Aging

Why learning gets harder as we get older

February, 2013

A mouse study shows that weakening unwanted or out-of-date connections is as important as making new connections, and that neurological changes as we age reduces our ability to weaken old connections.

A new study adds more support to the idea that the increasing difficulty in learning new information and skills that most of us experience as we age is not down to any difficulty in acquiring new information, but rests on the interference from all the old information.

Memory is about strengthening some connections and weakening others. A vital player in this process of synaptic plasticity is the NMDA receptor in the hippocampus. This glutamate receptor has two subunits (NR2A and NR2B), whose ratio changes as the brain develops. Children have higher ratios of NR2B, which lengthens the time neurons talk to each other, enabling them to make stronger connections, thus optimizing learning. After puberty, the ratio shifts, so there is more NR2A.

Of course, there are many other changes in the aging brain, so it’s been difficult to disentangle the effects of this changing ratio from other changes. This new study genetically modified mice to have more NR2A and less NR2B (reflecting the ratio typical of older humans), thus avoiding the other confounds.

To the researchers’ surprise, the mice were found to be still good at making strong connections (‘long-term potentiation’ - LTP), but instead had an impaired ability to weaken existing connections (‘long-term depression’ - LTD). This produces too much noise (bear in mind that each neuron averages 3,000 potential points of contact (i.e., synapses), and you will see the importance of turning down the noise!).

Interestingly, LTD responses were only abolished within a particular frequency range (3-5 Hz), and didn’t affect 1Hz-induced LTD (or 100Hz-induced LTP). Moreover, while the mice showed impaired long-term learning, their short-term memory was unaffected. The researchers suggest that these particular LTD responses are critical for ‘post-learning information sculpting’, which they suggest is a step (hitherto unknown) in the consolidation process. This step, they postulate, involves modifying the new information to fit in with existing networks of knowledge.

Previous work by these researchers has found that mice genetically modified to have an excess of NR2B became ‘super-learners’. Until now, the emphasis in learning and memory has always been on long-term potentiation, and the role (if any) of long-term depression has been much less clear. These results point to the importance of both these processes in sculpting learning and memory.

The findings also seem to fit in with the idea that a major cause of age-related cognitive decline is the failure to inhibit unwanted information, and confirm the importance of keeping your mind actively engaged and learning, because this ratio is also affected by experience.

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Hearing loss accelerates cognitive decline in older adults

February, 2013

A large study finds that hearing loss significantly increases the rate of cognitive decline in old age.

I’ve written before about the gathering evidence that sensory impairment, visual impairment and hearing loss in particular, is a risk factor for age-related cognitive decline and dementia. Now a large long-running study provides more support for the association between hearing loss and age-related cognitive decline.

The study involved 1,984 older adults (aged 75-84) whose hearing and cognition was tested at the start of the study, with cognitive performance again assessed three, five, and six years later.

Those with hearing loss showed significantly faster cognitive decline than those with normal hearing — some 30-40% faster (41% on the MMSE; 32% on the Digit Symbol Substitution Test), with rate directly related to the amount of hearing loss.

On average, older adults with hearing loss developed significant cognitive impairment 3.2 years sooner than those with normal hearing — a very significant difference indeed.

It has been suggested that increasing social isolation and loneliness may underlie some, if not all, of this association. It may also be that difficulties in hearing force the brain to devote too much of its resources to processing sound, leaving less for cognition. A third possibility is that some common factor underlies both hearing loss and cognitive decline — however, the obvious risk factors, such as high blood pressure, diabetes and stroke, were taken account of in the analysis.

The findings emphasize the importance of getting help for hearing difficulties, rather than regarding them as ‘natural’ in old age.

Reference: 

[3293] Lin, F. R., Yaffe K., Xia J., & et al
(2013).  Hearing loss and cognitive decline in older adults.
JAMA Internal Medicine. 1 - 7.

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Menopause forgetfulness greatest early in postmenopause

January, 2013

A smallish study suggests that the cognitive effects of menopause are greatest in the first year after menopause.

Being a woman of a certain age, I generally take notice of research into the effects of menopause on cognition. A new study adds weight, perhaps, to the idea that cognitive complaints in perimenopause and menopause are not directly a consequence of hormonal changes, but more particularly, shows that early post menopause may be the most problematic time.

