Health aging

Multimorbidity score linked to cognitive decline

  • A very large study found that older adults with multiple health conditions showed much greater cognitive decline than those with fewer chronic conditions, even when the conditions weren't directly related to brain health.

Data from more than 14,265 people older adults (51+) multiple times over a decade or more through the University of Michigan Health and Retirement Study has found that people with higher “multimorbidity scores” showed much faster cognitive decline than those with lower scores, even though most of the chronic conditions included in the index had no direct relationship with brain health. The higher the score, the faster the decline.

The multimorbidity index was calculated using three long-term studies of more than 250,000 health professionals, and takes into account the different ways different conditions affect people and how they interact.

The tool is free and available at the ePrognosis website for clinicians.




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Older adults with type 2 diabetes show reduced blood flow linked to worse cognition

July, 2015

A study involving 65 older adults (average age 66), of whom 35 had type 2 diabetes, has found that after two years, those with diabetes had decreases in their ability to regulate blood flow in the brain, and a reduced ability to regulate blood flow was associated with lower cognitive scores.

Specifically, at the start of the study those with diabetes scored an average 46 points on a cognitive test, compared with 55 in the control group. After two years, the diabetics' scores had fallen to an average of 41, while the scores of the control group hadn't fallen at all.

Greater decreases in blood flow regulation were also associated with higher levels of inflammation.

It's suggested that inflammation impairs blood flow regulation, and this accelerates cognitive decline.


Chung, C.-C., Pimentel, D., Jor’dan, A. J., Hao, Y., Milberg, W., & Novak, V. (2015). Inflammation-associated declines in cerebral vasoreactivity and cognition in type 2 diabetes. Neurology, 85(5), 450–458.

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Some chronic viral infections could contribute to age-related cognitive decline

  • A longitudinal study confirms findings from cross-sectional studies that certain common viral infections are factors in age-related cognitive decline.

Growing research has implicated infections as a factor in age-related cognitive decline, but these have been cross-sectional (comparing different individuals, who will have a number of other, possibly confounding, attributes). Now a large longitudinal study provides more evidence that certain chronic viral infections could contribute to subtle cognitive deterioration in apparently healthy older adults.

The study involved 1,022 older adults (65+), who had annual evaluations for five years. It revealed an association between cognitive decline and exposure to several viruses: cytomegalovirus (CMV), herpes simplex (HSV 2), and the protozoa Toxoplasma gondii.

More specifically, the IgG levels for HSV-2 were significantly associated with baseline cognitive scores, while the IgG levels for HSV-2 (genital herpes), TOX (which has been much in the news in recent years for being harbored in domestic cats, and being implicated in various neurological disorders), and CMV (a common virus which unfortunately rarely causes symptoms), but not HSV-1 (the cold sore virus), were significantly associated with greater temporal cognitive decline that varied by type of infection.

More research is obviously needed to determine more precisely what the role of different infectious agents is in cognitive decline, but the findings do point to a need for a greater emphasis on preventing and treating infections. They also add to the growing evidence that age-related cognitive decline isn't 'normal', but something that occurs when other health-related factors come into play.



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Risk Factors

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

High protein diet shrinks brain in Alzheimer’s mice

A study using genetically engineered mice has tested the effects of four diets for their effects on Alzheimer’s pathology: a regular diet, a high fat/low carbohydrate custom diet, a high protein/low carb version, or a high carbohydrate/low fat option. Unexpectedly, mice fed the high protein/low carbohydrate diet had brains 5% lighter that all the others, and regions of their hippocampus were less developed. Mice on the high fat diet had higher levels of amyloid-beta protein, although no effect on plaque burden was detected.

