreover, this effect was not seen among those with Medicaid or no health insurance, suggesting that lower socioeconomic status (or perhaps poorer access to health care) is associated with negative factors that counteract the benefits of exercise. Previous research has found that lower SES is associated with higher cardiovascular disease regardless of access to care.

Of the participants, 65% were Hispanic, 17% non-Hispanic black, and 15% non-Hispanic white. Over half (53%) had less than high school education, and 47% were on Medicaid or had no health insurance.

Reference: 

[2350] Willey, J. Z., Moon Y. P., Paik M. C., Yoshita M., DeCarli C., Sacco R. L., et al.
(2011).  Lower prevalence of silent brain infarcts in the physically active.
Neurology. 76(24), 2112 - 2118.

Full text available at http://www.natap.org/2011/HIV/NeurWNL013e31821f4472.pdf

Source: 

http://www.eurekalert.org/pub_releases/2011-06/aaon-mti060111.php

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Why our brains produce fewer new neurons in old age

August, 2011

New research explains why fewer new brain cells are created in the hippocampus as we get older.

It wasn’t so long ago we believed that only young brains could make neurons, that once a brain was fully matured all it could do was increase its connections. Then we found out adult brains could make new neurons too (but only in a couple of regions, albeit critical ones). Now we know that neurogenesis in the hippocampus is vital for some operations, and that the production of new neurons declines with age (leading to the idea that the reduction in neurogenesis may be one reason for age-related cognitive decline).

What we didn’t know is why this happens. A new study, using mice genetically engineered so that different classes of brain cells light up in different colors, has now revealed the life cycle of stem cells in the brain.

Adult stem cells differentiate into progenitor cells that ultimately give rise to mature neurons. It had been thought that the stem cell population remained stable, but that these stem cells gradually lose their ability to produce neurons. However, the mouse study reveals that during the mouse's life span, the number of brain stem cells decreased 100-fold. Although the rate of this decrease actually slows with age, and the output per cell (the number of progenitor cells each stem cell produces) increases, nevertheless the pool of stem cells is dramatically reduced over time.

The reason this happens (and why it wasn’t what we expected) is explained in a computational model developed from the data. It seems that stem cells in the brain differ from other stem cells. Adult stem cells in the brain wait patiently for a long time until they are activated. They then undergo a series of rapid divisions that give rise to progeny that differentiate into neurons, before ‘retiring’ to become astrocytes. What this means is that, unlike blood or gut stem cells (that renew themselves many times), brain stem cells are only used once.

This raises a somewhat worrying question: if we encourage neurogenesis (e.g. by exercise or drugs), are we simply using up stem cells prematurely? The researchers suggest the answer depends on how the neurogenesis has been induced. Parkinson's disease and traumatic brain injury, for example, activate stem cells directly, and so may reduce the stem cell population. However, interventions such as exercise stimulate the progenitor cells, not the stem cells themselves.

Reference: 

[2339] Encinas, J M., Michurina T V., Peunova N., Park J-H., Tordo J., Peterson D A., et al.
(2011).  Division-Coupled Astrocytic Differentiation and Age-Related Depletion of Neural Stem Cells in the Adult Hippocampus.
Cell Stem Cell. 8(5), 566 - 579.

Source: 

http://www.eurekalert.org/pub_releases/2011-05/cshl-scc050411.php

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Religious factors may influence brain shrinkage in old age

July, 2011
  • An intriguing new study suggests life-changing religious experiences may result in greater brain shrinkage in old age.

The brain tends to shrink with age, with different regions being more affected than others. Atrophy of the hippocampus, so vital for memory and learning, is associated with increased risk of developing Alzheimer’s, and has also been linked to depression.

In a study involving 268 older adults (58+), the hippocampus of those reporting a life-changing religious experience was found to be shrinking significantly more compared to those not reporting such an experience. Significantly greater hippocampal atrophy was also found among born-again Protestants, Catholics, and those with no religious affiliation, compared with Protestants not identifying as born-again.

The participants are not a general sample — they were originally recruited for the NeuroCognitive Outcomes of Depression in the Elderly. However, some of the participants were from the control group, who had no history of depression. Brain scans were taken at the beginning of the study, and then every two years. The length of time between the baseline scan and the final scan ranged from 2 to 8 years (average was 4).

Questions about religious experiences were asked in an annual survey, so could change over time. Two-thirds of the group was female, and 87% were white. The average age was 68. At baseline, 42% of the group was non-born-again Protestant, 36% born-again Protestant; 8% Catholic; 6% other religion. Only 7% reported themselves as having no religion. By the end of the study, 44% (119 participants) reported themselves born-again, and 13% (36) reported having had life-changing religious experiences.

These associations persisted after depression status, acute stress, and social support were taken into account. Nor did other religious factors (such as prayer, meditation, or Bible study) account for the changes.