The study followed 117 women from four stages of life: late reproductive, early and late menopausal transition, and early postmenopause. The late reproductive period is defined as when women first begin to notice subtle changes in their menstrual periods, but still have regular menstrual cycles. Women in the transitional stage (which can last for several years) experience fluctuation in menstrual cycles, and hormone levels begin to fluctuate significantly.

Women in the early stage of post menopause (first year after menopause), as a group, were found to perform more poorly on measures of verbal learning, verbal memory, and fine motor skill than women in the late reproductive and late transition stages. They also performed significantly worse than women in the late menopausal transition stage on attention/working memory tasks.

Surprisingly, self-reported symptoms such as sleep difficulties, depression, and anxiety did not predict memory problems. Neither were the problems correlated with hormone levels (although fluctuations could be a factor).

This seemingly contradicts earlier findings from the same researchers, who in a slightly smaller study found that those experiencing poorer working memory and attention were more likely to have poorer sleep, depression, and anxiety. That study, however, only involved women approaching and in menopause. Moreover, these aspects were not included in the abstract of the paper but only in the press release, and because I don’t have access to this particular journal, I cannot say whether there is something in the data that explains this. Because of this, I am not inclined to put too much weight on this point.

But we may perhaps take the findings as support for the view that cognitive problems experienced earlier in the menopause cycle are, when they occur, not a direct result of hormonal changes.

The important result of this study is the finding that the cognitive problems often experienced by women in their 40s and 50s are most acute during the early period of post menopause, and the indication that the causes and manifestations are different at different stages of menopause.

It should be noted, however, that there were only 14 women in the early postmenopause stage. So, we shouldn’t put too much weight on any of this. Nevertheless, it does add to the picture research is building up about the effects of menopause on women’s cognition.

While the researchers said that this effect is probably temporary — which was picked up as the headline in most media — this was not in fact investigated in this study. It would be nice to have some comparison with those, say, two or three and five years post menopause (but quite possibly this will be reported in a later paper).

Reference: 

[3237] Weber, M. T., Rubin L. H., & Maki P. M.
(2013).  Cognition in perimenopause.
Menopause: The Journal of The North American Menopause Society.

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Dopamine decline underlies episodic memory decline in old age

December, 2012

Findings supporting dopamine’s role in long-term episodic memory point to a decline in dopamine levels as part of the reason for cognitive decline in old age, and perhaps in Alzheimer’s.

The neurotransmitter dopamine is found throughout the brain and has been implicated in a number of cognitive processes, including memory. It is well-known, of course, that Parkinson's disease is characterized by low levels of dopamine, and is treated by raising dopamine levels.

A new study of older adults has now demonstrated the effect of dopamine on episodic memory. In the study, participants (aged 65-75) were shown black and white photos of indoor scenes and landscapes. The subsequent recognition test presented them with these photos mixed in with new ones, and required them to note which photos they had seen before. Half of the participants were first given Levodopa (‘L-dopa’), and half a placebo.

Recognition tests were given two and six hours after being shown the photos. There was no difference between the groups at the two-hour test, but at the six-hour test, those given L-dopa recognized up to 20% more photos than controls.

The failure to find a difference at the two-hour test was expected, if dopamine’s role is to help strengthen the memory code for long-term storage, which occurs after 4-6 hours.

Individual differences indicated that the ratio between the amount of Levodopa taken and body weight is key for an optimally effective dose.

The findings therefore suggest that at least part of the reason for the decline in episodic memory typically seen in older adults is caused by declining levels of dopamine.

Given that episodic memory is one of the first and greatest types of memory hit by Alzheimer’s, this finding also has implications for Alzheimer’s treatment.

Caffeine improves recognition of positive words

Another recent study also demonstrates, rather more obliquely, the benefits of dopamine. In this study, 200 mg of caffeine (equivalent to 2-3 cups of coffee), taken 30 minutes earlier by healthy young adults, was found to improve recognition of positive words, but had no effect on the processing of emotionally neutral or negative words. Positive words are consistently processed faster and more accurately than negative and neutral words.

Because caffeine is linked to an increase in dopamine transmission (an indirect effect, stemming from caffeine’s inhibitory effect on adenosine receptors), the researchers suggest that this effect of caffeine on positive words demonstrates that the processing advantage enjoyed by positive words is driven by the involvement of the dopaminergic system.