Franciosi, S., Gama Sosa, M., English, D., Oler, E., Oung, T., Janssen, W., et al. (2009). Novel cerebrovascular pathology in mice fed a high cholesterol diet. Molecular Neurodegeneration, 4(1), 42. doi: 10.1186/1750-1326-4-42. Full text available at

Infections may lead to faster memory loss in Alzheimer's disease

A 6-month study involving 222 people with Alzheimer's disease (average age 83) has found that people who had infections or even bumps and bruises from a fall were more likely to have high blood levels of tumor necrosis factor-α, a protein involved in the inflammatory process, and were also more likely to experience memory loss or cognitive decline than people who did not have infections and who had low levels of the protein. Nearly half the participants experienced an infection or injury that led to inflammation during the study, and they experienced memory loss that was at twice the rate of those who did not have infections or injuries. Those with high levels of the protein in their blood at the beginning of the study had memory loss at four times the rate of those with low levels of the protein at the start of the study, and those with high levels who also experienced acute infections during the study had memory loss at 10 times the rate of those who started with low levels and had no infections over the six-month period.

Holmes, C. et al. 2009. Systemic inflammation and disease progression in Alzheimer disease. Neurology, 73, 768-774.

Poor sleep linked to later development of Alzheimer's

A mouse study has found that amyloid-beta significantly increases during periods of sleep deprivation. The discovery follows observation that peptide levels in both mice and humans increase significantly during the day and drop at night. When mice were only allowed to sleep four hours a day for 21 days, they had higher amyloid-beta plaque build-up in their brain than similar-aged mice with regular sleeping habits. The circadian fluctuation was found to reflect the activity of orexin, a hormone that regulates wakefulness. The findings suggest insomnia, late-night habits, and irregular sleep schedules during mid-life may be linked to the later development of Alzheimer's disease.

Kang, J-E. et al. 2009. Amyloid- Dynamics Are Regulated by Orexin and the Sleep-Wake Cycle. Science, Published Online September 24 
Alzheimers linked to lack of Zzzzs

Greater dementia risk in former N.F.L. players

A study commissioned by the National Football League reports that Alzheimer’s disease or similar memory-related diseases appear to have been diagnosed in the league’s former players vastly more often than in the national population: five times the national average among those 50 and older (6.1%)and 19 times for those aged 30 through 49. The findings are consistent with several recent studies regarding N.F.L. players and the effects of their occupational head injuries. The study involved a phone survey of 1,063 retired players (from an original random list of 1,625), who were asked questions derived from the standard National Health Interview Survey. Some health issues were reported at higher than the population rate (sleep apnea and elevated cholesterol — both risk factors for cognitive problems).

Oxygen treatment hastens memory loss in Alzheimer's mice

A study using genetically engineered mice has found that young adult Alzheimer's mice exposed to 100% oxygen during several 3-hour sessions demonstrated substantial memory loss, while those exposed to normal air had no measurable memory loss, and neither did normal mice without any genetic predisposition for Alzheimer's disease. The results suggest that people genetically predisposed to Alzheimer's disease or with excessive amounts of beta amyloid in their brains are at increased risk of developing the disease earlier if they receive high concentrations of oxygen, for example during or after surgery. The findings may help explain why some elderly patients develop memory loss after major surgery.

Arendash, G.W. et al. 2009. Oxygen treatment triggers cognitive impairment in Alzheimer's transgenic mice. NeuroReport, 20 (12), 1087-1092.

Delirium rapidly accelerates memory decline in Alzheimer's patients

A new analysis of data spanning 15 years and involving 408 Alzheimer’s patients, has revealed that among those 72 patients who developed delirium at some point, the average decline on cognitive tests was 2.5 points per year before the episode of delirium, and 4.9 points per year after. Across groups, the rate of decline was about three times faster in those who had delirium compared to those who did not. Delirium often develops in elderly patients following a medical disturbance, surgery or infection, but it is preventable in up to 40% of cases.

Fong, T.G. et al. 2009. Delirium accelerates cognitive decline in Alzheimer disease. Neurology, 72, 1570-1575.

