risk factors

Vascular & Mixed Dementia

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Vascular dementia, as its name suggests, is caused by poor blood flow, produced by a single, localized stroke, or series of strokes.

It is the second most common dementia, accounting for perhaps 17% of dementias. It also co-occurs with Alzheimer's in 25-45% of cases. Although there are other types of dementia that also co-occur with Alzheimer's, mixed dementia generally refers to the co-occurrence of Alzheimer's and vascular dementia.

Risk factors

In general, unsurprisingly, vascular dementia has the same risk factors as cerebrovascular disease.

A study1 of 173 people from the Scottish Mental Survey of 1932 who have developed dementia has found that, compared to matched controls, those with vascular dementia were 40% more likely to have low IQ scores when they were children than the people who did not develop dementia. Because this was not true for those with Alzheimer's disease, it suggests that low childhood IQ may act as a risk factor for vascular dementia through vascular risks rather than the "cognitive reserve" theory.

Prevention

The exciting thing about vascular dementia is that it is far more preventable than other forms of dementia. As with risk, as a general rule, the same things that help you protect you from heart attacks and stroke will help protect you from vascular dementia. This means diet, and it means exercise.

A four-year study2 involving 749 older adults has found that the top one-third of participants who exerted the most energy in moderate activities such as walking were significantly less likely to develop vascular dementia than those people in the bottom one-third of the group.

Treatment

Apart from normal medical treatment for cerebrovascular problems, there are a couple of interesting Chinese studies that have looked specifically at vascular dementia.

The herb gastrodine has been used in China for centuries to treat disorders such as dizziness, headache and even ischemic stroke. A 12-week, randomized, double-blind trial3 involving 120 stroke patients who were diagnosed with mild to moderate vascular dementia has found that  gastrodine and Duxil® (a drug used to treat stroke patients in China) produced similar overall levels of cognitive improvement -- although more patients showed 'much improvement' with gastrodine (23% vs 14%).

A Chinese pilot study4 involving 25 patients with mild to moderate vascular dementia found that ginseng compound significantly improved their average memory function after 12 weeks, but more research (larger samples, placebo-controls) is needed before this finding can be confirmed. Five years on I have still not seen such a study.

References: 

  1. McGurn, B., Deary, I.J. & Starr, J.M. 2008. Childhood cognitive ability and risk of late-onset Alzheimer and vascular dementia. Neurology, first published on June 25, 2008 as doi: doi:10.1212/01.wnl.0000319692.20283.10
  2. Ravaglia, G. et al. 2007. Physical activity and dementia risk in the elderly. Findings from a prospective Italian study. Neurology, published online ahead of print December 19.
  3. Tian, J.Z. et al. 2003. A double-blind, randomized controlled clinical trial of compound of Gastrodine in treatment of mild and moderate vascular dementia in Beijing, China. Presented at the American Heart Association's Second Asia Pacific Scientific Forum in Honolulu on June 10.
  4. Tian, J.Z. et al. 2003. Presented at the American Stroke Association's 28th International Stroke Conference on February 14 in Phoenix. Press release

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Dementia: A general introduction

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Dementia is estimated1 to afflict over 35.5 million people worldwide -- this includes nearly 10 million people in Europe, nearly 4.4 million in North America, nearly 7 million in South and Southeast Asia, about 5.5 million in China and East Asia and about 3 million in Latin America.

The estimated prevalence for over 60s is 4.7% worldwide. Because this is a disorder of age, prevalence is of course greatly affected by the proportion of people reaching their senior years. Hence the prevalence is higher in the more developed countries: the estimated prevalence in Western Europe and North America is 7.2% and 6.9% respectively, compared to 2.6% in Africa.

What kinds of dementia are most common?

The prevalence of the various dementia types is a complicated story. Certainly Alzheimer's disease is by far the most common type of dementia, accounting for perhaps 70% of all dementias (although a 2006 study13 suggested that non-Alzheimer dementias were as common as Alzheimer's — however this was based on dementia among military veterans). The second most common dementia is almost certainly vascular dementia, which may account for some 17% of dementias. However, the actual numbers are made uncertain by the fact that these two dementias often occur together.

At minimum, around a quarter of Alzheimer's cases have been found, on autopsy, to also have vascular pathology; this proportion reaches higher levels when the samples are not restricted to dementia clinics. One such community-based study2, for example, found 45% of the Alzheimer's cases also showed significant vascular pathology. Another, U.K., study3 found a similar proportion (46%).

