Good news for Alzheimer's patients

In The New York Times, Pam Belluck reports,

The long, discouraging quest for a medication that works to treat Alzheimer’s reached a potentially promising milestone on Wednesday. For the first time in a large clinical trial, a drug was able to both reduce the plaques in the brains of patients and slow the progression of dementia.

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Alzheimer's research

David Nield reports at sciencealert.com,

Researchers have identified a new link between Alzheimer's and a protein called tau that could help treat the disease in the future.

..."Once tau accumulates, the brain degenerates," says senior researcher David Holtzman, from the Washington University School of Medicine in St. Louis.

"What we found was that when ApoE is there, it amplifies the toxic function of tau, which means that if we can reduce ApoE levels we may be able to stop the disease process."

ApoE (or Apolipoprotein E) helps to move cholesterol around the body. In rare cases, people can be born without the ApoE gene, leading to very high cholesterol levels and associated health problems.

To take a closer look at how ApoE could be linked to Alzheimer's and other brain diseases, researchers studied mice given variants of the ApoE gene: ApoE2, ApoE3, and ApoE4. Some mice lacked the gene altogether.

In the absence of the ApoE proteins produced by these genes, especially the ApoE4 variant, tangled clumps of the tau protein were much less harmful to brain cells, so reducing the influence of ApoE could be a promising avenue for future research into treatments.

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Progress in predicting Alzheimer's

Pam Belluck writes in the New York Times,

The largest analysis to date of amyloid plaques in people’s brains confirms that the presence of the substance can help predict who will develop Alzheimer’s and determine who has the disease.

Two linked studies, published Tuesday in JAMA, also support the central early role in Alzheimer’s of beta amyloid, the protein that creates plaques. Data from nearly 9,500 people on five continents shows that amyloid can appear 20 to 30 years before symptoms of dementia, that the vast majority of Alzheimer’s patients have amyloid and that the ApoE4 gene, known to increase Alzheimer’s risk, greatly accelerates amyloid accumulation.

The findings also confirm that amyloid screening, by PET scan or cerebral spinal fluid test, can help identify people for clinical trials of drugs to prevent Alzheimer’s.

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