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Old honeybees can regain youthful cognition when they return to youthful duties

August, 2012

A honey bee study shows how old foraging bees quickly start to decline cognitively, and how this can be reversed in some if they return to more social domestic duties in the hive.

I often talk about the importance of attitudes and beliefs for memory and cognition. A new honey bee study provides support for this in relation to the effects of aging on the brain, and suggests that this principle extends across the animal kingdom.

Previous research has shown that bees that stay in the nest and take care of the young remain mentally competent, but they don’t nurse for ever. When they’re older (after about 2-3 weeks), they become foragers, and foraging bees age very quickly — both physically and mentally. Obviously, you would think, bees ‘retire’ to foraging, and their old age is brief (they begin to show cognitive decline after just two weeks).

But it’s not as simple as that, because in artificial hives where worker bees are all the same age, nurse bees of the same age as foragers don’t show the same cognitive and sensory decline. Moreover, nurse bees have been found to maintain their cognitive abilities for more than 100 days, while foragers die within 18 days and show cognitive declines after 13-15 days (although their ability to assess sweetness remains intact).

The researchers accordingly asked a very interesting question: what happens if the foragers return to babysitting?

To achieve this, they removed all of the younger nurse bees from the nest, leaving only the queen and babies. When the older, foraging bees returned to the nest, activity slowed down for several days, and then they re-organized themselves: some of the old bees returned to foraging; others took on the babysitting and housekeeping duties (cleaning, building the comb, and tending to the queen). After 10 days, around half of these latter bees had significantly improved their ability to learn new things.

This cognitive improvement was also associated with a change in two specific proteins in their brains: one that has been associated with protection against oxidative stress and inflammation associated with Alzheimer disease and Huntington disease in humans (Prx6), and another dubbed a “chaperone” protein because it protects other proteins from being damaged when brain or other tissues are exposed to cell-level stress.

Precisely what it is about returning to the hive that produces this effect is a matter of speculation, but this finding does show that learning impairment in old bees can be reversed by changes in behavior, and this reversal is correlated with specific changes in brain protein.

Having said this, it shouldn’t be overlooked that only some of the worker bees showed this brain plasticity. This is not, apparently, due to differences in genotype, but may depend on the amount of foraging experience.

The findings add weight to the idea that social interventions can help our brains stay younger, and are consistent with growing evidence that, in humans, social engagement helps protect against dementia and age-related cognitive impairment.

The (probably) experience-dependent individual differences shown by the bees is perhaps mirrored in our idea of cognitive reserve, but with a twist. The concept of cognitive reserve emphasizes that accumulating a wealth of cognitive experience (whether through education or occupation or other activities) protects your brain from the damage that might occur with age. But perhaps (and I’m speculating now) we should also consider the other side of this: repeated engagement in routine or undemanding activities may have a deleterious effect, independent of and additional to the absence of more stimulating activities.

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Controlling diabetes important for slowing cognitive decline

August, 2012
  • Findings from a large, long-running study adds to growing evidence that poorly controlled diabetes is associated with faster cognitive decline.

The latest finding from the large, long-running Health, Aging, and Body Composition (Health ABC) Study adds to the evidence that preventing or controlling diabetes helps prevent age-related cognitive decline.

The study involves 3,069 older adults (70+), of whom 717 (23%) had diabetes at the beginning of the study in 1997. Over the course of the study, a further 159 developed diabetes. Those with diabetes at the beginning had lower cognitive scores, and showed faster decline. Those who developed diabetes showed a rate of decline that was between that faster rate and the slower rate of those who never developed diabetes.

Among those with diabetes, those who had higher levels of a blood marker called glycosylated hemoglobin had greater cognitive impairment. Higher levels of this blood marker reflect poorer control of blood sugar.

In other words, both duration and severity of diabetes are important factors in determining rate of cognitive decline in old age.

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Effect of blood pressure on the aging brain depends on genetics

July, 2012

For those with the Alzheimer’s gene, higher blood pressure, even though within the normal range, is linked to greater brain shrinkage and reduced cognitive ability.

