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B vitamins may slow cognitive decline

28 Aug

Dr. Greger takes a look at the most recent work on the cognitive effects of B vitamins:

Initially, the results were disappointing. Vitamin supplementation did not seem to work, but the studies were tracking neuropsychological assessments, which are more subjective compared to structural neuroimaging—that is, actually seeing what’s happening to the brain. A double-blind randomized controlled trial found that homocysteine-lowering by B vitamins can slow the rate of accelerated brain atrophy in people with mild cognitive impairment. As we age, our brains slowly atrophy, but the shrinking is much accelerated in patients suffering from Alzheimer’s disease. An intermediate rate of shrinkage is found in people with mild cognitive impairment. The thinking is if we could slow the rate of brain loss, we may be able to slow the conversion to Alzheimer’s disease. Researchers tried giving people B vitamins for two years and found it markedly slowed the rate of brain shrinkage. The rate of atrophy in those with high homocysteine levels was cut in half. A simple, safe treatment can slow the accelerated rate of brain loss.

A follow-up study went further by demonstrating that B-vitamin treatment reduces, by as much as seven-fold, the brain atrophy in the regions specifically vulnerable to the Alzheimer’s disease process.

Some thoughts on memory and age

14 Aug

There is a general decline in memory with age that seems to affect all of us, this is called benign senescent forgetting  and is not considered pathological. Naturally, we find this forgetting disconcerting. Fortunately, however, there is evidence that we can reduce the effects of benign senescent forgetting. We know that environmental factors must be important because there are differences between generations in performance on memory tests. Standard scores for psychological tests are set by administering the large representative samples of the general population. When tests are restandardized we can compare changes in test performance across generations. For example, one study found that 61 – 75 years olds tested in 2007, performed better than 61 – 75 year olds tested in 1985. The improvements were substantial and must have some environmental cause since the human genome could not have substantially changed in the intervening decades.
The fact that environmental factors must affect memory is heartening news, because it suggests that memory improvement is possible.
However, benign senescent forgetting remains frightening and we worry that it may be an early sign of dementia. Our fear of Alzheimer’s disease and other forms of dementia may not be misplaced. Even if average memory performance of older people has been improving, as life expectancy increases a larger percentage of us may succumb to dementia.
Dementia is a degenerative brain disorder. Memory loss is the major symptom of dementia, but patients also exhibit other forms of intellectual decline.
In the United States 5% of those between the ages of 71 and 79 years suffer from dementia, while 37.4% of those 90 and older suffer from dementia. Alzheimer’s disease accounts for 69.9 cases of dementia. Vascular dementia accounts for another 17.4%. The reaming 12.7% includes Parkinson’s dementia, traumatic brain injuries, alcoholic dementia, and other causes.
There is evidence that we can reduce our risks of dementia. Physical exercise, healthy diet, cognitive engagement, and memory training do seem to offer some protection.

Higher childhood IQ related to a lower risk mortality

3 Jul

The Lothian birth-cohort studies continue to contribute to our understanding of cognitive aging. Here is the latest paper, published in the journal Intelligence. And here are the paper’s highlights;

• 94% of the participants of the Scottish Mental Survey 1947 were traced.
• Higher childhood IQ was related to a lower risk of all-cause mortality by age 79.
• The effect was slightly stronger in women than in men.
• The decline in risk across categories of IQ scores was graded across the full range.
•This is the only study of IQ and mortality in an entire year-of-birth cohort.

Here is Ian Deary’s brief description of the Lothian birth-cohort studies

Even moderate alcohol consumption increases risk of cognitive decline

30 Jun

This month The British Medical Journal published a paper titled : “Moderate alcohol consumption as risk factor for adverse brain outcomes and cognitive decline: longitudinal cohort study.” Here is the abstract:

Objectives To investigate whether moderate alcohol consumption has a favourable or adverse association or no association with brain structure and function.

Design Observational cohort study with weekly alcohol intake and cognitive performance measured repeatedly over 30 years (1985-2015). Multimodal magnetic resonance imaging (MRI) was performed at study endpoint (2012-15).

Setting Community dwelling adults enrolled in the Whitehall II cohort based in the UK (the Whitehall II imaging substudy).

Participants 550 men and women with mean age 43.0 (SD 5.4) at study baseline, none were “alcohol dependent” according to the CAGE screening questionnaire, and all safe to undergo MRI of the brain at follow-up. Twenty three were excluded because of incomplete or poor quality imaging data or gross structural abnormality (such as a brain cyst) or incomplete alcohol use, sociodemographic, health, or cognitive data.

Main outcome measures Structural brain measures included hippocampal atrophy, grey matter density, and white matter microstructure. Functional measures included cognitive decline over the study and cross sectional cognitive performance at the time of scanning.

Results Higher alcohol consumption over the 30 year follow-up was associated with increased odds of hippocampal atrophy in a dose dependent fashion. While those consuming over 30 units a week were at the highest risk compared with abstainers (odds ratio 5.8, 95% confidence interval 1.8 to 18.6; P≤0.001), even those drinking moderately (14-21 units/week) had three times the odds of right sided hippocampal atrophy (3.4, 1.4 to 8.1; P=0.007). There was no protective effect of light drinking (1-<7 units/week) over abstinence. Higher alcohol use was also associated with differences in corpus callosum microstructure and faster decline in lexical fluency. No association was found with cross sectional cognitive performance or longitudinal changes in semantic fluency or word recall.