Connection between heart disorder and Alzheimer's

A very large study, involving over 37,000 patients, has found that those with atrial fibrillation, regardless of age, were 44% more likely to develop dementia, and those younger than 70 were 130% more likely to develop Alzheimer's. Previous studies have shown a connection between atrial fibrillation and vascular dementia. Atrial fibrillation is the most common heart rhythm problem, and has a strong genetic link. It is also a risk factor for stroke.

The findings were presented Friday, May 15, at "Heart Rhythm 2009," the annual scientific sessions of the Heart Rhythm Society in Boston.

Inflammatory response to infection and injury may worsen dementia

Systemic inflammation – inflammation in the body as a whole – is known to have direct effects on brain function, but there has been little research into the impact of systemic inflammation on the progress of dementia and neurodegenerative diseases. Now, in a study to mimic the effect of bacterial infection in people with dementia, a mouse study has revealed that that the inflammatory response to infection in mice with prior neurodegenerative disease leads to exaggerated symptoms of the infection, causes changes in memory and learning and leads to accelerated progression of dementia.

Cunningham, C. et al. In press. Systemic Inflammation Induces Acute Behavioral and Cognitive Changes and Accelerates Neurodegenerative Disease. Biological Psychiatry

Physical frailty may be linked to Alzheimer's disease

Autopsies of the brains of 165 people who had been participants in a larger community study of chronic diseases of aging has revealed that Alzheimer's disease pathology (plaques and tangles) was associated with physical frailty in older persons regardless of whether they had dementia. The level of frailty was approximately twice as high in a person with a high level of Alzheimer’s pathology, and this was true regardless of medical history or level of physical activity. These findings raise the possibility that Alzheimer's disease may contribute to frailty or that frailty and Alzheimer's disease share a common cause. Studies show that about 7% of people over age 65 are considered frail; 45% after age 85.

Buchman, A.S., Schneider, J.A., Leurgans, S. & Bennett, D.A. 2008. Physical frailty in older persons is associated with Alzheimer disease pathology. Neurology, 71, 499-504.

Thyrotropin levels associated with Alzheimer's risk in women

A clinically detectable over- or under-active thyroid has long been recognized as a potentially reversible cause of cognitive impairment. Now a large long-running study of thyrotropin (a hormone secreted by the pituitary gland that helps regulate thyroid gland function) levels has found that women with the lowest and highest levels of thyrotropin had more than double the risk of developing Alzheimer's disease. No relationship was observed between thyrotropin levels and Alzheimer's disease risk in men.

Tan, Z.S. et al. 2008. Thyroid Function and the Risk of Alzheimer Disease: The Framingham Study. Archives of Internal Medicine, 168(14), 1514-1520.

Short arms and legs linked to risk of dementia

Several studies have shown that early life environment plays an important role in susceptibility to chronic disease later in life. Data from the Cardiovascular Health Cognition Study (involving 2,798 people for an average of five years) has now found that women with the shortest arm spans were 1.5 times more likely to develop dementia and Alzheimer’s disease than women with longer arm spans. For every inch longer a woman’s leg, the risk of dementia and Alzheimer’s disease was reduced by 16%. In men, only arm span was associated with a lower risk of dementia. With every increased inch in arm span, men had a 6% decrease in risk of dementia. The association between short limbs and dementia risk may be due to poor nutrition in early life, which can affect limb growth (which implies that there should be no such connection if your short limbs are due to genetics).

Szekely, C.A. et al. 2008. No advantage of Aβ42-lowering NSAIDs for prevention of Alzheimer dementia in six pooled cohort studies. Neurology, 70, 2291-2298.

Inhaled anesthetics might increase the risk of Alzheimer's

A study using a new imaging technique has been able to see why anesthetics might cause amyloid β peptides to clump together, and whether one method of anesthesia was better than another. Previous studies have found that the inhaled anesthetics halothane and isoflurane and the intravenous anesthetic propofol encouraged the growth and clumping of Aβ in a test tube experiment. The new study found that the inhaled anesthetics caused the highest levels of Aβ aggregation, while the injected anesthetic propofol only interacted and caused aggregation at high concentrations, and thiopental did not cause the clustering of Aβ peptides even at high concentrations.

