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Alzheimer's & Dementia

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Rates of new dementia cases may be falling
  • Data from the very long-running Framingham Heart Study adds to evidence that, for those with at least a high school education, the rate of dementia is declining. Improved cardiovascular health and treatment appears to be an important factor in this decline.

As we all know, people are living longer and obesity is at appalling levels. For both these (completely separate!) reasons, we expect to see growing rates of dementia. A new analysis using data from the long-running Framingham Heart Study offers some hope to individuals, however.

Rigorous exercise does not slow dementia decline
  • A study involving nearly 500 people with dementia has found that a rigorous physical exercise program did nothing to slow their decline.

A number of studies have found that physical exercise can help delay the onset of dementia, however the ability of exercise to slow the decline once dementia has set in is a more equivocal question. A large new study answers this question in the negative.

Impaired waste management in the brain a cause of Alzheimer's?
  • A mouse study has shown that, as cells age, their ability to remove damaged proteins and structures (autophagy) declines, due to a decrease in the cell components (autophagosomes) that collect the damaged proteins.
  • A study found that the process of breaking down defective mitochondria and recycling the components (mitophagy) is impaired in those with Alzheimer's.
  • Microglia clear damage by engulfing the damaged matter then releasing it inside exosomes, which can be absorbed by other cells. Studies have now shown that these exosomes, designed to transmit information, can also spread harmful tau & amyloid-beta protein.
  • A mouse study has shown how amyloid plaques lead to tau tangles, and that weakened microglia facilitate this. It also links weak microglia to the risky variant of the TREM2 gene.
  • However, the common TREM2 variant is linked to faster plaque growth at later stages.
  • TREM2 appears to modify the way immune cells respond to tau tangles.
  • Another mouse study found that overactive microglia (achieved by turning off another gene) were linked to both better removal of amyloid-beta, and loss of synapses. This may help explain why reducing amyloid plaques often fails to improve cognition.

Aging linked to impaired garbage collection in the brain

A mouse study has shown that, as cells age, their ability to remove damaged proteins and structures declines.

Does mental stimulation help fight age-related cognitive decline?
  • A large study found that mentally stimulating activities in mid-life and later were linked to a lower risk or delay of MCI.
  • A very large study found that the more regularly older adults played puzzles such as crosswords and Sudoku, the better they performed on tasks assessing attention, reasoning and memory.
  • A review of 32 studies has concluded that mind-body exercises such as tai chi do help improve cognition in older adults.

Can computer use, crafts and games slow or prevent age-related memory loss?

High cholesterol intake & eggs don't increase dementia risk

A large, long-running Finnish study looking at the dietary habits of 2,497 men aged 42-60 has found that a high intake of dietary cholesterol was not associated with the risk of dementia or Alzheimer's disease, even among carriers of the ‘Alzheimer’s gene’ APOE4.

Exercise helps MCI

A pilot study involving 17 older adults with mild cognitive impairment and 18 controls (aged 60-88; average age 78) has found that a 12-week exercise program significantly improved performance on a semantic memory task, and also significantly improved brain efficiency, for both groups.

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.

Brain proteins involved in the development of Alzheimer's
  • When a particular fat molecule in the brain doesn't break down properly, cognition gets harder, and there's an increase in amyloid precursor proteins (which are part of the Alzheimer's cascade).
  • Tau proteins are also involved in the Alzheimer's cascade. A new study shows that individuals vary markedly in how quickly they spread in the brain.
  • A protein called SIRT6 has now been found to be crucially involved in DNA repair, to be severely deficient in those with Alzheimer's, and to be associated with learning impairment in mice.
  • A protein called NPTX2 may explain why some brains can cope with high levels of amyloid-beta much better than others.

Disrupted fat breakdown in the brain involved in Alzheimer’s?

Gender differences in Alzheimer's disease may be linked to tau spread
  • Brain scans suggest that tau proteins may spread more rapidly through women’s brains, increasing Alzheimer's risk and speeding its progression.

Accumulating evidence suggests that tau spreads through brain tissue like an infection, traveling from neuron to neuron and turning other proteins into abnormal tangles, subsequently killing brain cells.

Alzheimer's produces early brain atrophy
  • A large study finds those who go on to develop Alzheimer's show atrophy of the hippocampus before age 40, and in the amygdala around age 40.

Brain scans from over 4,000 people, across the age range (9 months to 94 years) and including 1,385 Alzheimer's patients, has revealed an early divergence between those who go on to develop Alzheimer’s and those who age normally.

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