Parkinson's Disease Dementia

Poor sleep drives Alzheimer’s progression

  • Getting a good night’s sleep is given greater importance with the discovery that sleep deprivation appears to rapidly increase the spread of tau tangles.

Poor sleep has been associated with the development of Alzheimer's disease, and this has been thought to be in part because the protein amyloid beta increases with sleep deprivation. A new study explains more.

Experiments with mice show that sleep deprivation also rapidly increases levels of the other key Alzheimer’s disease protein, tau tangles.

The work built on findings that tau is high in older people who sleep poorly, and that, when people are kept awake all night, their tau levels rise by about 50%.

When mice had tau proteins seeded in the hippocampus of their brains, those who were kept awake for long periods each day (mice are nocturnal), showed significantly greater spread of tau tangles than those mice allowed to sleep normally. Moreover, the new tangles appeared in the same areas of the brain affected in people with Alzheimer’s.

Disrupted sleep also increased release of synuclein protein, a hallmark of Parkinson’s disease. People with Parkinson’s—like those with Alzheimer’s—often have sleep problems.

All of this supports the idea that sleep directly protects against the development of Alzheimer's.

https://www.futurity.org/alzheimers-disease-sleep-tau-1966962/

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Deep brain therapy effective in early Parkinson’s

A 2-year trial involving 251 patients with Parkinson's disease and early motor complications (mean age, 52 years; mean duration of disease, 7.5 years) has found that those given deep brain stimulation surgery significantly improved their quality of life, motor disability, activities of daily living, levodopa-induced motor complications, and time with good mobility and no dyskinesia. Those given normal medical therapy, on the other hand, declined or at best got no worse.

03/2013

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Why HIV-associated dementia occurs & implications for other disorders

October, 2012

A new understanding of why dementia sometimes occurs with HIV, even when treated, may also suggest a new approach to other neurological disorders, including age-related cognitive decline.

HIV-associated dementia occurs in around 30% of untreated HIV-positive patients. Surprisingly, it also is occasionally found in some patients (2-3%) who are being successfully treated for HIV (and show no signs of AIDS).

A new study may have the answer for this mystery, and suggest a solution. Moreover, the answer may have general implications for those experiencing cognitive decline in old age.

The study found that HIV, although it doesn’t directly infect neurons, tries to stop the development of BDNF. Long known to be crucial for memory and learning, the reduced production of mature BDNF results in axons and dendrites shortening — meaning connections between neurons are lost. That in turn, brings about the death of some neurons.

It seems that the virus interferes with the normal process of development in BDNF, whereby one form of it, called proBDNF, is cut by certain enzymes into a new form called mature BDNF. It is in this form that it has its beneficial effect on neuron growth. Unfortunately, in its earlier form it is toxic to neurons.

This imbalance in the proportions of mature BDNF and proBDNF also appears to occur as we age, and in depression. It may also be a risk factor in Parkinson's and Huntington's diseases.

However, these findings suggest a new therapeutic approach.

Compounds in green tea and chocolate may help protect brain cells

In which context, it is interesting to note another new study, which has been busy analyzing the effects on brain cells of 2000 compounds, both natural and synthetic. Of the 256 that looked to have protective effects, nine were related to epicatechin, which is found in cocoa and green tea leaves.

While we’ve been aware for some time of these positive qualities, the study specifically identified epicatechin and epigallocatechin gallate (EGCG) as being the most effective at helping protect neurons by inducing production of BDNF.

One of the big advantages these compounds have is in their ability to cross the blood-brain barrier, making them a good candidate for therapy.

While green tea, dark chocolate, and cocoa are particularly good sources, many fruits also have good levels, in particular, black grapes, blackberries, apples, cherries, pears, and raspberries. (see this University of Davis document (pdf) for more detail)

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Poor sleep in old age increases risk of cognitive impairment

May, 2012

Two recent studies add to evidence that sleeping poorly is a risk factor for several disorders in old age, including mild cognitive impairment, Parkinson’s, cardiovascular disease and diabetes.

Older adults who sleep poorly react to stress with increased inflammation

A study involving 83 older adults (average age 61) has found that poor sleepers reacted to a stressful situation with a significantly greater inflammatory response than good sleepers. High levels of inflammation increase the risk of several disorders, including cardiovascular disease and diabetes, and have been implicated in Alzheimer’s.