I’ve reported before on the evidence suggesting that carriers of the ‘Alzheimer’s gene’, APOE4, tend to have smaller brain volumes and perform worse on cognitive tests, despite being cognitively ‘normal’. However, the research hasn’t been consistent, and now a new study suggests the reason.

The e4 variant of the apolipoprotein (APOE) gene not only increases the risk of dementia, but also of cardiovascular disease. These effects are not unrelated. Apoliproprotein is involved in the transportation of cholesterol. In older adults, it has been shown that other vascular risk factors (such as elevated cholesterol, hypertension or diabetes) worsen the cognitive effects of having this gene variant.

This new study extends the finding, by looking at 72 healthy adults from a wide age range (19-77).

Participants were tested on various cognitive abilities known to be sensitive to aging and the effects of the e4 allele. Those abilities include speed of information processing, working memory and episodic memory. Blood pressure, brain scans, and of course genetic tests, were also performed.

There are a number of interesting findings:

  • The relationship between age and hippocampal volume was stronger for those carrying the e4 allele (shrinkage of this brain region occurs with age, and is significantly greater in those with MCI or dementia).
  • Higher systolic blood pressure was significantly associated with greater atrophy (i.e., smaller volumes), slower processing speed, and reduced working memory capacity — but only for those with the e4 variant.
  • Among those with the better and more common e3 variant, working memory was associated with lateral prefrontal cortex volume and with processing speed. Greater age was associated with higher systolic blood pressure, smaller volumes of the prefrontal cortex and prefrontal white matter, and slower processing. However, blood pressure was not itself associated with either brain atrophy or slower cognition.
  • For those with the Alzheimer’s variant (e4), older adults with higher blood pressure had smaller volumes of prefrontal white matter, and this in turn was associated with slower speed, which in turn linked to reduced working memory.

In other words, for those with the Alzheimer’s gene, age differences in working memory (which underpin so much of age-related cognitive impairment) were produced by higher blood pressure, reduced prefrontal white matter, and slower processing. For those without the gene, age differences in working memory were produced by reduced prefrontal cortex and prefrontal white matter.

Most importantly, these increases in blood pressure that we are talking about are well within the normal range (although at the higher end).

The researchers make an interesting point: that these findings are in line with “growing evidence that ‘normal’ should be viewed in the context of individual’s genetic predisposition”.

What it comes down to is this: those with the Alzheimer’s gene variant (and no doubt other genetic variants) have a greater vulnerability to some of the risk factors that commonly increase as we age. Those with a family history of dementia or serious cognitive impairment should therefore pay particular attention to controlling vascular risk factors, such as hypertension and diabetes.

This doesn’t mean that those without such a family history can safely ignore such conditions! When they get to the point of being clinically diagnosed as problems, then they are assuredly problems for your brain regardless of your genetics. What this study tells us is that these vascular issues appear to be problematic for Alzheimer’s gene carriers before they get to that point of clinical diagnosis.

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Menopause ‘brain fog’ a product of poor sleep and depression?

May, 2012

A smallish study of women approaching and in menopause found that some experienced poorer working memory and attention, and these were more likely to have poorer sleep, depression, and anxiety.

A study involving 75 perimenopausal women aged 40 to 60 has found that those with memory complaints tended to show impairments in working memory and attention. Complaints were not, however, associated with verbal learning or memory.

Complaints were also associated with depression, anxiety, somatic complaints, and sleep disturbance. But they weren’t linked to hormone levels (although estrogen is an important hormone for learning and memory).

What this suggests to me is that a primary cause of these cognitive impairments may be poor sleep, and anxiety/depression. A few years ago, I reported on a study that found that, although women’s reports of how many hot flashes they had didn’t correlate with memory impairment, an objective measure of the number of flashes they experienced during sleep did. Sleep, as I know from personal experience, is of sufficient importance that my rule-of-thumb is: don’t bother looking for any other causes of attention and memory deficits until you have sorted out your sleep!

Having said that, depressive symptoms showed greater relationship to memory complaints than sleep disturbance.

It’s no big surprise to hear that it is working memory in particular that is affected, because what many women at this time of life complain of is ‘brain fog’ — the feeling that your brain is full of cotton-wool. This doesn’t mean that you can’t learn new information, or remember old information. But it does mean that these tasks will be impeded to the extent that you need to hold on to too many bits of information. So mental arithmetic might be more difficult, or understanding complex sentences, or coping with unexpected disruptions to your routine, or concentrating on a task for a long time.