Another, large long-running, study14 has found that only 30% of people with signs of dementia had Alzheimer’s disease alone. 42% had Alzheimer’s disease with cerebral infarcts (strokes) and 16% had Alzheimer’s disease with Parkinson’s disease (including two people with all three conditions). Infarcts alone caused another 12% of the cases. Vascular dementia caused another 12%.

Although there are other types of dementia that also co-occur with Alzheimer's, mixed dementia generally refers to the co-occurrence of Alzheimer's and vascular dementia.

The other important dementia type that co-occurs with Alzheimer's at a high rate is dementia with Lewy bodies, also considered to be one of the most common dementias (although, due to inconsistent criteria, estimates of its actual prevalence vary wildly). It is estimated to co-occur with Alzheimer's pathology around half the time. At a lesser frequency, but still high, is Parkinson's disease dementia — about 20% of Alzheimer's patients also have Parkinson's disease.

But it is probably fair to say that the distinction between these dementia types is not clear-cut. Lewy bodies are found in a high proportion of both Alzheimer's and Parkinson's patients — the number of cases of 'pure' Lewy body dementia is much smaller. It's been said, in fact, that the main difference between Lewy body dementia and Parkinson's disease dementia lies in the timing — Parkinson's disease dementia will be preceded by at least a year and more likely a number of years, by full-blown Parkinson's disease.

Regardless of the difficulties in establishing clear clinical criteria, however, there is no doubt that Alzheimer's co-occurs with vascular pathology or Lewy body pathology at a startlingly high rate.

One of the problems with clearly distinguishing between these types of dementia is a happy one: vascular and Alzheimer's pathology can be found, at autopsy, in many elderly brains that have not shown symptoms of dementia.

For example, in one community-based study4, in which the median age at death was around 85 for the 209 individuals, 48% had had dementia, of whom 64% showed Alzheimer's pathology. However, 33% of those who had not had dementia showed similar levels of Alzheimer's plaques. Similarly, some amount of tau tangles (another aspect of Alzheimer's pathology) was found in 61% of the demented and 34% of the non-demented individuals. Finally, multiple vascular pathology was found in 46% of the demented group and 33% of the non-demented, and vascular lesions were equally common in both.

And in the large long-running study mentioned earlier14, in those without dementia, brain autopsy revealed the presence of Alzheimer’s in 24% of cases, and infarctions in 18%.

How likely am I to develop dementia?

The question of how likely any person is to develop dementia must begin with estimates of prevalence, but this of course is only the very beginning of the story.

Estimating prevalence is complicated by the fact that dementia is greatly affected by lifestyle, environmental, and genetic factors, and consequently prevalence varies a lot depending on geographic region.

Different dementia sub-types have different causes, and some give a much greater weight to genetic or environmental factors than others. However, the finding that dementia risk is much greater in those with more than one pathology, and that Alzheimer’s pathology with cerebral infarcts is a very common combination, adds to growing evidence that dementia risk might be reduced with the same tools we use for cardiovascular disease such as control of blood cholesterol levels and hypertension.

Age as a factor

The first American study to use nationally representative data5 (rather than extrapolating from regional data) came up with a figure of 13.9% of those aged 71 and older (one in seven). But age of course makes all the difference in the world. The study found 5% of those aged 71 to 79, rising to 37.4% of those age 90 and older.

Although all the dementia types show an increase with age, Alzheimer's is particularly a disorder of age: although the study found only 46.7% of those with dementia in their 70s had Alzheimer's, for those in their 90s, Alzheimer's was the dementia type for 79.5% of them.

An Italian study of over 2000 seniors over 80 years old6 confirms that dementia does indeed keep increasing with age (it had been thought that risk leveled off for those who reached their 90s). The study found that 13.5% of those aged 80 to 84 had dementia, rising sharply to 30.8% of those 85 to 89, 39.5% of those 90 to 94, and 52.8% among those older than 94.

Gender as a factor

A number of studies have found differences between men and women, or between difference ethnicities, but this large, nationally representative study found that, although on the face of it there were race and gender differences, these differences disappeared once age, years of education, and presence of at least one "Alzheimer's gene" was taken into account.

However, an American study of over 900 seniors over 90 years old7 found that women of this age were much more likely to have dementia than men (some 45% of them, compared to 28% of the men), and that the likelihood of having dementia kept increasing with age for the women, but not for the men. Of course, more women than men survive to this age (some two-thirds of the participants were women).

