risk factors

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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More evidence linking poor sleep to Alzheimer’s risk

March, 2012

Two recent studies add to the evidence linking sleep disorders to the later development of Alzheimer’s disease.

A small study of the sleep patterns of 100 people aged 45-80 has found a link between sleep disruption and level of amyloid plaques (characteristic of Alzheimer’s disease). The participants were recruited from the Adult Children Study, of whom half have a family history of Alzheimer’s disease.

Sleep was monitored for two weeks. Those who woke frequently (more than five times an hour!) and those who spent less than 85% of their time in bed actually asleep, were more likely to have amyloid plaques. A quarter of the participants had evidence of amyloid plaques.

The study doesn’t tell us whether disrupted sleep leads to the production of amyloid plaques, or whether brain changes in early Alzheimer's disease lead to changes in sleep, but evidence from other studies do, I think, give some weight to the first idea. At the least, this adds yet another reason for making an effort to improve your sleep!

The abstract for this not-yet-given conference presentation, or the press release, don’t mention any differences between those with a family history of Alzheimer’s and those without, suggesting there was none — but since the researchers made no mention either way, I wouldn’t take that for granted. Hopefully we’ll one day see a journal paper providing more information.

The main findings are supported by another recent study. A Polish study involving 150 older adults found that those diagnosed with Alzheimer’s after a seven-year observation period were more likely to have experienced sleep disturbances more often and with greater intensity, compared to those who did not develop Alzheimer’s.

Reference: 

Ju, Y., Duntley, S., Fagan, A., Morris, J. & Holtzman, D. 2012. Sleep Disruption and Risk of Preclinical Alzheimer Disease. To be presented April 23 at the American Academy of Neurology's 64th Annual Meeting in New Orleans.

Bidzan L, Grabowski J, Dutczak B, Bidzan M. 2011. [Sleep disorders in the preclinical period of the Alzheimer's disease]. Psychiatria Polska, 45(6), 851-60. http://www.ncbi.nlm.nih.gov/pubmed/22335128

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Walking speed and grip strength may predict dementia, stroke risk

March, 2012

More evidence comes for a link between lower physical fitness and increased risk of dementia in a large study that extends earlier findings to middle-aged and younger-old.

Following on from research showing an association between lower walking speed and increased risk of dementia, and weaker hand grip strength and increased dementia risk, a large study has explored whether this association extends to middle-aged and younger-old adults.

Part of the long-running Framingham study, the study involved 2,410 men and women with an average age of 62, who underwent brain scans and tests for walking speed, hand grip strength and cognitive function. During the follow-up period of up to 11 years, 34 people (1.4%) developed dementia (28 Alzheimer’s) and 79 people (3.3%) had a stroke.

Those who had a slower walking speed at the start of the study were one-and-a-half times more likely to develop dementia compared to people with faster walking speed, while stronger hand grip strength was associated with a 42% lower risk of stroke or transient ischemic attack in people over age 65.

Slower walking speed and weaker hand grip strength were also associated with lower brain volume and poorer cognitive performance. Specifically, those with slower walking speed scored significantly worse on tests of visual reproduction, paired associate learning, executive function, visual organization, and language (Boston Naming test). Higher hand grip strength was associated with higher scores on tests of visual reproduction, executive function, visual organization, language and abstraction (similarities test).

While the nature of the association is not yet understood, the findings do seem to support the benefits of physical fitness. At the least, these physical attributes can serve as pointers to the need for more investigation of an older person’s brain health. But they might also serve as a warning to improve physical fitness.

Reference: 

Camargo, E.C., Beiser, A., Tan, Z.S., Au, R., DeCarli, C., Pikula, A., Kelly-Hayes, M., Kase, C., Wolf, P. & Seshadri, S. 2012. Walking Speed, Handgrip Strength and Risk of Dementia and Stroke: The Framingham Offspring Study. To be presented April 25 at the American Academy of Neurology's 64th Annual Meeting in New Orleans.

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Higher risk of mild cognitive impairment among older men

February, 2012

Significant differences in the risk of mild cognitive impairment for men and women, and in the risk of developing the two sub-types, suggests that risk factors should be considered separately for genders and sub-type.

More data from the long-running Mayo Clinic Study of Aging has revealed that, in this one part of the U.S. at least, MCI develops at an overall rate of 6.4% a year among older adults (70+), with a higher rate for men and the less-educated.