It is still possible that long-term stress might play a part in this association — the study measured acute rather than cumulative stress. The researchers suggest that life-changing religious experiences can be stressful, if they don’t fit in with your existing beliefs or those of your family and friends, or if they lead to new social systems that add to your stress.

Of course, the present results can be interpreted in several ways — is it the life-changing religious experience itself that is the crucial factor? Or the factors leading up to that experience? Or the consequences of that experience? Still, it’s certainly an intriguing finding, and it will be interesting to see more research expanding and confirming (or not!) this result.

More generally, the findings may help clarify the conflicting research about the effects of religion on well-being, by pointing to the fact that religion can’t be considered a single factor, but one subject to different variables, some of which may be positive and others not.

Reference: 

[2296] Owen, A. D., Hayward D. R., Koenig H. G., Steffens D. C., & Payne M. E.
(2011).  Religious Factors and Hippocampal Atrophy in Late Life.
PLoS ONE. 6(3), e17006 - e17006.

Full text at http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0017006
 

Source: 

http://medicalxpress.com/news/2011-05-religious-factors-brain.html http://www.scientificamerican.com/article.cfm?id=religious-experiences-s...

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Childhood musical training helps auditory processing in old age

June, 2011

Another study confirms the cognitive benefits of extensive musical training that begins in childhood, at least for hearing.

A number of studies have demonstrated the cognitive benefits of music training for children. Now research is beginning to explore just how long those benefits last. This is the second study I’ve reported on this month, that points to childhood music training protecting older adults from aspects of cognitive decline. In this study, 37 adults aged 45 to 65, of whom 18 were classified as musicians, were tested on their auditory and visual working memory, and their ability to hear speech in noise.

The musicians performed significantly better than the non-musicians at distinguishing speech in noise, and on the auditory temporal acuity and working memory tasks. There was no difference between the groups on the visual working memory task.

Difficulty hearing speech in noise is among the most common complaints of older adults, but age-related hearing loss only partially accounts for the problem.

The musicians had all begun playing an instrument by age 8 and had consistently played an instrument throughout their lives. Those classified as non-musicians had no musical experience (12 of the 19) or less than three years at any point in their lives. The seven with some musical experience rated their proficiency on an instrument at less than 1.5 on a 10-point scale, compared to at least 8 for the musicians.

Physical activity levels were also assessed. There was no significant difference between the groups.

The finding that visual working memory was not affected supports the idea that musical training helps domain-specific skills (such as auditory and language processing) rather than general ones.

Reference: 

[2299] Parbery-Clark, A., Strait D. L., Anderson S., Hittner E., & Kraus N.
(2011).  Musical Experience and the Aging Auditory System: Implications for Cognitive Abilities and Hearing Speech in Noise.
PLoS ONE. 6(5), e18082 - e18082.

Source: 

http://www.eurekalert.org/pub_releases/2011-05/nu-meo050611.php Full text at http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0018082

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Why it gets harder to remember as we get older

June, 2011

A new study finds that older adults have more difficulty in recognizing new information as ‘new’, and this is linked to degradation of the path leading into the hippocampus.

As we get older, when we suffer memory problems, we often laughingly talk about our brain being ‘full up’, with no room for more information. A new study suggests that in some sense (but not the direct one!) that’s true.

To make new memories, we need to recognize that they are new memories. That means we need to be able to distinguish between events, or objects, or people. We need to distinguish between them and representations already in our database.

We are all familiar with the experience of wondering if we’ve done something. Is it that we remember ourselves doing it today, or are we remembering a previous occasion? We go looking for the car in the wrong place because the memory of an earlier occasion has taken precedence over today’s event. As we age, we do get much more of this interference from older memories.

In a new study, the brains of 40 college students and older adults (60-80) were scanned while they viewed pictures of everyday objects and classified them as either "indoor" or "outdoor." Some of the pictures were similar but not identical, and others were very different. It was found that while the hippocampus of young students treated all the similar pictures as new, the hippocampus of older adults had more difficulty with this, requiring much more distinctiveness for a picture to be classified as new.

Later, the participants were presented with completely new pictures to classify, and then, only a few minutes later, shown another set of pictures and asked whether each item was "old," "new" or "similar." Older adults tended to have fewer 'similar' responses and more 'old' responses instead, indicating that they could not distinguish between similar items.

The inability to recognize information as "similar" to something seen recently is associated with “representational rigidity” in two areas of the hippocampus: the dentate gyrus and CA3 region. The brain scans from this study confirm this, and find that this rigidity is associated with changes in the dendrites of neurons in the dentate/CA3 areas, and impaired integrity of the perforant pathway — the main input path into the hippocampus, from the entorhinal cortex. The more degraded the pathway, the less likely the hippocampus is to store similar memories as distinct from old memories.

Apart from helping us understand the mechanisms of age-related cognitive decline, the findings also have implications for the treatment of Alzheimer’s. The hippocampus is one of the first brain regions to be affected by the disease. The researchers plan to conduct clinical trials in early Alzheimer's disease patients to investigate the effect of a drug on hippocampal function and pathway integrity.

