Early Warning System?
The accumulation of amyloid-beta and tau proteins in the brain is linked to Alzheimer’s disease, and now research shows that such accumulation can disrupt connections between brain structures important for memory.
The new study, led by investigators at Harvard Medical School and Massachusetts General Hospital and published April 5 in PNAS, revealed that these disrupted connections were present years before signs of cognitive impairment were observed. The researchers hope that their findings may eventually lead to strategies for earlier detection of Alzheimer’s disease.
For years, researchers have known that amyloid-beta and tau pathologies, the hallmarks of Alzheimer’s disease, can cause the death of neurons—the brain’s most abundant cells—eventually leading to impairment and dementia.
“But we did not know how the brain’s connections respond to the accumulation of these proteins very early in the disease process, even before symptoms,” said senior author Yakeel Quiroz, HMS associate professor of psychology in the Department of Psychiatry at Mass General and the director of the the Familial Dementia Neuroimaging Lab and the Multicultural Alzheimer’s Prevention Program at Mass General.
To learn more about this phenomenon, Quiroz and colleagues studied the brains of individuals from a large family with more than 6,000 living members from Antioquia, Colombia, who have a high prevalence of Alzheimer’s disease.
Quiroz and her colleagues have formed a unique relationship with this family, creating the Colombia-Boston study in 2015 to learn more about how Alzheimer’s disease progresses before cognitive impairment emerges and to find sensitive biomarkers for predicting who is at high risk for dementia.
Members of the family with the mutation known as Presenilin-1 E280A are almost certain to develop Alzheimer’s disease, usually showing signs of mild cognitive impairment at age 44 and dementia by the age of 49.
Previously, the research team showed that these individuals exhibit high levels of amyloid-beta protein almost two decades before onset of mild cognitive impairment, and tau pathology close to six years before onset.
“Studying this unique population can really help us understand how amyloid-beta and tau pathologies could affect how the brain communicates years before individuals develop dementia,” said co-first author Edmarie Guzmán-Vélez, an HMS instructor in psychology in the Department of Psychiatry at Mass General.
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