Mandal, P.K., Williams, J.P. & Mandal, R. 2007. Molecular Understanding of Aβ Peptide Interaction with Isoflurane, Propofol, and Thiopental: NMR Spectroscopic Study. Biochemistry, 46 (3), 762 –771.

Anesthetics a risk factor for Alzheimer’s?

The link between surgery and cognitive problems has long been noted, but it’s never been clear whether postoperative cognitive dysfunction was the result of the surgery itself or the anaesthetics. Now animal studies and test tube experiments are beginning to show that certain anaesthetics reduce the rate at which brain cells are born and develop. The latest study reveals that the inhaled anaesthetics halothane and isoflurane encourage clumping of beta amyloid protein, as does the commonly used intravenous anaesthetic propofol, at least at higher concentrations — suggesting that giving elderly patients certain general anaesthetics could increase their risk of developing Alzheimer's disease. The intravenous anaesthetic thiopental appears to have no effect on the proteins.

The study was presented at the annual Society for Neuroscience Meeting held in Atlanta, Georgia, October 14-18.

Brain activity, drugs could affect Alzheimer's progression

Mouse studies have revealed that the activity of connections among brain cells significantly affects levels of the toxic protein beta-amyloid, suggesting that the kind of mental activity people practice or drugs they might take fo affect their risk of Alzheimer’s or the disease progression. The researchers suggest that enriched environments may increase overall synaptic activity in some brain regions and decrease it in others. Increased activity in some brain regions might result in increased susceptibility to beta-amyloid deposition if the activated neural circuits contain high levels of human APP expression. Drugs used to treat neuropsychiatric disorders directly influence neurotransmitters, and their receptors, thereby altering synaptic activity.

Cirrito, J.R. et al. 2005. Synaptic Activity Regulates Interstitial Fluid Amyloid-b Levels In Vivo. Neuron, 48, 913–922.

New research suggests heart bypass surgery increases risk of Alzheimer's disease

Patients who have either coronary artery bypass graft surgery or coronary angioplasty are at an increased risk of developing Alzheimer's disease, according to a study involving 5,216 people who underwent coronary artery bypass graft surgery (CABG) and 3,954 people who had a percutaneous transluminal coronary angioplasty (PTCA) in 1996 and 1997. The researchers suggest the trauma to the brain during surgery is the principle cause.

Lee, T.A., Wolozin, B., Weiss, K.B. & Bednar, M.M. 2005. Assessment of the Emergence of Alzheimer's Disease Following Coronary Artery Bypass Graft Surgery or Percutaneous Transluminal Coronary Angioplasty. Journal of Alzheimer's Disease, 7 (4), 319-324.

Testosterone loss may lead to Alzheimer's

A new study suggests that, like estrogen loss in older women, decreased levels of testosterone may put aging men at risk for Alzheimer's disease. The research suggests that testosterone both protects neurons from injury, and reduces levels of beta-amyloid.

Rosario, E.R., Chang, L., Stanczyk, F.Z. & Pike, C.J. 2004. Age-Related Testosterone Depletion and the Development of Alzheimer Disease. JAMA, 292, 1431-1432.

Coronary artery bypass surgery not a risk factor for dementia

A comparison of dementia patients with controls has found that dementia patients are no more likely than those without dementia to have had coronary artery bypass surgery.

Minorities hardest hit by Alzheimer's disease

A study of 119 Latinos and 55 non-Latino white Alzheimer patients suggests that Latinos in the U.S. develop Alzheimer's symptoms much earlier than their white, non-Latino peers. There are several known factors which may be responsible for this apparent vulnerability in Latinos: high rates of vascular disease, leave school earlier, and less likely to use medical services or have health insurance than other Americans.

