Beyond Increased Risk: APOE4 a Direct Cause of Alzheimer's?

homozygotes in a large multicohort study had higher levels of AD biomarkers by age 55 years than did those with othergene variants. By age 65 years, most had developed AD symptoms and showed abnormal amyloid levels in cerebrospinal fluid and on PET.

Other biomarkers showed a biologic penetrance of AD that increased with age. By age 80 years, penetrance for all amyloid and tau biomarkers reached 88%. homozygotes, with AD symptoms present at age 65 years, minor cognitive impairment at 72 years, dementia at 74 years, and death at 77 years (When they limited analysis to only those who developed AD dementia, investigators found no difference in amyloid or tau accumulation betweenhomozygotes.

"We may need to start treating these homozygotes as a separate group in our research so we can really understand the relation between amyloid and tau and symptoms inhomozygotes in a way that we have not been able to because of our practice in the field of thinking thatis this unitary risk effect," co-investigator Sterling Johnson, PhD, professor of geriatrics and dementia, University of Wisconsin-Madison, said at a press briefing.

"This is important for preventing Alzheimer's-related dementia and a real movement forward in defining the disease on the basis of genetics and biomarkers," she added.

Study funders included Fondo de Investigaciones Sanitario, Carlos III Health Institute, Fondo Europeo de Desarrollo Regional, Unión Europea, National Institutes of Health, the Department de Salut de la Generalitat de Catalunya, Horizon 2020–Research and Innovation Framework Programme from the European Union, La Caixa Foundation, EIT Digital, and the Alzheimer Association.

Source: Healthcare Press (healthcarepress.net)

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