The study involved 1,450 older adults (aged 70-89), who underwent memory testing every 15 months for an average of three years. By the end of the study period, 296 people had developed MCI, a rate of 6.4% per year. For men, the rate was 7.2% compared to 5.7% for women.

It should be noted that these rates apply to a relatively homogeneous group of people. Participants come from one county in Minnesota, an overwhelmingly white part of the U.S.

MCI comes in two types: amnestic (involving memory loss) and non-amnestic. Amnestic MCI was more than twice as common as non-amnestic MCI. The incidence rate of aMCI was also higher for men (4.4%) than women (3.3%), as was the risk of naMCI (2% vs 1.1%).

Those who had less education also had higher rates of MCI. For aMCI, the rate for those with 12 years or less of education was 4.3%, compared to 3.25% for those with more education. Similarly, for naMCI, the rates were 2% and 1%, respectively.

While the great majority of people diagnosed with MCI continued to have the disorder or progressed to dementia, some 12% were later re-diagnosed as not having it. This, I would presume, probably reflects temporary ‘dips’ in cognitive performance as a consequence of physical or emotional problems.

The differences between aMCI and naMCI, and between genders, suggest that risk factors for these should be considered separately.

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Diet linked to brain atrophy in old age

January, 2012
  • A more rigorous measurement of diet finds that dietary factors account for nearly as much brain shrinkage as age, education, APOE genotype, depression and high blood pressure combined.

The study involved 104 healthy older adults (average age 87) participating in the Oregon Brain Aging Study. Analysis of the nutrient biomarkers in their blood revealed that those with diets high in omega 3 fatty acids and in vitamins C, D, E and the B vitamins had higher scores on cognitive tests than people with diets low in those nutrients, while those with diets high in trans fats were more likely to score more poorly on cognitive tests.

These were dose-dependent, with each standard deviation increase in the vitamin BCDE score ssociated with a 0.28 SD increase in global cognitive score, and each SD increase in the trans fat score associated with a 0.30 SD decrease in global cognitive score.

Trans fats are primarily found in packaged, fast, fried and frozen food, baked goods and margarine spreads.

Brain scans of 42 of the participants found that those with diets high in vitamins BCDE and omega 3 fatty acids were also less likely to have the brain shrinkage associated with Alzheimer's, while those with high trans fats were more likely to show such brain atrophy.

Those with higher omega-3 scores also had fewer white matter hyperintensities. However, this association became weaker once depression and hypertension were taken into account.

Overall, the participants had good nutritional status, but 7% were deficient in vitamin B12 (I’m surprised it’s so low, but bear in mind that these are already a select group, being healthy at such an advanced age) and 25% were deficient in vitamin D.

The nutrient biomarkers accounted for 17% of the variation in cognitive performance, while age, education, APOE genotype (presence or absence of the ‘Alzheimer’s gene’), depression and high blood pressure together accounted for 46%. Diet was more important for brain atrophy: here, the nutrient biomarkers accounted for 37% of the variation, while the other factors accounted for 40% (meaning that diet was nearly as important as all these other factors combined!).

The findings add to the growing evidence that diet has a significant role in determining whether or not, and when, you develop Alzheimer’s disease.

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Why a select group of seniors retain their cognitive abilities

December, 2011
  • Comparison of the brains of octogenarians whose memories match those of middle-aged people reveals important differences between their brains and those of cognitively-normal seniors.

A certain level of mental decline in the senior years is regarded as normal, but some fortunate few don’t suffer from any decline at all. The Northwestern University Super Aging Project has found seniors aged 80+ who match or better the average episodic memory performance of people in their fifties. Comparison of the brains of 12 super-agers, 10 cognitively-normal seniors of similar age, and 14 middle-aged adults (average age 58) now reveals that the brains of super-agers also look like those of the middle-aged. In contrast, brain scans of cognitively average octogenarians show significant thinning of the cortex.

The difference between the brains of super-agers and the others was particularly marked in the anterior cingulate cortex. Indeed, the super agers appeared to have a much thicker left anterior cingulate cortex than the middle-aged group as well. Moreover, the brain of a super-ager who died revealed that, although there were some plaques and tangles (characteristic, in much greater quantities, of Alzheimer’s) in the mediotemporal lobe, there were almost none in the anterior cingulate. (But note an earlier report from the researchers)

Why this region should be of special importance is somewhat mysterious, but the anterior cingulate is part of the attention network, and perhaps it is this role that underlies the superior abilities of these seniors. The anterior cingulate also plays a role error detection and motivation; it will be interesting to see if these attributes are also important.

