Alzheimer's & Other Dementias

Latest news

  • A new test can quickly detect reduced blood capillaries in the back of the eye that are an early indication of Alzheimer's, and shows that it can help distinguish Alzheimer's from MCI.

A study has shown new technology can quickly and non-invasively detect reduced blood capillaries in the back of the eye that are an early indication of Alzheimer's.

  • A long-running study found subtle cognitive deficits evident 11-15 years before clear impairment, as were changes in tau protein.

A very long-running study involving 290 people at risk of Alzheimer's has found that, in those 81 people who developed

  • A large study found that most of those who were very poor at identifying common odors developed dementia within 5 years.
  • A study of older adults with a parent who had Alzheimer's found that those who were poorest at identifying odors showed the most Alzheimer's biomarkers.
  • A largish study found that poorer odor identification in older adults (average age 80) )was associated with a transition to dementia and with cognitive decline.
  • An animal study found olfactory dysfunction precedes cognitive problems, and relates amyloid-beta protein in the olfactory epithelium.
  • A large 13-year study found that a poor sense of smell was linked to a greater risk of death within 10 years, and of death from dementia and Parkinson’s disease in particular.

A long-term study of nearly 3,000 older adults (57-85) has found that those who couldn’t identify at least four out of five common odors were more than twice as likely as those with a normal sense of smell to develop dementia within five years.

  • A blood-clotting protein called fibrinogen has been shown to provoke the brain's immune cells into destroying synapses. The process begins with fibrinogen leaking from the blood into the brain.
  • Another study has found that nearly half of all dementias begin with a breakdown of the gatekeeper cells (pericytes) that help keep fibrinogen out of the brain.

Alzheimer's disease is associated with abnormalities in the vast network of blood vessels in the brain, but it hasn’t been known how this affects cognition. A study has now shown that a blood-clotting protein called fibrinogen plays a part.

  • Blood flow deficits in the brain, seen early on in Alzheimer's, have now been linked to some capilleries being block by white blood cells.

It’s been known that decreased blood flow in the brain occurs in people with Alzheimer's, and recent studies suggest that brain blood flow deficits are one of the earliest detectable symptoms of dementia.

  • Age-related changes in gene enhancers have been linked to faster cognitive decline in Alzheimer's brains.

New findings identify a mechanism that accelerates aging in the brain and gives rise to Alzheimer's disease.

  • 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

  • Study indicates APOE4 carriers are only at greater Alzheimer's risk if they have chronic inflammation.
  • Large study finds increasing inflammation linked to more white matter damage.
  • Common causes of chronic inflammation include cardiovascular disease, heart failure, diabetes, high blood pressure and infections.

Link found between chronic inflammation and Alzheimer's gene risk

  • Synapses in Alzheimer's brains found to be clogged with clusterin and amyloid-beta proteins, and APOE4 carriers had more protein clumps than those without the gene variant.
  • APOE4 decreases activity in hippocampus that is critical for memory consolidation.
  • Study of Amazonian hunter-gatherers show APOE4 gene can provide benefits when exposure to parasites is high.

Alzheimer's gene linked to damage to brain connections

A study has found that synapses in people who had died with Alzheimer's contained clumps of clusterin and clumps of amyloid beta. These protein clumps may be damaging the links between neurons.

  • More evidence that Alzheimer's disease is not a single disease with a single cause and single pathway comes from a large study classifying patients into 6 groups, only two of which showed strong genetic association.
  • Another study using post-mortem brain tissue found that different genes were associated with different types of brain damage.

A study involving 4,050 people with late-onset Alzheimer's disease (mean age 80) has classified them into six groups based on their cognitive functioning at the time of diagnosis. A genetic study found two of the groups showed strong genetic associations.

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