These sorts of problems are typical of those produced by on-going sleep deprivation, stress, and depression.

One caveat to the findings is that the study participants tended to be of above-average intelligence and education. This would protect them to a certain extent from cognitive decline — those with less cognitive reserve might display wider impairment. Other studies have found verbal memory, and processing speed, impaired during menopause.

Note, too, that a long-running, large population study has found no evidence for a decline in working memory, or processing speed, in women as they pass through perimenopause and menopause.

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Fluctuating sense of control linked to cognitive ability in older adults

April, 2012

A small study has found that, in older adults, their sense of control fluctuates over the course of a day, and this affects their cognitive abilities.

Previous research has pointed to a typical decline in our sense of control as we get older. Maintaining a sense of control, however, appears to be a key factor in successful aging. Unsurprisingly, in view of the evidence that self-belief and metacognitive understanding are important for cognitive performance, a stronger sense of control is associated with better cognitive performance. (By metacognitive understanding I mean the knowledge that cognitive performance is malleable, not fixed, and strategies and training are effective in improving cognition.)

In an intriguing new study, 36 older adults (aged 61-87, average age 74) had their cognitive performance and their sense of control assessed every 12 hours for 60 days. Participants were asked questions about whether they felt in control of their lives and whether they felt able to achieve goals they set for themselves.

The reason I say this is intriguing is that it’s generally assumed that a person’s sense of control — how much they feel in control of their lives — is reasonably stable. While, as I said, it can change over the course of a lifetime, until recently we didn’t think that it could fluctuate significantly in the course of a single day — which is what this study found.

Moreover, those who normally reported having a low sense of control performed much better on inductive reasoning tests during periods when they reported feeling a higher sense of control. Similarly, those who normally reported feeling a high sense of control scored higher on memory tests when feeling more in control than usual.

Although we can’t be sure (since this wasn’t directly investigated), the analysis suggests that the improved cognitive functioning stems from the feeling of improved control, not vice versa.

The study builds on an earlier study that found weekly variability in older adults’ locus of control and competency beliefs.

Assessment was carried out in the form of a daily workbook, containing a number of measures, which participants completed twice daily. Each assessment took around 30-45 minutes to complete. The measures included three cognitive tests (14 alternate forms of each of these were used, to minimize test familiarity):

  • Letter series test: 30 items in which the next letter in a series had to be identified. [Inductive reasoning]
  • Number comparison: 48 items in which two number strings were presented beside each other, and participants had to identify where there was any mismatch. [Perceptual speed]
  • Rey Auditory Verbal Learning Task: participants have to study a list of 15 unrelated words for one minute, then on another page recall as many of the words as they could. [Memory]

Sense of control over the previous 12 hours was assessed by 8 questions, to which participants indicated their agreement/disagreement on a 6-point scale. Half the questions related to ‘locus of control’ and half to ‘perceived competence’.

While, unsurprisingly, compliance wasn’t perfect (it’s quite an arduous regime), participants completed on average 115 of 120 workbooks. Of the possible 4,320 results (36 x 120), only 166 were missing.

One of the things that often annoys me is the subsuming of all within-individual variability in cognitive scores into averages. Of course averages are vital, but so is variability, and this too often is glossed over. This study is, of course, all about variability, so I was very pleased to see people’s cognitive variability spelled out.

Most of the variance in locus of control was of course between people (86%), but 14% was within-individual. Similarly, the figures for perceived competence were 88% and 12%. (While locus of control and perceived competence are related, only 26% of the variability in within-person locus of control was associated with competence, meaning that they are largely independent.)

By comparison, within-individual variability was much greater for the cognitive measures: for the letter series (inductive reasoning), 32% was within-individual and 68% between-individual; for the number matching (perceptual speed), 21% was within-individual and 79% between-individual; for the memory test, an astounding 44% was within-individual and 56% between-individual.

Some of this within-individual variability in cognitive performance comes down to practice effects, which were significant for all cognitive measures. For the memory test, time of day was also significant, with performance being better in the morning. For the letter and number series tests, previous performance also had a small effect on perceived competence. For the number matching, increase in competence subsequent to increased performance was greatest for those with lower scores. However, lagged analyses indicated that beliefs preceded performance to a greater extent than performance preceding beliefs.