While the precise reason for the anterior cingulate to be critical to retaining cognitive abilities might be mysterious, the lack of cortical atrophy, and the suggestion that super-agers’ brains have much reduced levels of the sort of pathological damage seen in most older brains, adds weight to the growing evidence that cognitive aging reflects clinical problems, which unfortunately are all too common.

Sadly, there are no obvious lifestyle factors involved here. The super agers don’t have a lifestyle any different from their ‘cognitively average’ counterparts. However, while genetics might be behind these people’s good fortune, that doesn’t mean that lifestyle choices don’t make a big difference to those of us not so genetically fortunate. It seems increasingly clear that for most of us, without ‘super-protective genes’, health problems largely resulting from lifestyle choices are behind much of the damage done to our brains.

It should be emphasized that these unpublished results are preliminary only. This conference presentation reported on data from only 12 of 48 subjects studied.

Reference: 

Harrison, T., Geula, C., Shi, J., Samimi, M., Weintraub, S., Mesulam, M. & Rogalski, E. 2011. Neuroanatomic and pathologic features of cognitive SuperAging. Presented at a poster session at the 2011 Society for Neuroscience conference.

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How neighborhood status affects cognitive function in older adults

November, 2011

New research confirms the correlation between lower neighborhood socioeconomic status and lower cognitive function in older adults, and accounts for most of it through vascular health, lifestyle, and psychosocial factors.

In the last five years, three studies have linked lower neighborhood socioeconomic status to lower cognitive function in older adults. Neighborhood has also been linked to self-rated health, cardiovascular disease, and mortality. Such links between health and neighborhood may come about through exposure to pollutants or other environmental stressors, access to alcohol and cigarettes, barriers to physical activity, reduced social support, and reduced access to good health and social services.

Data from the large Women’s Health Initiative Memory Study has now been analyzed to assess whether the relationship between neighborhood socioeconomic status can be explained by various risk and protective factors for poor cognitive function.

Results confirmed that higher neighborhood socioeconomic status was associated with higher cognitive function, even after individual factors such as age, ethnicity, income, education, and marital status have been taken into account. A good deal of this was explained by vascular factors (coronary heart disease, diabetes, stroke, hypertension), health behaviors (amount of alcohol consumed, smoking, physical activity), and psychosocial factors (depression, social support). Nevertheless, the association was still (barely) significant after these factors were taken account of, suggesting some other factors may also be involved. Potential factors include cognitive activity, diet, and access to health services.

In contradiction of earlier research, the association appeared to be stronger among younger women. Consistent with other research, the association was stronger for non-White women.

Data from 7,479 older women (65-81) was included in the analysis. Cognitive function was assessed by the Modified MMSE (3MSE). Neighborhood socioeconomic status was assessed on the basis of: percentage of adults over 25 with less than a high school education, percentage of male unemployment, percentage of households below the poverty line, percentage of households receiving public assistance, percentage of female-headed households with children, and median household income. Around 87% of participants were White, 7% Black, 3% Hispanic, and 3% other. Some 92% had graduated high school, and around 70% had at least some college.

Reference: 

[2523] Shih, R. A., Ghosh-Dastidar B., Margolis K. L., Slaughter M. E., Jewell A., Bird C. E., et al.
(2011).  Neighborhood Socioeconomic Status and Cognitive Function in Women.
Am J Public Health. 101(9), 1721 - 1728.

Previous:

Lang IA, Llewellyn DJ, Langa KM, Wallace RB, Huppert FA, Melzer D. 2008. Neighborhood deprivation, individual socioeconomic status, and cognitive function in older people: analyses from the English Longitudinal Study of Ageing. J Am Geriatr Soc., 56(2), 191-198.

Sheffield KM, Peek MK. 2009. Neighborhood context and cognitive decline in older Mexican Americans: results from the Hispanic Established Populations for Epidemiologic Studies of the Elderly. Am J Epidemiol., 169(9), 1092-1101.

Wight RG, Aneshensel CS, Miller-Martinez D, et al. 2006. Urban neighborhood context, educational attainment, and cognitive function among older adults. Am J Epidemiol., 163(12), 1071-1078.

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Common health complaints increase Alzheimer's risk

October, 2011

Two large studies respectively find that common health complaints and irregular heartbeat are associated with an increased risk of developing Alzheimer’s, while a rat study adds to evidence that stress is also a risk factor.