South Carolina, as the only U.S. state that keeps a comprehensive database of people with a diagnosis of Alzheimer's disease, has found that African Americans aged 55 to 64 years were more than three times as likely to have Alzheimer's as their European American counterparts. At ages 65 to 84, African Americans were more than twice as likely to have Alzheimer's. South Carolina has greater rates of obesity, diabetes, and related health problems than the rest of the country, especially amongst African Americans.

Another study has found that, in order to avoid overestimating the number of African Americans who may have early signs of Alzheimer's disease, screening tests must be adapted to cultural differences. The study involved 635 people over the age of 60. Researchers found that, using current scoring methods, African Americans scored lower on various neuropsychological tests. Even when education was taken into account, 35% of African Americans scored low enough to warrant a diagnosis of MCI, compared to only 15% of European Americans. However, when the researchers applied new, racially sensitive scoring methods they've developed, the difference in MCI rates disappeared.

Reported at The 9th International Conference on Alzheimer's Disease and Related Disorders (ICAD), July 17-22, at the Pennsylvania Convention Center in Philadelphia, Pennsylvania:

Christopher Clark – Latino Patients with AD Have An Earlier Age of Symptoms Onset Compared to Anglos (P1-041)

James Laditka – Epidemiology of Alzheimer's Disease: Race Effects, Area Variation, and Clustering (P3-132)

Marjorie Marenberg – Racial Differences in Screening of MCI in a Primary Care Population (O4-01-02)

Alzheimer's Association offers information about providing culturally sensitive care at

Low free testosterone levels linked to Alzheimer's disease in older men

A study evaluating the testosterone levels of 574 men, ages 32 to 87, who participated in the Baltimore Longitudinal Study of Aging (BLSA), found that older men with lower levels of free, or unbound, testosterone circulating in their bloodstreams were apparently at higher risk of developing Alzheimer's than their peers. This is believed to be the first study to associate low circulating blood levels of free testosterone with Alzheimer’s years before diagnosis. Previously, the same researchers had found that older men with high levels of circulating free testosterone have better visual and verbal memory and perform spatial tasks more adeptly than their peers.

Moffat, S.D., Zonderman, A.B., Metter, E.J., Kawas, C., Blackman, M.R., Harman, S.M. & Resnick, S.M. 2004. Free testosterone and risk for Alzheimer disease in older men. Neurology, 62, 188-193.

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Common drugs that can cause memory problems in older adults

A large study, involving 3,690 older adults, has found that drugs with strong anticholinergic effects cause memory and cognitive impairment when taken continuously for a mere two months. Moreover, taking multiple drugs with weaker anticholinergic effects, such as many common over-the-counter digestive aids, affected cognition after 90 days’ continuous use. In both these cases, the risk of cognitive impairment doubled (approximately).



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Cognitive decline in old age related to poorer sleep

February, 2013
  • A new study confirms the role slow-wave sleep plays in consolidating memories, and reveals that one reason for older adults’ memory problems may be the quality of their sleep.

Recent research has suggested that sleep problems might be a risk factor in developing Alzheimer’s, and in mild cognitive impairment. A new study adds to this gathering evidence by connecting reduced slow-wave sleep in older adults to brain atrophy and poorer learning.

The study involved 18 healthy young adults (mostly in their 20s) and 15 healthy older adults (mostly in their 70s). Participants learned 120 word- nonsense word pairs and were tested for recognition before going to bed. Their brain activity was recorded while they slept. Brain activity was also measured in the morning, when they were tested again on the word pairs.

As has been found previously, older adults showed markedly less slow-wave activity (both over the whole brain and specifically in the prefrontal cortex) than the younger adults. Again, as in previous studies, the biggest difference between young and older adults in terms of gray matter volume was found in the medial prefrontal cortex (mPFC). Moreover, significant differences were also found in the insula and posterior cingulate cortex. These regions, like the mPFC, have also been associated with the generation of slow waves.