Interestingly, education was protective for the women (the risk of dementia decreasing the more years of education the individual had had) but not for the men. The study participants were not, however, a random sampling -- they all came from the same retirement community, and most were white and of high socioeconomic status. Given that, and considering the times in which they were born, it seems likely that there would be far more variability in educational level among the women than the men. The men, while less likely to develop dementia, did tend to decline faster if they did develop it.

The Italian oldest-old study, too, found more women than men had dementia: across all ages, 25.8% of the women and 17.1% of the men.

These figures don't of course tell us how many develop dementia at those ages. Obviously, survival rates are a factor, and as we saw in the other study, male and female survival rates do vary. The figures for new cases of dementia developing in these age bands were:

  • 6% at 80 to 84 years;
  • 12.4% at 85 to 89 years;
  • 13.1% from 90 to 94 years; and
  • 20.7% among those over 94.

These figures make even more clear what was apparent in the earlier figures: dementia jumps suddenly in the later half of the 80s, and again in the later half of the 90s.

Importantly, however, the incidence of new cases shows us how important the gender difference in survival rates is: the difference in prevalence is much smaller in these terms --9.2% among women and 7.2% among men.

The study, which canvassed everyone in the age group within a specific geographical area and had an 88% response rate, had a ratio of 74 women to 26 men. Because the number of men at the very highest ages was so small, we can't draw any firm conclusions about gender differences at those ages.

The Italian study involves a very different population from that of the American study: Varese is in a heavily industrialised part of northern Italy, with a high immigrant population, and the average amount of education was only 5.1 years.

A review of 26 studies looking at dementia prevalence in Europe8 confirmed rates for men rising from 1.8% in the 65-69 years age range up to 30% in the over 90 years age group, and for women rising from 1.5% to 30% in the 80-85 years age band. However (and confirming the American study), rates in the oldest old for women rose to over 50% in those over 95 years.

Early onset of dementia

The average age at the onset of dementia is around 80 years. Early-onset dementia is defined arbitrarily (and variably) as occurring before 60-65. Early-onset cases have been estimated to make upabout 6-7% of all cases of Alzheimer's disease, and though a lot of attention has been given to them, only about 7% of early-onset cases are in fact familial9.

Familial cases involve mutations in specific genes (the APP or presenilin genes); they do not include what is popularly referred to as the "Alzheimer's gene" — variants of APOE. A 1995 study10 calculated that a person with no family history of Alzheimer's disease who has an e4 allele has a lifetime risk of 29%, compared to a risk of 9% if they don't have an e4 allele. In other words, if you don't have any of the Alzheimer's risk genes, or any family history, you only have a 9% risk of developing Alzheimer's, and even if you do have the "Alzheimer's gene", your chance of not getting Alzheimer's is still over 70%. Your risk does, however, go up dramatically if both your APOE alleles are e4.

A large study11 found, however, that there were both ethnic and gender differences for the risk of this genetic factor. The effect of having an e4 allele was much greater among Japanese compared to Caucasian, and greater for Caucasian compared to African American and Hispanic. Additionally, the effect of having an e4 allele becomes less significant after 70.

There is evidence12 that the age of onset for both Alzheimer's and Parkinson's diseases, for those genetically disposed, is controlled by genes on chromosome 10.

References: 