While it wasn’t an aspect of this study, it should also be noted that a person’s sense of control may well vary according to domain (e.g., cognition, social interaction, health) and context. In this regard, it’s interesting to note the present findings that sense of control affected inductive reasoning for low-control individuals, but memory for high-control individuals, suggesting that the cognitive domain also matters.

Now this small study was a preliminary one and there are several limitations that need to be tightened up in subsequent research, but I think it’s important for three reasons:

  • as a demonstration that cognitive performance is not a fixed attribute;
  • as a demonstration of the various factors that can affect older adults’ cognitive performance;
  • as a demonstration that your beliefs about yourself are a factor in your cognitive performance.

Reference: 

[2794] Neupert, S. D., & Allaire J. C.
(2012).  I think I can, I think I can: Examining the within-person coupling of control beliefs and cognition in older adults.
Psychology and Aging. No Pagination Specified - No Pagination Specified.

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Alzheimer's protein may impair mental function even in healthy adults

March, 2012

The protein associated with Alzheimer's disease appears to impair cognitive function many years before symptoms manifest. Higher levels of this protein are more likely in carriers of the Alzheimer’s gene, and such carriers may be more affected by the protein’s presence.

Another study adds to the evidence that changes in the brain that may lead eventually to Alzheimer’s begin many years before Alzheimer’s is diagnosed. The findings also add to the evidence that what we regard as “normal” age-related cognitive decline is really one end of a continuum of which the other end is dementia.

In the study, brain scans were taken of 137 highly educated people aged 30-89 (participants in the Dallas Lifespan Brain Study). The amount of amyloid-beta (characteristic of Alzheimer’s) was found to increase with age, and around a fifth of those over 60 had significantly elevated levels of the protein. These higher amounts were linked with worse performance on tests of working memory, reasoning and processing speed.

More specifically, across the whole sample, amyloid-beta levels affected processing speed and fluid intelligence (in a dose-dependent relationship — that is, as levels increased, these functions became more impaired), but not working memory, episodic memory, or crystallized intelligence. Among the elevated-levels group, increased amyloid-beta was significantly associated with poorer performance for processing speed, working memory, and fluid intelligence, but not episodic memory or crystallized intelligence. Among the group without elevated levels of the protein, increasing amyloid-beta only affected fluid intelligence.

These task differences aren’t surprising: processing speed, working memory, and fluid intelligence are the domains that show the most decline in normal aging.

Those with the Alzheimer’s gene APOE4 were significantly more likely to have elevated levels of amyloid-beta. While 38% of the group with high levels of the protein had the risky gene variant, only 15% of those who didn’t have high levels carried the gene.

Note that, while the prevalence of carriers of the gene variant matched population estimates (24%), the proportion was higher among those in the younger age group — 33% of those under 60, compared to 19.5% of those aged 60 or older. It seems likely that many older carriers have already developed MCI or Alzheimer’s, and thus been ineligible for the study.

The average age of the participants was 64, and the average years of education 16.4.

Amyloid deposits varied as a function of age and region: the precuneus, temporal cortex, anterior cingulate and posterior cingulate showed the greatest increase with age, while the dorsolateral prefrontal cortex, orbitofrontal cortex, parietal and occipital cortices showed smaller increases with age. However, when only those aged 60+ were analyzed, the effect of age was no longer significant. This is consistent with previous research, and adds to evidence that age-related cognitive impairment, including Alzheimer’s, has its roots in damage occurring earlier in life.

In another study, brain scans of 408 participants in the Mayo Clinic Study of Aging also found that higher levels of amyloid-beta were associated with poorer cognitive performance — but that this interacted with APOE status. Specifically, carriers of the Alzheimer’s gene variant were significantly more affected by having higher levels of the protein.

This may explain the inconsistent findings of previous research concerning whether or not amyloid-beta has significant effects on cognition in normal adults.

As the researchers of the first study point out, what’s needed is information on the long-term course of these brain changes, and they are planning to follow these participants.

In the meantime, all in all, the findings do provide more strength to the argument that your lifestyle in mid-life (and perhaps even younger) may have long-term consequences for your brain in old age — particularly for those with a genetic susceptibility to Alzheimer’s.

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