A ten-year study involving 7,239 older adults (65+) has found that each common health complaint increased dementia risk by an average of about 3%, and that these individual risks compounded. Thus, while a healthy older adult had about an 18% chance of developing dementia after 10 years, those with a dozen of these health complaints had, on average, closer to a 40% chance.

It’s important to note that these complaints were not for serious disorders that have been implicated in Alzheimer’s. The researchers constructed a ‘frailty’ index, involving 19 different health and wellbeing factors: overall health, eyesight, hearing, denture fit, arthritis/rheumatism, eye trouble, ear trouble, stomach trouble, kidney trouble, bladder control, bowel control, feet/ankle trouble, stuffy nose/sneezing, bone fractures, chest problems, cough, skin problems, dental problems, other problems.

Not all complaints are created equal. The most common complaint — arthritis/rheumatism —was only slightly higher among those with dementia. Two of the largest differences were poor eyesight (3% of the non-demented group vs 9% of those with dementia) and poor hearing (3% and 6%).

At the end of the study, 4,324 (60%) were still alive, and of these, 416 (9.6%) had Alzheimer's disease, 191 (4.4%) had another sort of dementia and 677 (15.7%) had other cognitive problems (but note that 1,023 were of uncertain cognitive ability).

While these results need to be confirmed in other research — the study used data from broader health surveys that weren’t specifically designed for this purpose, and many of those who died during the study will have probably had dementia — they do suggest the importance of maintaining good general health.

Common irregular heartbeat raises risk of dementia

In another study, which ran from 1994 to 2008 and followed 3,045 older adults (mean age 74 at study start), those with atrial fibrillation were found to have a significantly greater risk of developing Alzheimer’s.

At the beginning of the study, 4.3% of the participants had atrial fibrillation (the most common kind of chronically irregular heartbeat); a further 12.2% developed it during the study. Participants were followed for an average of seven years. Over this time, those with atrial fibrillation had a 40-50% higher risk of developing dementia of any type, including probable Alzheimer's disease. Overall, 18.8% of the participants developed some type of dementia during the course of the study.

While atrial fibrillation is associated with other cardiovascular risk factors and disease, this study shows that atrial fibrillation increases dementia risk more than just through this association. Possible mechanisms for this increased risk include:

  • weakening the heart's pumping ability, leading to less oxygen going to the brain;
  • increasing the chance of tiny blood clots going to the brain, causing small, clinically undetected strokes;
  • a combination of these plus other factors that contribute to dementia such as inflammation.

The next step is to see whether any treatments for atrial fibrillation reduce the risk of developing dementia.

Stress may increase risk for Alzheimer's disease

And a rat study has shown that increased release of stress hormones leads to cognitive impairment and that characteristic of Alzheimer’s disease, tau tangles. The rats were subjected to stress for an hour every day for a month, by such means as overcrowding or being placed on a vibrating platform. These rats developed increased hyperphosphorylation of tau protein in the hippocampus and prefrontal cortex, and these changes were associated with memory deficits and impaired behavioral flexibility.

Previous research has shown that stress leads to that other characteristic of Alzheimer’s disease: the formation of beta-amyloid.

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Depression & Cognition

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

Psychological distress, not depression, linked to increased risk of stroke

A study following 20,627 people for an average of 8.5 years has found that psychological distress was associated with an increased risk of stroke and that the risk of stroke increased the more distress the participants reported. This association remained the same regardless of cigarette smoking, systolic blood pressure, overall blood cholesterol, obesity, previous heart attack, diabetes, social class, education, high blood pressure treatment, family history of stroke and recent antidepressant medication use. However, there was no increased risk for people who had experienced an episode of major depression in the past year or at any point in their lifetime.

[1298] Surtees, P. G., Wainwright N. W. J., Luben R. N., Wareham N. J., Bingham S. A., & Khaw K. - T.
(2008).  Psychological distress, major depressive disorder, and risk of stroke.
Neurology. 70(10), 788 - 794.

http://www.eurekalert.org/pub_releases/2008-03/aaon-pdn022608.php

Depression increases risk of executive dysfunction in older people

A two-year study of more than 700 older adults (65 and older) has found that depression increased the risk of declining executive function (high-level mental processes, such a making decisions, organizing, planning and doing a series of things in sequence).