  1. From the 2009 World Alzheimer's Report: http://www.alz.co.uk/research/worldreport/
  2. Lim A, Tsuang D, Kukull W, et al. 1999. Cliniconeuropathological correlation of Alzheimer’s disease in a community-based case series. Journal of the American Geriatric Society, 47, 564-569.
  3. Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS). 2001. Pathological correlates of late-onset dementia in a multicentre, community-based population in England and Wales. Lancet, 357, 169-175.
  4. Langa, K.M., Foster, N.L. & Larson, E.B. 2004. Mixed Dementia: Emerging Concepts and Therapeutic Implications. JAMA, 292(23), 2901-2908.
  5. Plassman, B.L. et al. 2007. Prevalence of Dementia in the United States: The Aging, Demographics, and Memory Study. Neuroepidemiology, 29, 125-132. 
  6. Lucca, U. et al. 2009. Risk of dementia continues to rise in the oldest old: The Monzino 80-plus Study. Presented on July 14, 2009, at the annual International Conference on Alzheimer's Disease in Vienna. http://www.alz.org/icad/documents/abstracts/abstracts_prev_ICAD09.pdf
  7. Corrada, M.M. et al. 2008. Prevalence of dementia after age 90: Results from The 90+ Study. Neurology, 71 (5), 337-343.
  8. Reynish, E. et al. 2009. Systematic Review and Collaborative Analysis of the Prevalence of Dementia in Europe. Presented on July 14, 2009, at the annual International Conference on Alzheimer's Disease in Vienna. http://www.alz.org/icad/documents/abstracts/abstracts_prev_ICAD09.pdf
  9. Nussbaum, R.L. & Ellis, C.E. 2003. Alzheimer's Disease and Parkinson's Disease. New England Journal of Medicine, 348 (14), 1356-1364. http://content.nejm.org/cgi/content/full/348/14/1356#R23
  10. Seshadri S, Drachman DA, Lippa CF. 1995. Apolipoprotein E epsilon 4 allele and the lifetime risk of Alzheimer's disease: what physicians know, and what they should know. Archives of Neurology, 52, 1074-1079. http://tinyurl.com/ya7vss7
  11. Farrer LA, Cupples LA, Haines JL, et al. Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease: a meta-analysis. JAMA 1997;278:1349-1356. http://tinyurl.com/yb9tdju
  12. Li, Y. et al. 2002. Age at Onset in Two Common Neurodegenerative Diseases Is Genetically Controlled. American Journal of Human Genetics, 70, 985-993. Press release
  13. Ross, E.D. et al. 2006. Changing Relative Prevalence of Alzheimer Disease versus Non-Alzheimer Disease Dementias: Have We Underestimated the Looming Dementia Epidemic? Dementia and Geriatric Cognitive Disorders, 22 (4), 273-277.
  14. Schneider, J.A., Arvanitakis, Z., Bang, W. & Bennett, D.A. 2007. Mixed brain pathologies account for most dementia cases in community-dwelling older persons. Neurology, published ahead of print June 13.

 

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Rapid blood pressure drops in middle age linked to dementia in old age

  • A large study indicates that an inclination to dizziness on standing up is associated with a greater risk of developing cognitive impairment and dementia decades later.

Data from over 11,500 participants in the Atherosclerosis Risk in Communities (ARIC) cohort has found evidence that orthostatic hypotension in middle age may increase the risk of cognitive impairment and dementia 20 years later.

Orthostatic hypotension is the name for the experience of dizziness or light-headedness on standing up. Previous research has suggested an association between orthostatic hypotension and cognitive decline in older adults.

In this study, participants aged 45-64 were tested for orthostatic hypotension in 1987. Those with it (703, around 6%) were 40% more likely to develop dementia in the next 20 years. They also had some 15% more cognitive decline.

Orthostatic hypotension was defined as a drop of 20 mmHg or more in systolic blood pressure or 10 mmHg or more in diastolic blood pressure, when the individual stood up after 20 minutes lying down.

More work is needed to understand the reason for the association.

https://www.eurekalert.org/pub_releases/2017-03/jhub-rbp030817.php

Rawlings, Andreea. 2017. Orthostatic Hypotension is Associated with 20-year Cognitive Decline and Incident Dementia: The Atherosclerosis Risk in Communities (ARIC) Study. Presented March 10 at the American Heart Association's EPI|LIFESTYLE 2017 Scientific Sessions in Portland, Oregon.

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Higher coffee consumption linked to lower dementia risk in women

  • A large study adds to evidence that caffeine helps older women fight cognitive impairment and dementia.
  • This is supported by two animal studies showing precisely how caffeine is valuable for keeping the brain healthy.

Data from the Women's Health Initiative Memory Study, involving 6,467 postmenopausal women (65+) who reported some level of caffeine consumption, has found that those who consumed above average amounts of coffee had a lower risk of developing dementia.

Caffeine intake was estimated from a questionnaire. The median intake was 172 mg per day (an 8-ounce cup of brewed coffee contains 95mg of caffeine, 8-ounces of brewed black tea contains 47mg, so slightly less than 2 cups of coffee or less than 4 cups of tea). The women were cognitively assessed annually.

Over ten years, 388 were diagnosed with probable dementia (209) or MCI (179). Those who consumed above the median amount of caffeine had a 36% reduction in risk. The average intake in this group was 261 mg (3 cups of coffee), while the average intake for those below the median was 64 mg per day (less than one cup).

Risk factors such as hormone therapy, age, race, education, body mass index, sleep quality, depression, hypertension, prior cardiovascular disease, diabetes, smoking, and alcohol consumption, were taken into account.