Each participant completed a self-report of sleep quality, perceived stress, loneliness and medication use. Around 27% were categorized as poor sleepers. Participants were given a series of tests of verbal and working memory designed to increase stress, with blood being taken before and after testing, as well as three more times over the next hour. The blood was tested for levels of a protein marker for inflammation (interleukin-6).

Poor sleepers reported more depressive symptoms, more loneliness and more perceived stress compared to good sleepers. Before cognitive testing, levels of IL-6 were the same for poor and good sleepers. However, while both groups showed increases in IL-6 after testing, poor sleepers showed a significantly larger increase — as much as four times larger and at a level found to increase risk for illness and death in older adults.

After accounting for loneliness, depression or perceived stress, this association remained. Surprisingly, there was no evidence that poor sleep led to worse cognitive performance, thus causing more stress. Poor sleepers did just as well on the tests as the good sleepers (although I note that we cannot rule out that poor sleepers were having to put in more effort to achieve the same results). Although there was a tendency for poor sleepers to be in a worse mood after testing (perhaps because they had to put in more effort? My own speculation), this mood change didn’t predict the increased inflammatory response.

The findings add to evidence that poor sleep (unfortunately common as people age) is an independent risk factor for cognitive and physical health, and suggest we should put more effort into dealing with it, rather than just accepting it as a corollary of age.

REM sleep disorder doubles risk of MCI, Parkinson's

A recent Mayo Clinic study has also found that people with rapid eye movement sleep behavior disorder (RBD) have twice the risk of developing mild cognitive impairment or Parkinson’s disease. Some 34% of those diagnosed with probable RBD developed MCI or Parkinson's disease within four years of entering the study, a rate 2.2 times greater than those with normal REM sleep.

Earlier research has found that 45% of those with RBD developed MCI or Parkinson's disease within five years of diagnosis, but these findings were based on clinical patients. The present study involved cognitively healthy older adults (70-89) participating in a population-based study of aging, who were diagnosed for probable RBD on the basis of the Mayo Sleep Questionnaire.

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Reviving a failing sense of smell through training

January, 2012

A rat study reveals how training can improve or impair smell perception.

The olfactory bulb is in the oldest part of our brain. It connects directly to the amygdala (our ‘emotion center’) and our prefrontal cortex, giving smells a more direct pathway to memory than our other senses. But the olfactory bulb is only part of the system processing smells. It projects to several other regions, all of which are together called the primary olfactory cortex, and of which the most prominent member is the piriform cortex. More recently, however, it has been suggested that it would be more useful to regard the olfactory bulb as the primary olfactory cortex (primary in the sense that it is first), while the piriform cortex should be regarded as association cortex — meaning that it integrates sensory information with ‘higher-order’ (cognitive, contextual, and behavioral) information.

Testing this hypothesis, a new rat study has found that, when rats were given training to distinguish various odors, each smell produced a different pattern of electrical activity in the olfactory bulb. However, only those smells that the rat could distinguish from others were reflected in distinct patterns of brain activity in the anterior piriform cortex, while smells that the rat couldn’t differentiate produced identical brain activity patterns there. Interestingly, the smells that the rats could easily distinguish were ones in which one of the ten components in the target odor had been replaced with a new component. The smells they found difficult to distinguish were those in which a component had simply been deleted.

When a new group of rats was given additional training (8 days vs the 2 days given the original group), they eventually learned to discriminate between the odors the first animals couldn’t distinguish, and this was reflected in distinct patterns of brain activity in the anterior piriform cortex. When a third group were taught to ignore the difference between odors the first rats could readily distinguish, they became unable to tell the odors apart, and similar patterns of brain activity were produced in the piriform cortex.

The effects of training were also quite stable — they were still evident after two weeks.

These findings support the idea of the piriform cortex as association cortex. It is here that experience modified neuronal activity. In the olfactory bulb, where all the various odors were reflected in different patterns of activity right from the beginning (meaning that this part of the brain could discriminate between odors that the rat itself couldn’t distinguish), training made no difference to the patterns of activity.

Having said that, it should be noted that this is not entirely consistent with previous research. Several studies have found that odor training produces changes in the representations in the olfactory bulb. The difference may lie in the method of neural recording.