Conclusions Alcohol consumption, even at moderate levels, is associated with adverse brain outcomes including hippocampal atrophy. These results support the recent reduction in alcohol guidance in the UK and question the current limits recommended in the US.

There is a good account in The Washington Post

An acceleration of cognitive decline?

26 Jun

Here a disturbing finding published in the most recent issue of the journal Intelligence, I have underlined the key sentence :

The cohort process of cognitive aging is a contested topic in population research. The literature is largely in disagreement over how and why inter-cohort trends in cognitive aging occur in the United States. This paper examines significant trends in the rate of cognitive decline and conceptualizes the role of the depression trajectory as a late life course process that accelerates cognitive aging at the individual and population level. To this end, I draw my study sample from the Health and Retirement Study (N = 24,678) and use aging-vector models as an extension of parallel-process latent growth modeling to analyze repeated measures of cognition and depression. Findings show the acceleration of cognitive decline (“negative” Flynn Effect) and worsening of depression risk for recent cohorts. The upward trends in depression account for significant acceleration in cognitive decline among later cohorts, thus providing a new insight into sociogenic population dynamics of cognitive aging.

From the body of the paper:

Taken together, the findings of the study strongly support the “negative” Flynn Effect on cognitive aging (Alwin, 2008). That is, later cohorts not only perform cognitive tasks more poorly, but also experience a faster rate of cognitive decline. As a result, considerable intercohort gaps occur particularly in old age. Further, the present study shows that the acceleration of cognitive decline is largely driven by depression symptomatology that concurrently evolves in late life, rather than by differences in cognitive reserves during adulthood (e.g., socioeconomic environments). Thus, the negative Flynn Effect is not necessarily paradoxical with regard to a continuous increase in educational attainment, which does not significantly predict the rate of cognitive decline. In contrast, depression risk in later life have significant impacts on cognitive decline at the individual and population levels. The results show that individuals develop an average of 1 to 2 additional depression symptoms in late life. Because later cohorts, particularly Non-Hispanic Blacks and Hispanics, are at higher risk of developing depression symptoms, their exposure to cognitive risk factors should be of public health concern.

Transcranial direct current stimulation for dementia?

1 May

Possibly, according to a paper presented at the recent American Academy of Neurology Annual Meeting:

To assess efficacy of transcranial direct current stimulation (tDCS) for improving picture naming abilities in individuals with mild dementia, researchers conducted a double-blind, cross-over study among 12 individuals. Study participants received 10 sessions of training on picture naming plus 30 minutes of anodal tDCS applied to the parietal lobe or sham simulation. Evaluation occurred before stimulation, at the final stimulation session, 2 weeks after stimulation and 2 months after stimulation.

Study participants who received tDCS significantly improved in picture naming, compared with those who received sham stimulation.

This seems like a strong study design and the results are striking. Normally, you would not expect improvement in a memory test on people suffering from dementia. Indeed, drugs, such as Donepezil,  used for treatment of dementia, only claim to reduce the rate of decline, not to cause improvement.

Note that this is a conference paper and has not yet been published in a peer reviewed journal. It would be important to know the magnitude of the effect and to see the research replicated.

“Sugary beverage intake and preclinical Alzheimer’s disease”

26 Apr

For some years I have been intrigued by the idea that Alzheimer’s disease might be a special type of diabetes (sometimes called Type 3 Diabetes). You can read the evidence for this hypothesis here.

A recent study published in the journal Alzheimer’s and Dementia reports the observation that sugary drink consumption may be linked to Alzheimer’s disease. Here is the abstract:

Introduction
Excess sugar consumption has been linked with Alzheimer’s disease (AD) pathology in animal models.

Methods
We examined the cross-sectional association of sugary beverage consumption with neuropsychological (N = 4276) and magnetic resonance imaging (N = 3846) markers of preclinical Alzheimer’s disease and vascular brain injury (VBI) in the community-based Framingham Heart Study. Intake of sugary beverages was estimated using a food frequency questionnaire.

Results
Relative to consuming less than one sugary beverage per day, higher intake of sugary beverages was associated with lower total brain volume (1–2/day, β ± standard error [SE] = −0.55 ± 0.14 mean percent difference, P = .0002; >2/day, β ± SE = −0.68 ± 0.18, P < .0001), and poorer performance on tests of episodic memory (all P < .01). Daily fruit juice intake was associated with lower total brain volume, hippocampal volume, and poorer episodic memory (all P < .05). Sugary beverage intake was not associated with VBI in a consistent manner across outcomes.

Discussion
Higher intake of sugary beverages was associated cross-sectionally with markers of preclinical AD.

This result would be consistent with the Type 3 Diabetes hypothesis. But note that the study is correlational and based on self-report. Sugary beverage consumption might be a proxy for some other variable.

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