The findings are consistent with other research finding a benefit for older women. It should not be assumed that the findings apply to men. It also appears that there may be a difference depending on education level. This sample had a high proportion of college-educated women.

It should also be noted that there was no clear dose-response effect — we could put more weight on the results if there was a clear relationship between amount of caffeine and benefit. Part of the problem here, however, is that it’s difficult to accurately assess the amount of caffeine, given that it’s based on self-report intake of coffee and tea, and the amount of caffeine in different beverages varies significantly.

Moreover, we do have a couple of mechanisms for caffeine to help fight age-related cognitive decline.

A recent study using rats modified to have impaired receptors for the adenosine A2A produced rats showing typical characteristics of an aging brain. In humans, too, age-related cognitive decline has been associated with over-activation of these receptors and dysfunction in glucocorticoid receptors.

The rat study shows that over-activation of the adenosine A2A receptors reduces the levels of glucocorticoid receptors in the hippocampus, which in turn impairs synaptic plasticity and cognition. In other words, it is the over-activation of the adenosine receptors that triggers a process that ends with cognitive impairment.

The point of all this is that caffeine inhibits the adenosine A2A receptors, and when the rats were given a caffeine analogue, their memory deficits returned to normal.

Another more recent study has found that caffeine increases the production of an enzyme that helps prevent tau tangles.

Building on previous research finding that an enzyme called NMNAT2 not only protects neurons from stress, but also helps prevent misfolded tau proteins (linked to Alzheimer’s, and other neurodegenerative disorders), the study identified 24 compounds (out of 1,280 tested) as having potential to increase the production of NMNAT2. One of the most effective of these was caffeine.

When caffeine was given to mice modified to produce lower levels of NMNAT2, the mice began to produce the same levels of the enzyme as normal mice.

https://www.eurekalert.org/pub_releases/2016-10/oupu-fwc100316.php

https://www.eurekalert.org/pub_releases/2016-08/ind-cai083016.php

https://www.eurekalert.org/pub_releases/2017-03/iu-cbe030717.php

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Age-related drop in body temperature worsens Alzheimer's disease

  • A mouse study suggests that some Alzheimer’s symptoms are made worse by falling body temperature — and are helped by improving body temperature.

Our bodies’ ability to regulate its temperature gets worse with age, along with a slowing metabolism. We also become more vulnerable to Alzheimer's as we age. A study compared mice genetically engineered to manifest Alzheimer's symptoms as they age with normal mice. They found that these transgenic mice were worse at maintaining their body temperature as they aged, with the difference reaching almost 1° Celsius by the age of 12 months.

Moreover, there was an increase in Alzheimer’s symptoms (such as a greater increase in abnormal tau proteins and loss of synaptic proteins) in transgenic mice when they were exposed to low temperatures.

But — and this is the exciting bit — when the mice were given one week in a 28°C environment, and their body temperature increased by 1°C, beta-amyloid production dropped substantially, and memory test results were comparable to those of normal mice.

While obviously these results need to be replicated in humans, the findings do suggest that improving body temperature might be helpful for those in early stages of Alzheimer’s. Body temperature can be increased through physical activity, diet, drugs, or simply by turning the heat up.

http://www.eurekalert.org/pub_releases/2016-04/ul-dib040716.php

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Tau tangles why TBI increases risk of Alzheimer's

  • Mouse study shows tau tangles may be behind increased Alzheimer's risk for those who have suffered a traumatic brain injury.

We know that traumatic brain injury increases the risk of later developing neurodegenerative disorders such as Alzheimer's disease, but we haven't known why. New mouse studies suggest a reason.

In the research, mice who had a toxic form of tau protein (taken from mice who had suffered TBI) injected into their hippocampus, showed impaired memory and cognition. Moreover, levels of the aggregated tau protein not only increased in the hippocampus, but also in the cerebellum (which is quite some distance away from the hippocampus). This is consistent with other research showing that tau tangles spread from the initial injection site, using mice modeling Alzheimer's disease.

The study followed on from previous research showing that this form of tau protein increases after a traumatic brain injury and may contribute to development of chronic traumatic encephalopathy (a condition experienced by many professional athletes and military personnel).

