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Alzheimer’s Risk in Middle Age

Cedars-Sinai investigators used PET imaging to look at abnormal protein levels in the mid-life brain. Photo by Getty.
Cedars-Sinai investigators used PET imaging to look at abnormal protein levels in the mid-life brain. Photo by Getty.
Cedars-Sinai investigators used PET imaging to look at abnormal protein levels in the mid-life brain. Photo by Getty.

Cedars-Sinai Investigators Find Links Between Alzheimer’s-Associated Proteins and Poorer Cognition in Adults 55 and Younger

Mitzi Gonzales, PhD

Mitzi Gonzales, PhD

Higher-than-average levels of two Alzheimer’s-associated proteins—amyloid beta and tau—in the brain are linked with poorer cognition in middle-aged adults, according to a study led by Cedars-Sinai investigators and published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

“In older adults, higher levels of amyloid beta and tau have been associated with poorer memory and cognition," said Mitzi Gonzales, PhD, director of Translational Research in the Jona Goldrich Center for Alzheimer’s and Memory Disorders at Cedars-Sinai and lead author of the study. “Our study found that this was also true in adults age 55 and younger—a period thought to be important for prevention. We also found higher levels in individuals with a higher genetic risk for Alzheimer's disease. Future studies should examine memory and cognitive changes over time and look at why some individuals remain mentally sharp despite having high levels of these proteins, to provide important clues about maintaining cognitive health over the lifespan.”

The findings highlight the importance of understanding the effects of amyloid beta and tau proteins on memory and thinking abilities at earlier ages. The work could also help focus dementia-prevention efforts in younger at-risk populations.

Additional authors: Adrienne O’Donnell, Saptaparni Ghosh, Emma Thibault, Georges El Fakhri, Sudha Seshadri, Jeremy Tanner, Claudia L. Satizabal, Charles S. Decarli, Keith A. Johnson, Alexa S. Beiser, Matthew Pase.

Funding: National Institutes of Health, Grant/Award Numbers: N01-HC-25195, HHSN268201500001I, 75N92019D00031; National Institute on Aging, Grant/Award Numbers: RF1AG059421, R01AG054076, R01AG049607, R01AG033090, R01AG066524, R01NS017950, R01AG077472, P30AG066546; National Health and Medical Research Council of Australia Investigator, Grant/Award Number: GTN2009264. 


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