[1417] Cui, X., Lyness J. M., Tu X., King D. A., & Caine E. D.
(2007).  Does Depression Precede or Follow Executive Dysfunction? Outcomes in Older Primary Care Patients.
Am J Psychiatry. 164(8), 1221 - 1228.

http://www.eurekalert.org/pub_releases/2007-10/uorm-dcf100807.php

Depressed older adults more likely to become cognitively impaired

A study involving 2,220 participants in the Cardiovascular Health Study, a longitudinal prospective study of adults 65 and older, has found that 19.7% of subjects with moderate to high depression developed mild cognitive impairment within six years, compared to 10% of subjects with no depressive symptoms and 13.3% of subjects with low depressive symptoms. There was no correlation between depression and vascular disease, although it has been hypothesized that vascular disease might lead to both depression and cognitive impairment by causing inadequate blood flow to different brain structures.

[409] Barnes, D. E., Alexopoulos G. S., Lopez O. L., Williamson J. D., & Yaffe K.
(2006).  Depressive Symptoms, Vascular Disease, and Mild Cognitive Impairment: Findings From the Cardiovascular Health Study.
Arch Gen Psychiatry. 63(3), 273 - 279.

http://www.eurekalert.org/pub_releases/2006-03/uoc--doa030206.php

Treatable depression often accompanies mild memory loss

A large-scale study of older adults begun in 1989 has revealed that 43% of those with mild cognitive impairment had psychiatric symptoms (such as depression, irritability, loss of interest in activities, or changes in sleep or appetite) in the month before examination. Such symptoms are often shrugged off as emotional reactions to memory decline, but they may be due to changes in brain function, and may respond to treatment.

[1275] Lyketsos, C. G., Lopez O., Jones B., Fitzpatrick A. L., Breitner J., & DeKosky S.
(2002).  Prevalence of Neuropsychiatric Symptoms in Dementia and Mild Cognitive Impairment: Results From the Cardiovascular Health Study.
JAMA. 288(12), 1475 - 1483.

http://www.eurekalert.org/pub_releases/2002-09/wfub-tdo092702.php

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Diabetes & Cognition

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

Diabetic episodes affect memory

A study involving 62 children with type 1 diabetes, of whom 33 had experienced diabetic ketoacidosis, has found those with such experience performed significantly worse on a memory test that tested their ability to recall events in association with specific details. The finding points to the importance of avoiding diabetic ketoacidosis, which is avoidable in those known to have diabetes.

[1384] Ghetti, S., Lee J. K., Sims C. E., DeMaster D. M., & Glaser N. S.
(2010).  Diabetic Ketoacidosis and Memory Dysfunction in Children with Type 1 Diabetes.
The Journal of Pediatrics. 156(1), 109 - 114.

http://www.eurekalert.org/pub_releases/2009-10/uoc--dea101909.php

Poor glucose control linked to cognitive impairment in diabetics

The ongoing Memory in Diabetes (MIND) study, involving some 3,000 type 2 diabetics 55 years and older, has found that cognitive functioning abilities drop as average blood sugar levels rise. However, there was no connection between daily blood glucose levels and cognitive performance. The study adds to growing evidence that poorer blood glucose control is strongly associated with poorer memory function, that may eventually lead to mild cognitive impairment, vascular dementia and Alzheimer's disease. It is also possible that people with impaired cognitive ability are less compliant in taking medications and controlling their diabetes. Further research will test the hypothesis that improving glucose control results in improved cognitive function.

[797] Marcovina, S. M., Launer L. J., Cukierman-Yaffe T., Gerstein H. C., Williamson J. D., Lazar R. M., et al.
(2009).  Relationship Between Baseline Glycemic Control and Cognitive Function in Individuals With Type 2 Diabetes and Other Cardiovascular Risk Factors.
Diabetes Care. 32(2), 221 - 226.

http://www.eurekalert.org/pub_releases/2009-02/wfub-hbs021109.php

Adult-onset diabetes slows mental functioning in several ways, with deficits appearing early

A comparison of 41 adults with diabetes and 424 adults in good health, aged between 53 and 90, has revealed that healthy adults performed significantly better than adults with diabetes on two of the five domains tested: executive functioning and speed of processing. There were no significant differences on tests of episodic and semantic memory, verbal fluency, reaction time and perceptual speed. The effect remained even when only the younger group (those below 70) were analyzed, indicating that the diabetes-linked cognitive deficits appear early and remain stable.