When mPFC volume was taken into account, age no longer significantly predicted the extent of the decline in slow-wave activity — in other words, the decline in slow-wave activity appears to be due to the brain atrophy in the medial prefrontal cortex. Atrophy in other regions of the brain (precuneus, hippocampus, temporal lobe) was not associated with the decline in slow-wave activity when age was considered.

Older adults did significantly worse on the delayed recognition test than young adults. Performance on the immediate test did not predict performance on the delayed test. Moreover, the highest performers on the immediate test among the older adults performed at the same level as the lowest young adult performers — nevertheless, these older adults did worse the following day.

Slow-wave activity during sleep was significantly associated with performance on the next day’s test. Moreover, when slow-wave activity was taken into account, neither age nor mPFC atrophy significantly predicted test performance.

In other words, age relates to shrinkage of the prefrontal cortex, this shrinkage relates to a decline in slow-wave activity during sleep, and this decline in slow-wave sleep relates to poorer cognitive performance.

The findings confirm the importance of slow-wave brainwaves for memory consolidation.

All of this suggests that poorer sleep quality contributes significantly to age-related cognitive decline, and that efforts should be made to improve quality of sleep rather than just assuming lighter, more disturbed sleep is ‘natural’ in old age!




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Early surgical menopause linked to faster cognitive decline

February, 2013

Women who undergo surgical menopause at an earlier age may have an increased risk of cognitive decline.

The issue of the effect of menopause on women’s cognition, and whether hormone therapy helps older women fight cognitive decline and dementia, has been a murky one. Increasing evidence suggests that the timing and type of therapy is critical. A new study makes clear that we also need to distinguish between women who experience early surgical menopause and those who experience natural menopause.

The study involved 1,837 women (aged 53-100), of whom 33% had undergone surgical menopause (removal of both ovaries before natural menopause). For these women, earlier age of the procedure was associated with a faster decline in semantic and episodic memory, as well as overall cognition. The results stayed the same after factors such as age, education and smoking were taken into consideration.

There was also a significant association between age at surgical menopause and the plaques characteristic of Alzheimer's disease. However, there was no significant association with Alzheimer’s itself.

On the positive side, hormone replacement therapy was found to help protect those who had surgical menopause, with duration of therapy linked to a significantly slower decline in overall cognition.

Also positively, age at natural menopause was not found to be associated with rate of cognitive decline.


Bove, R. et al. 2013. Early Surgical Menopause Is Associated with a Spectrum of Cognitive Decline. To be presented at the American Academy of Neurology's 65th Annual Meeting in San Diego, March 21, 2013.




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Immune system may protect against Alzheimer's

July, 2012

New studies involving genetically-engineered mice and older adult humans support a connection between the immune system and cognitive impairment in old age.

A number of studies have come out in recent years linking age-related cognitive decline and dementia risk to inflammation and infection (put inflammation into the “Search this site” box at the top of the page and you’ll see what I mean). New research suggests one important mechanism.

In a mouse study, mice engineered to be deficient in receptors for the CCR2 gene — a crucial element in removing beta-amyloid and also important for neurogenesis — developed Alzheimer’s-like pathology more quickly. When these mice had CCR2 expression boosted, accumulation of beta-amyloid decreased and the mice’s memory improved.

In the human study, the expression levels of thousands of genes from 691 older adults (average age 73) in Italy (part of the long-running InCHIANTI study) were analyzed. Both cognitive performance and cognitive decline over 9 years (according to MMSE scores) were significantly associated with the expression of this same gene. That is, greater CCR2 activity was associated with lower cognitive scores and greater decline.

Expression of the CCR2 gene was also positively associated with the Alzheimer’s gene — meaning that those who carry the APOE4 variant are more likely to have higher CCR2 activity.

The finding adds yet more weight to the importance of preventing / treating inflammation and infection.


[2960] Harries, L. W., Bradley-Smith R. M., Llewellyn D. J., Pilling L. C., Fellows A., Henley W., et al.
(2012).  Leukocyte CCR2 Expression Is Associated with Mini-Mental State Examination Score in Older Adults.
Rejuvenation Research. 120518094735004 - 120518094735004.

