Tag Archives: Alzheimer

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.

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“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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“Prevention may prove the best way to manage the dementia epidemic”

20 Mar

So argues this important piece in Scientific American (sorry, it’s behind a paywall). So far drugs that target Alzheimer’s have been disappointing. Our best evidence suggests that lifestyle interventions (exercise, improvements in diet, and cognitive engagement) really do help.

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LED light flickering as a treatment for Alzheimer’s?

14 Dec

Don’t get your hopes up yet. The findings reflect animal research, but here is the story from ScienceDaily:

Using LED lights flickering at a specific frequency, researchers have shown that they can significantly reduce the beta amyloid plaques seen in Alzheimer’s disease in the visual cortex of mice. This treatment appears to work by stimulating brain waves known as gamma oscillations, which the researchers discovered help the brain suppress beta amyloid production and invigorate cells responsible for destroying the plaques.

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Dementia rates fall

23 Nov

A very surprising finding reported in The New York Times:

Despite fears that rates were going to explode as the population grows older and fatter, and has more, a large nationally representative survey has found the reverse. Dementia is actually on the wane. And when people do get dementia, they get it at older and older ages.

You can read the original study here. The key points:

Question Has the prevalence of dementia among older adults in the United States changed between 2000 and 2012?

Findings In this observational cohort study of more than 21 000 US adults 65 years or older from the nationally representative Health and Retirement Study, dementia prevalence declined significantly, from 11.6% in 2000 to 8.8% in 2012.

Meaning Population brain health seemed to improve between 2000 and 2012; increasing educational attainment and better control of cardiovascular risk factors may have contributed to the improvement, but the full set of social, behavioral, and medical factors contributing to the improvement is still uncertain.

What are the causes of this good news?:

Increases in the level of education among the later-born cohort accounted for some of the decreased dementia risk, and there was some evidence that improvements in treatments for cardiovascular risk factors (eg, diabetes) may also have played a role. However, the full set of social, behavioral, and medical factors contributing to the decline in dementia prevalence is still uncertain.

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Air pollution and Alzheimer’s?

16 Sep

A paper published in PNAS titled “Magnetite pollution nanoparticles in the human brain,” makes the argument:

We identify the abundant presence in the human brain of magnetite nanoparticles that match precisely the high-temperature magnetite nanospheres, formed by combustion and/or friction-derived heating, which are prolific in urban, airborne particulate matter (PM). Because many of the airborne magnetite pollution particles are <200 nm in diameter, they can enter the brain directly through the olfactory nerve and by crossing the damaged olfactory unit. This discovery is important because nanoscale magnetite can respond to external magnetic fields, and is toxic to the brain, being implicated in production of damaging reactive oxygen species (ROS). Because enhanced ROS production is causally linked to neurodegenerative diseases such as Alzheimer’s disease, exposure to such airborne PM-derived magnetite nanoparticles might need to be examined as a possible hazard to human health.

It’s hard not the find the idea of pollution induced magnetite nanospheres in your brain disturbing. The paper reports:

The specific presence of magnetite in the brain is important because it has been causally linked with potential cellular responses to external magnetic fields

suggesting that the nanoparticles in conjunction with magnetic fields may be a factor. This may explain some of the inconsistent findings on the effects of magnetic fields on humans.

 

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An Alzheimer’s breakthrough?

2 Sep

This story has received a lot of attention in media. The paper appeared in Nature, perhaps the most prestigious science journal in the world. Here is the abstract:

Alzheimer’s disease (AD) is characterized by deposition of amyloid-β (Aβ) plaques and neurofibrillary tangles in the brain, accompanied by synaptic dysfunction and neurodegeneration. Antibody-based immunotherapy against Aβ to trigger its clearance or mitigate its neurotoxicity has so far been unsuccessful. Here we report the generation of aducanumab, a human monoclonal antibody that selectively targets aggregated Aβ. In a transgenic mouse model of AD, aducanumab is shown to enter the brain, bind parenchymal Aβ, and reduce soluble and insoluble Aβ in a dose-dependent manner. In patients with prodromal or mild AD, one year of monthly intravenous infusions of aducanumab reduces brain Aβ in a dose- and time-dependent manner. This is accompanied by a slowing of clinical decline measured by Clinical Dementia Rating—Sum of Boxes and Mini Mental State Examination scores. The main safety and tolerability findings are amyloid-related imaging abnormalities. These results justify further development of aducanumab for the treatment of AD. Should the slowing of clinical decline be confirmed in ongoing phase 3 clinical trials, it would provide compelling support for the amyloid hypothesis.

These are truly exciting results. The paper reports that a  “dose-dependent slowing of clinical progression on the Mini Mental State Examination (MMSE) with aducanumab treatment was also observed.” In other words, the larger the dose the slower the cognitive decline. You can find details about Aducanumab here.

 

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