How far does this generalize to the human brain? Human studies have suggested that odors are represented in the posterior piriform cortex rather than the anterior piriform cortex. They have also suggested that the anterior piriform cortex is involved in expectations relating to the smells, rather than representing the smells themselves. Whether these differences reflect species differences, task differences, or methodological differences, remains to be seen.

But whether or not the same exact regions are involved, there are practical implications we can consider. The findings do suggest that one road to olfactory impairment is through neglect — if you learn to ignore differences between smells, you will become increasingly less able to do so. An impaired sense of smell has been found in Alzheimer’s disease, Parkinson's disease, schizophrenia, and even normal aging. While some of that may well reflect impairment earlier in the perception process, some of it may reflect the consequences of neglect. The burning question is, then, would it be possible to restore smell function through odor training?

I’d really like to see this study replicated with old rats.

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Animal studies indicate caffeine may slow dementia and cognitive decline but human studies less conclusive

July, 2010

Several recent studies and reviews suggest that the benefits of caffeine for age-related cognitive impairment and dementia are limited. It may be that the association only exists for women.

A special supplement in the Journal of Alzheimer's Disease focuses on the effects of caffeine on dementia and age-related cognitive decline. Here are the highlights:

A mouse study has found memory restoration and lower levels of amyloid-beta in Alzheimer’s mice following only 1-2 months of caffeine treatment. The researchers talk of “ a surprising ability of moderate caffeine intake to protect against or treat AD”, and define moderate intake as around 5 cups of coffee a day(!).

A review of studies into the relation between caffeine intake, diabetes, cognition and dementia, concludes that indications that coffee/caffeine consumption is associated with a decreased risk of Type 2 diabetes and possibly also with a decreased dementia risk, cannot yet be confirmed with any certainty.

A study involving 351 older adults without dementia found the association between caffeine intake and cognitive performance disappeared once socioeconomic status was taken into account.

A study involving 641 older adults found caffeine consumption was significantly associated with less cognitive decline for women only. Supporting this, white matter lesions were significantly fewer in women consuming more than 3 units of caffeine per day (after adjustment for age) than in women consuming less.

A Portuguese study involving 648 older adults found that caffeine intake was associated with a lower risk of cognitive decline in women, but not significantly in men.

A review of published studies examining the relation between caffeine intake and cognitive decline or dementia shows a trend towards a protective effect of caffeine, but because of the limited number of epidemiological studies, and the methodological differences between them, is unable to come up with a definitive conclusion.

A review of published epidemiological studies looking at the association between caffeine intake and Parkinson’s Disease confirms that higher caffeine intake is associated with a lower risk of developing Parkinson’s Disease (though this association may be stronger for men than women). Other studies provide evidence of caffeine’s potential in treatment, improving both the motor deficits and non-motor symptoms of Parkinson’s.

Reference: 

Arendash, G.W. & Cao, C. Caffeine and Coffee as Therapeutics Against Alzheimer’s Disease. Journal of Alzheimer's Disease, 20 (Supp 1), 117-126.
Biessels, G.J. Caffeine, Diabetes, Cognition, and Dementia. Journal of Alzheimer's Disease, 20 (Supp 1), 143-150.
Kyle, J., Fox, H.C. & Whalley, L.J. Caffeine, Cognition, and Socioeconomic Status. Journal of Alzheimer's Disease, 20 (Supp 1), 151-159.
Ritchie, K. et al. Caffeine, Cognitive Functioning, and White Matter Lesions in the Elderly: Establishing Causality from Epidemiological Evidence. Journal of Alzheimer's Disease, 20 (Supp 1), 161-161
Santos, C. et al. Caffeine Intake is Associated with a Lower Risk of Cognitive Decline: A Cohort Study from Portugal. Journal of Alzheimer's Disease, 20 (Supp 1), 175-185.
Santos, C. et al. Caffeine Intake and Dementia: Systematic Review and Meta-Analysis. Journal of Alzheimer's Disease, 20 (Supp 1), 187-204.
Costa, J. et al. Caffeine Exposure and the Risk of Parkinson’s Disease: A Systematic Review and Meta-Analysis of Observational Studies. Journal of Alzheimer's Disease, 20 (Supp 1), 221-238.
Prediger, R.D.S. Effects of Caffeine in Parkinson’s Disease: From Neuroprotection to the Management of Motor and Non-Motor Symptoms. Journal of Alzheimer's Disease, 20 (Supp 1), 205-220.

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