Dialing up the activity of a protein called SYK in the brain’s “janitors” could provide an avenue to treat Alzheimer’s and other neurodegenerative diseases.

The APOE4 variant causes cholesterol buildup in the cells that make protective fatty sheaths for neurons, possibly helping explain its role in neurodegeneration.

Damaged lysosomes are repaired by a lipid-based signaling pathway dubbed PITT that could be targeted to treat neurodegenerative disease, its discoverers say.

The MIT biologist studies how RNA molecules self-assemble and the role these accumulations may play in diseases such as ALS and Huntington’s.

The Biogen-developed treatment, called lecanemab, appears to have a more clear-cut effect on slowing the disease than the company’s previous Alzheimer’s drug, Aduhelm.

Mice with overactive LINE-1 retrotransposons in their brains exhibit movement difficulties, suggesting the genetic elements may play a role in ataxia in humans. 

The Middlebury College neuroscientist explores enzymes that affect brain cell development and neurodegeneration.

Research traces the evolution of a gene variant that reduces the risk of Alzheimer’s disease, finding that it originally evolved in response to infectious bacteria.

Maligned peptides such as the Alzheimer’s-associated amyloid precursor protein may have critical roles in the healthy brain.

The normal functions of peptides that aggregate in Alzheimer’s, Parkinson’s, and Huntington’s have been largely overlooked by scientists, but some argue that they are critical for understanding the development of disease.

Observational evidence for the connection is solidifying, and some clues are emerging about the mechanisms that may explain it.

His work was pivotal to understanding the mechanisms of neurodegenerative diseases, particularly Alzheimer’s and Parkinson’s.

Researchers find a way to wipe out the brain’s immune cell corps and send in new and improved versions.