[796] Yeung, S. E., Fischer A. L., & Dixon R. A.
(2009).  Exploring effects of type 2 diabetes on cognitive functioning in older adults.
Neuropsychology. 23(1), 1 - 9.

http://www.eurekalert.org/pub_releases/2009-01/apa-ads123008.php

Blood sugar linked to normal cognitive aging

Following research showing that decreasing brain function in the area of the hippocampus called the dentate gyrus is a main contributor of normal age-related cognitive decline, an imaging study has been investigating the cause of this decreasing function by looking at measures that typically change during aging, like rising blood sugar, body mass index, cholesterol and insulin levels. The study of 240 community-based nondemented elders (average age 80 years), of whom 60 had type 2 diabetes, found that decreasing activity in the dentate gyrus only correlated with levels of blood glucose. The same association was also found in aging rhesus monkeys and in mice. The finding suggests that maintaining blood sugar levels, even in the absence of diabetes, could help maintain aspects of cognitive health. It also suggests that one reason why physical exercise benefits memory may be its effect on lowering glucose levels.

[830] Mayeux, R., Vannucci S. J., Small S. A., Wu W., Brickman A. M., Luchsinger J., et al.
(2008).  The brain in the age of old: The hippocampal formation is targeted differentially by diseases of late life.
Annals of Neurology. 64(6), 698 - 706.

http://www.eurekalert.org/pub_releases/2008-12/cumc-rac121508.php

Diabetic seniors may experience memory declines after eating high-fat food

Growing evidence links diabetes to cognitive impairment. Now a small study of 16 adults (aged 50 years and older) with type 2 diabetes compared their cognitive performance on three separate occasions, fifteen minutes after consuming different meals. One meal consisted of high fat products – a danish pastry, cheddar cheese and yogurt with added whipped cream; the second meal was only water; and the third was the high-fat meal plus high doses of vitamins C (1000 mg) and E (800 IU) tablets. Researchers found that vitamin supplementation consistently improved recall scores relative to the meal alone, while those who ate the high fat meal without vitamin supplements showed significantly more forgetfulness of words and paragraph information in immediate and time delay recall tests. Those on water meal and meal with vitamins showed similar levels in cognitive performance. The finding indicates not only that diabetics can temporarily further worsen already underlying memory problems associated with the disease by consuming unhealthy meals, but also that this can be remedied by taking high doses of antioxidant vitamins C and E with the meal, suggesting that the effect of high-fat foods is to cause oxidative stress. However, this is hardly a recommended course of action, and the real importance of this finding is that it emphasizes the need for diabetics to consume healthy foods high in antioxidants, like fruits and vegetables. Of course, this is a very small study, and further replication is needed.

[1094] Chui, M., & Greenwood C.
(2008).  Antioxidant vitamins reduce acute meal-induced memory deficits in adults with type 2 diabetes.
Nutrition Research. 28(7), 423 - 429.

http://www.eurekalert.org/pub_releases/2008-06/bcfg-swt062408.php

Stress hormone impacts memory, learning in diabetic rodents

A rodent study sheds light on why diabetes can impair cognitive function. The study found that increased levels of a stress hormone (called cortisol in humans) in diabetic rats impaired synaptic plasticity and reduced neurogenesis in the hippocampus. When levels returned to normal, the hippocampus recovered. Cortisol production is controlled by the hypothalamic-pituitary axis (HPA). People with poorly controlled diabetes often have an overactive HPA axis and excessive cortisol.

[1050] Stranahan, A. M., Arumugam T. V., Cutler R. G., Lee K., Egan J. M., & Mattson M. P.
(2008).  Diabetes impairs hippocampal function through glucocorticoid-mediated effects on new and mature neurons.
Nature Neuroscience. 11(3), 309 - 317.

http://www.eurekalert.org/pub_releases/2008-02/nioa-shi021508.php

Tight diabetes control does not impact cognitive ability in type 1 diabetes

A long-running study involving 1,441 type 1 diabetics, aged 13 to 39, has demonstrated that multiple episodes of severe hypoglycaemia, though they can cause confusion, irrational behavior, convulsions and unconsciousness, do not lead to long-term loss of cognitive ability.