The findings support the hypothesis that many of the symptoms of TBI may be down to an increase in these tau tangles, and that this may also be responsible for the increased risk for neurodegenerative disease. As an obvious corollary, it also suggests that the tau tangles are an important therapeutic target.

http://www.eurekalert.org/pub_releases/2016-01/uotm-tbi011216.php

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More evidence that stress increases risk of Alzheimer's

  • A stress hormone has been found to be associated with more amyloid-beta protein, in mice and human neurons.
  • The finding helps explain why stress is a risk factor for Alzheimer's.
  • A previous 38-year study supports this with the finding that women who scored highly in "neuroticism" in middle age, had a greater chance of later developing Alzheimer's.
  • This link was largely accounted for by chronic stress experienced by these women over the four decades.

A study involving both mice and human cells adds to evidence that stress is a risk factor for Alzheimer's.

The study found that mice who were subjected to acute stress had more amyloid-beta protein in their brains than a control group. Moreover, they had more of a specific form of the protein, one that has a particularly pernicious role in the development of Alzheimer's disease.

When human neurons were treated with the stress hormone corticotrophin releasing factor (CRF), there was also a significant increase in the amyloid proteins.

It appears that CRF causes the enzyme gamma secretase to increase its activity. This produces more amyloid-beta.

The finding supports the idea that reducing stress is one part of reducing your risk of developing Alzheimer's.

A neurotic personality increases the risk of Alzheimer's disease

An interesting study last year supports this.

The study, involving 800 women who were followed up some 40 years after taking a personality test, found that women who scored highly in "neuroticism" in middle age, have a greater chance of later developing Alzheimer's. People who have a tendency to neuroticism are more readily worried, distressed, and experience mood swings. They often have difficulty in managing stress.

The women, aged 38 to 54, were first tested in 1968, with subsequent examinations in 1974, 1980, 1992, 2000, and 2005. Neuroticism and extraversion were assessed in 1968 using the Eysenck Personality Inventory. The women were asked whether they had experienced long periods of high stress at each follow-up.

Over the 38 years, 153 developed dementia (19%), of whom 104 were diagnosed with Alzheimer's (13% of total; 68% of those with dementia).

A greater degree of neuroticism in midlife was associated with a higher risk of Alzheimer's and long-standing stress. This distress accounted for a lot of the link between neuroticism and Alzheimer's.

Extraversion, while associated with less chronic stress, didn't affect Alzheimer's risk. However, high neuroticism/low extraversion (shy women who are easily worried) was associated with the highest risk of Alzheimer's.

The finding supports the idea that long periods of stress increase the risk of Alzheimer's, and points to people with neurotic tendencies, who are more sensitive to stress, as being particularly vulnerable.

http://www.eurekalert.org/pub_releases/2015-09/uof-uhr091615.php

http://www.eurekalert.org/pub_releases/2014-10/uog-anp101414.php

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Sleeping on your side best for clearing waste from brain

  • Waste products accumulate as the brain functions.
  • The process of clearing this waste is most effective during sleep.
  • Accumulation of waste products such as amyloid-beta and tau proteins are involved in Alzheimer's.
  • Rat study shows sleeping on your side is best for removing waste from the brain.

This sounds like pseudoscience, but it appears in Journal of Neuroscience, so … Weirdly, a rat study has found that sleeping on the side (the most common posture for humans and other animals) is the best position for efficiently removing waste from the brain.

Brain waste includes amyloid-beta and tau proteins, whose build-up is a critical factor in the development of Alzheimer's disease.

The study used imaging of the glymphatic pathway, which clears waste products from the brain by filtering cerebrospinal fluid through the brain and exchanging it with interstitial fluid. The process is most efficient during sleep, and its efficiency is affected by the level of consciousness. The researchers compared glymphatic transport during sleep when anesthetized rodents’ brains were in three positions—lateral (side), prone (down), and supine (up).

Of course, these findings need to be confirmed in humans (which might be tricky!), but there is, after all, no harm in changing your sleep position, if you don't already sleep on your side (though I concede it can be a difficult thing to change).

Apart from providing a practical tip for fighting age-related cognitive decline and dementia, the finding also supports the idea that one of the purposes of sleep is to ‘clean up’ the mess that accumulates while we are awake.

The finding is also consistent with increasing evidence that sleep disturbances are a factor in the development and progression of dementia.

http://www.futurity.org/side-sleeping-brains-979872/

Reference: 

[3956] Lee H, Xie L, Yu M, Kang H, Feng T, Deane R, Logan J, Nedergaard M, Benveniste H. The Effect of Body Posture on Brain Glymphatic Transport. The Journal of Neuroscience [Internet]. 2015 ;35(31):11034 - 11044. Available from: http://www.jneurosci.org/content/35/31/11034

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