In surprising twist, some Alzheimer’s plaques may be protective, not destructive
One of the characteristic hallmarks of Alzheimer’s disease (AD) is the buildup of amyloid-beta plaques in the brain. Most therapies designed to treat AD target these plaques, but they’ve largely failed in clinical trials. As detailed in Nature Immunology, Professor Greg Lemke and colleagues upend conventional views of the origin of one prevalent type of plaque, indicating a reason why treatments have been unsuccessful.
How brain cells repair their DNA reveals “hot spots” of aging and disease
Neurons lack the ability to replicate their DNA, so they’re constantly working to repair damage to their genome. A new study in the journal Science led by Professor and Salk President Rusty Gage finds that these repairs are not random, but instead focus on protecting certain genetic “hot spots” that appear to play a critical role in neural identity and function. The findings give novel insights into the genetic structures involved in aging and neurodegeneration, and could point to the development of potential new therapies for diseases such as Alzheimer’s, Parkinson’s and other age-related dementia disorders.
Salk scientists reveal how brain cells in Alzheimer’s go awry, lose their identity
Gage’s lab also revealed how brain cells in Alzheimer’s go awry and lose their identity. The team reported new insights in the journal Cell Stem Cell by growing neurons that resemble—more accurately than ever before—brain cells in older patients. And like patients themselves, the afflicted neurons appear to lose their cellular identity. Access to better models of the disease can give scientists an improved understanding of how it develops and help them propose novel treatments.
Parkinson’s, cancer and type 2 diabetes share a key element that drives disease
When cells are stressed, a flurry of activity takes place to protect the cell’s most important players. During the rush, a protein called Parkin hurries to protect the mitochondria, the power stations of the cell. Salk Professor Reuben Shaw and his team report in the journal Science Advances a direct link between a major sensor of cell stress and Parkin itself. The same pathway is also tied to type 2 diabetes and cancer, which could open a new avenue for treating all three diseases.
San Diego Nathan Shock Center announces first grant awardees at inaugural training workshop
The San Diego Nathan Shock Center (SD-NSC) of Excellence in the Basic Biology of Aging, a consortium between the Salk Institute for Biological Studies, Sanford Burnham Prebys (SBP) Medical Discovery Institute and the University of California San Diego, has announced the first class of pilot grant awardees at the center’s inaugural training workshop. Six recipients, each from a different institution, will receive up to $15,000 to pursue research that advances our understanding of how humans age, with the ultimate goal of extending the number of years of potentially healthy, disease-free life.
To read more about the Salk Institute’s collaborative and innovative aging research, keep an eye out for the Spring 2021 Inside Salk, available in May!
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This month’s image comes from a recent press release from the lab of Greg Lemke. This image shows a dense-core amyloid-beta plaque (red) surrounded by microglia that lack TAM receptors (white).