[1120] The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications(DCCT/EDIC) Study Research
(2007).  Long-Term Effect of Diabetes and Its Treatment on Cognitive Function.
N Engl J Med. 356(18), 1842 - 1852.

http://www.eurekalert.org/pub_releases/2007-05/jdc-sst050107.php

Brain function not impaired by tight diabetes control and hypoglycemia

Previous research had indicated that tight blood glucose control -- achieved by taking three or more insulin injections daily – meant type 1 diabetics were three times as likely to suffer episodes of severe hypoglycemia, raising the fear that it might lead to a long-term loss of cognitive ability. Now a follow-up study provides the reassuring news that there was no link between multiple severe hypoglycemic reactions and impaired cognitive function in people with type 1 diabetes.

Jacobson, A.M. et al. 2006. Effects of Intensive and Conventional Treatment on Cognitive Function Twelve Years after the Completion of the Diabetes Control and Complications Trial (DCCT). Abstract Number 750232, presented at the American Diabetes Association's 66th Annual Scientific Sessions held in Washington, D.C, June 9—13.

http://www.eurekalert.org/pub_releases/2006-06/jdc-lss060806.php

Fat hormone linked to learning and memory

A new study reveals why obese patients who have diabetes also may have problems with their long-term memory. Leptin — the so-called ‘fat’ hormone — doesn't cross into the brain to help regulate appetite in obese people. Leptin also acts in the hippocampus, suggesting that leptin plays a role in learning and memory. The new study supports this by demonstrating that mice navigated a maze better after they received leptin. Moreover, mice with elevated levels of amyloid-beta plaques (characteristic of Alzheimer's) were particularly sensitive to leptin.

[2400] Farr, S. A., Banks W. A., & Morley J. E.
(2006).  Effects of leptin on memory processing.
Peptides. 27(6), 1420 - 1425.

http://www.sciencedaily.com/releases/2006/06/060614090511.htm
http://www.eurekalert.org/pub_releases/2006-06/slu-alb061306.php

Age-related vision problems may be associated with cognitive impairment

Age-related macular degeneration (AMD) develops when the macula, the portion of the eye that allows people to see in detail, deteriorates. An investigation into the relationship between vision problems and cognitive impairment in 2,946 patients has been carried out by The Age-Related Eye Disease Study (AREDS) Research Group. Tests were carried out every year for four years. Those who had more severe AMD had poorer average scores on cognitive tests, an association that remained even after researchers considered other factors, including age, sex, race, education, smoking, diabetes, use of cholesterol-lowering medications and high blood pressure. Average scores also decreased as vision decreased. It’s possible that there is a biological reason for the association; it is also possible that visual impairment reduces a person’s capacity to develop and maintain relationships and to participate in stimulating activities.

Chaves, P.H.M. et al. 2006. Association Between Mild Age-Related Eye Disease Study Research Group. 2006. Cognitive Impairment in the Age-Related Eye Disease Study: AREDS Report No. 16. Archives of Ophthalmology,124, 537-543.

http://www.eurekalert.org/pub_releases/2006-04/jaaj-avp040606.php

Review supports link between lifestyle factors and cognitive function in older adults

A review of 96 papers involving 36 very large, ongoing epidemiological studies in North America and Europe looking at factors involved in maintaining cognitive and emotional health in adults as they age has concluded that controlling cardiovascular risk factors, such as reducing blood pressure, reducing weight, reducing cholesterol, treating (or preferably avoiding) diabetes, and not smoking, is important for maintaining brain health as we age. The link between hypertension and cognitive decline was the most robust across studies. They also found a consistent close correlation between physical activity and brain health. However, they caution that more research is needed before specific recommendations can be made about which types of exercise and how much exercise are beneficial. They also found protective factors most consistently reported for cognitive health included higher education level, higher socio-economic status, emotional support, better initial performance on cognitive tests, better lung capacity, more physical exercise, moderate alcohol use, and use of vitamin supplements. Psychosocial factors, such as social disengagement and depressed mood, are associated with both poorer cognitive and emotional health in late life. Increased mental activity throughout life, such as learning new things, may also benefit brain health.