Reference: 

[2304] Yassa, M. A., Mattfeld A. T., Stark S. M., & Stark C. E. L.
(2011).  Age-related memory deficits linked to circuit-specific disruptions in the hippocampus.
Proceedings of the National Academy of Sciences.

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http://medicalxpress.com/news/2011-05-tougher.html

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Discovery of more risky genes reveals more about the paths to Alzheimer’s

June, 2011

New genetic studies implicate myelin development, the immune system, inflammation, and lipid metabolism as critical pathways in the development of Alzheimer’s.

I commonly refer to ApoE4 as the ‘Alzheimer’s gene’, because it is the main genetic risk factor, tripling the risk for getting Alzheimer's. But it is not the only risky gene.

A mammoth genetic study has identified four new genes linked to late-onset Alzheimer's disease. The new genes are involved in inflammatory processes, lipid metabolism, and the movement of molecules within cells, pointing to three new pathways that are critically related to the disease.

Genetic analysis of more than 11,000 people with Alzheimer's and a nearly equal number of healthy older adults, plus additional data from another 32,000, has identified MS4A, CD2AP, CD33, and EPHA1 genes linked to Alzheimer’s risk, and confirmed two other genes, BIN1 and ABCA7.

A second meta-analysis of genetic data has also found another location within the MS4A gene cluster which is associated with Alzheimer's disease. Several of the 16 genes within the cluster are implicated in the activities of the immune system and are probably involved in allergies and autoimmune disease. The finding adds to evidence for a role of the immune system in the development of Alzheimer's.

Another study adds to our understanding of how one of the earlier-known gene factors works. A variant of the clusterin gene is known to increase the risk of Alzheimer’s by 16%. But unlike the ApoE4 gene, we didn’t know how, because we didn’t know what the CLU gene did. A new study has now found that the most common form of the gene, the C-allele, impairs the development of myelin.

The study involved 398 healthy adults in their twenties. Those carrying the CLU-C gene had poorer white-matter integrity in multiple brain regions. The finding is consistent with increasing evidence that degeneration of myelin in white-matter tracts is a key component of Alzheimer’s and another possible pathway to the disease. But this gene is damaging your brain (in ways only detectible on a brain scan) a good 50 years before any clinical symptoms are evident.

Moreover, this allele is present in 88% of Caucasians. So you could say it’s not so much that this gene variant is increasing your risk, as that having the other allele (T) is protective.

Reference: 

[2257] Naj, A. C., Jun G., Beecham G. W., Wang L-S., Vardarajan B. N., Buros J., et al.
(2011).  Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease.
Nat Genet. 43(5), 436 - 441.

Antunez, C. et al. 2011. The membrane-spanning 4-domains, subfamily A (MS4A) gene cluster contains a common variant associated with Alzheimer's disease. Genome Medicine,  3:33 doi:10.1186/gm249
Full text available at http://genomemedicine.com/content/3/5/33/abstract

[2254] Braskie, M. N., Jahanshad N., Stein J. L., Barysheva M., McMahon K. L., de Zubicaray G. I., et al.
(2011).  Common Alzheimer's Disease Risk Variant Within the CLU Gene Affects White Matter Microstructure in Young Adults.
The Journal of Neuroscience. 31(18), 6764 - 6770.

Source: 

http://www.eurekalert.org/pub_releases/2011-04/cumc-adc040111.php
http://www.eurekalert.org/pub_releases/2011-05/bc-aio052711.php
http://esciencenews.com/articles/2011/05/13/alzheimers.risk.gene.disrupt...

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Alzheimer's diagnostic guidelines updated

June, 2011
  • Updated clinical guidelines now cover three distinct stages of Alzheimer's disease.

For the first time in 27 years, clinical diagnostic criteria for Alzheimer's disease dementia have been revised, and research guidelines updated. They mark a major change in how experts think about and study Alzheimer's disease.

The updated guidelines now cover three distinct stages of Alzheimer's disease:

  • Preclinical – is currently relevant only for research. It describes the use of biomarkers that may precede the development of Alzheimer’s.
  • Mild Cognitive Impairment– Current biomarkers include elevated levels of tau or decreased levels of beta-amyloid in the cerebrospinal fluid, reduced glucose uptake in the brain, and atrophy of certain brain regions. Primarily for researchers, these may be used in specialized clinical settings.
  • Alzheimer's Dementia – Criteria outline ways clinicians should approach evaluating causes and progression of cognitive decline, and expand the concept of Alzheimer's dementia beyond memory loss to other aspects of cognition, such as word-finding, vision/spatial issues, and impaired reasoning or judgment.

The criteria are available at http://www.alzheimersanddementia.org/content/ncg

Source: 

http://www.eurekalert.org/pub_releases/2011-04/nioa-adg041511.php

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