Naert, G. & Rivest S. 2012. Hematopoietic CC-chemokine receptor 2-(CCR2) competent cells are protective for the cognitive impairments and amyloid pathology in a transgenic mouse model of Alzheimer's disease. Molecular Medicine, 18(1), 297-313.

El Khoury J, et al. 2007. Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease. Nature Medicine, 13, 432–8.




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Migraines and headaches linked to more brain lesions in older adults

March, 2011
  • Older adults who have a history of severe headaches are more likely to have a greater number of brain lesions, but do not show greater cognitive impairment (within the study time-frame).

Lesions of the brain microvessels include white-matter hyperintensities and the much less common silent infarcts leading to loss of white-matter tissue. White-matter hyperintensities are common in the elderly, and are generally regarded as ‘normal’ (although a recent study suggested we should be less blasé about them — that ‘normal’ age-related cognitive decline reflects the presence of these small lesions). However, the degree of white-matter lesions is related to the severity of decline (including increasing the risk of Alzheimer’s), and those with hypertension or diabetes are more likely to have a high number of them.

A new study has investigated the theory that migraines might also lead to a higher number of white-matter hyperintensities. The ten-year French population study involved 780 older adults (65+; mean age 69). A fifth of the participants (21%) reported a history of severe headaches, of which 71% had migraines.

Those with severe headaches were twice as likely to have a high quantity of white-matter hyperintensities as those without headaches. However, there was no difference in cognitive performance between the groups. Those who suffered from migraines with aura (2% of the total), also showed an increased number of silent cerebral infarcts — a finding consistent with other research showing that people suffering from migraine with aura have an increased risk of cerebral infarction (or strokes). But again, no cognitive decline was observed.

The researchers make much of their failure to find cognitive impairment, but I would note that, nevertheless, the increased number of brain lesions does suggest that, further down the track, there is likely to be an effect on cognitive performance. Still, headache sufferers can take comfort in the findings, which indicate the effect is not so great that it shows up in this decade-long study.





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Protein in the urine: A warning sign for cognitive decline

December, 2010

Two recent studies indicate that the presence of protein in the urine, even in small amounts, could be a warning sign that a patient may develop cognitive impairment with age.

A six-year study involving over 1200 older women (70+) has found that low amounts of albumin in the urine, at levels not traditionally considered clinically significant, strongly predict faster cognitive decline in older women. Participants with a urinary albumin-to-creatinine ratio of >5 mcg/mg at the start of the study experienced cognitive decline at a rate 2 to 7 times faster in all cognitive measures than that attributed to aging alone over an average 6 years of follow-up. The ability most affected was verbal fluency. Albuminuria may be an early marker of diffuse vascular disease.

Data from 19,399 individuals participating in the Renal Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, of whom 1,184 (6.1%) developed cognitive impairment over an average follow-up of 3.8 years, has found that those with albuminuria were 1.31-1.57 times more likely to develop cognitive impairment compared to individuals without albuminuria. This association was strongest for individuals with normal kidney function. Conversely, low kidney function was associated with a higher risk for developing cognitive impairment only among individuals without albuminuria. Surprisingly, individuals with albuminuria and normal kidney function had a higher probability for developing cognitive impairment as compared to individuals with moderate reductions in kidney function in the absence of albuminuria.

Both albuminuria and low kidney function are characteristics of kidney disease.


Lin, J., Grodstein, F., Kang, J.H. & Curhan, G. 2010. A Prospective Study of Albuminuria and Cognitive Decline in Women. Presented at ASN Renal Week 2010 on November 20 in Denver, CO.

Tamura, M.K. et al. 2010. Albuminuria, Kidney Function and the Incidence of Cognitive Impairment in US Adults. Presented at ASN Renal Week 2010 on November 20 in Denver, CO.




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