Wagster M, Hendrie H, Albert M, Butters M, Gao S, Knopman DS, Launer L, Yaffe K, Cuthbert B, Edwards E. The NIH Cognitive and Emotional Health ProjectReport of the Critical Evaluation Study Committee. Alzheimer's and Dementia [Internet]. 2006 ;2(1):12 - 32. Available from: http://www.alzheimersanddementia.com/article/S1552-5260(05)00503-0/abstract?articleId=&articleTitle=&citedBy=false&medlinePmidWithoutMDLNPrefix=&overridingDateRestriction=&related=false&restrictdesc_author=&restrictDescription=&restrictName.jalz=jalz&rest

http://www.eurekalert.org/pub_releases/2006-02/aa-nss021606.php

Risk for lowered cognitive performance greater in people at high risk for stroke

A new large-scale study supports earlier suggestions that those with a high risk for stroke within 10 years are also at risk for lowered cognitive function and show a pattern of deficits similar to that seen in mild vascular cognitive impairment. It is speculated that the reason may lie in structural and functional changes in the brain that do not rise to the level of clinical detection, and this is supported by a recent brain imaging study showing that abnormal brain atrophy is related both to higher risk of stroke and poorer cognitive ability. The probability of experiencing stroke within 10 years was calculated using weighted combinations of age, systolic blood-pressure, presence of diabetes, cigarette smoking, history of cardiovascular disease, treatment for hypertension and atrial fibrillation.

[1422] Elias, M. F., Sullivan L. M., D'Agostino R. B., Elias P. K., Beiser A., Au R., et al.
(2004).  Framingham stroke risk profile and lowered cognitive performance.
Stroke; a Journal of Cerebral Circulation. 35(2), 404 - 409.

http://www.eurekalert.org/pub_releases/2004-01/ama-rfl010804.php

Age-related changes in the brain's white matter affect cognitive function

From around age 60, "white-matter lesions" appear in the brain, significantly affecting cognitive function. But without cognitive data from childhood, it is hard to know how much of the difference in cognitive abilities between elderly individuals is due to aging. A longitudinal study has been made possible by the Scottish Mental Survey of 1932, which gave 11-year-olds a validated cognitive test. Scottish researchers have tracked down healthy living men and women who took part in this Survey and retested 83 participants. Testing took place in 1999, when most participants were 78 years old.
It was found that the amount of white-matter lesions made a significant contribution to general cognitive ability differences in old age, independent of prior ability. The amount of white-matter lesions contributed 14.4% of the variance in cognitive scores; early IQ scores contributed 13.7%. The two factors were independent.
Although white-matter lesions are viewed as a normal part of aging, they are linked with other health problems, in particular to circulatory problems (including hypertension, diabetes, heart disease and cardiovascular risk factors).

[442] Deary, I. J., Leaper S. A., Murray A. D., Staff R. T., & Whalley L. J.
(2003).  Cerebral white matter abnormalities and lifetime cognitive change: a 67-year follow-up of the Scottish Mental Survey of 1932.
Psychology and Aging. 18(1), 140 - 148.

http://www.eurekalert.org/pub_releases/2003-03/apa-aci031703.php

High sugar blood levels linked to poor memory

A new study takes an important step in explaining cognitive impairment in diabetics, and suggests a possible cause for some age-related memory impairment. The study assessed non-diabetic middle-aged and elderly people. Those with impaired glucose tolerance (a pre-diabetic condition) had a smaller hippocampus and scored worse on tests for recent memory. These results were independent of age or overall cognitive performance. The brain uses glucose almost exclusively as a fuel source. The ability to get glucose from the blood is reduced in diabetes. The study raises the possibility that exercise and weight loss, which help control blood sugar levels, may be able to reverse some of the memory loss that accompanies aging.

[543] Convit, A., Wolf O. T., Tarshish C., & de Leon M. J.
(2003).  Reduced glucose tolerance is associated with poor memory performance and hippocampal atrophy among normal elderly.
Proceedings of the National Academy of Sciences of the United States of America. 100(4), 2019 - 2022.

http://www.eurekalert.org/pub_releases/2003-02/nyum-hsb013003.php

Diabetes and high blood pressure linked to decline in mental ability

A large-scale six-year study of people aged 40 to 70 years old found that people with diabetes and high blood pressure are more likely to experience cognitive decline. Diabetes was associated with greater cognitive decline for those younger than 58 as well as those older than 58, but high blood pressure was a risk factor only for the 58 and older group.

[2534] Knopman, D. S., Boland L. L., Mosley T., Howard G., Liao D., Szklo M., et al.
(2001).  Cardiovascular risk factors and cognitive decline in middle-aged adults.
Neurology. 56(1), 42 - 48.

http://www.eurekalert.org/pub_releases/2001-01/MC-Nsld-0701101.php
http://www.eurekalert.org/pub_releases/2001-01/AAoN-Dahb-0801101.php

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