WEDNESDAY, Nov. 11, 2026 (HealthDay News) — A signature protein in Alzheimer’s disease builds up much faster and spreads more widely in the brain in people with early-onset Alzheimer’s disease, than in those diagnosed later, a new study says.
Tau is a natural protein that helps support cells, but it may also misbehave, forming damaging tangles and clumps inside brain cells. Tau buildup, along with amyloid protein deposits, are key markers of Alzheimer's disease in the brain, according to the National Institute on Aging.
In patients diagnosed with Alzheimer’s before age 65, tau builds up at more than twice the rate seen in older adults facing the condition, the study team found.
This rapid buildup of tau protein tangles in the brains of younger patients helps explain why they often face a faster decline in function and many have unusual symptoms at first, the team said.
While late-onset Alzheimer’s almost always begins with memory problems, early-onset cases may present differently. Some younger patients may first struggle with reading, judging distances, interpreting visual cues or managing everyday executive functions like problem-solving and planning, even though their speech remains intact, researchers said.
“Patients with early-onset Alzheimer’s are more likely than older patients to present with symptoms unrelated to memory, at least initially,” said co-senior author Renaud La Joie, a professor in Precision Care for Memory Disorders at the University of California, San Francisco.
For the study, the team analyzed hundreds of participants, including 390 early-onset patients (average age: 59) and 211 late-onset patients (average age: 78).
The team used PET scans to look for tau inside patients' brain tissue. Cognition was measured with standard clinical scoring tools.
Based on repeat tau PET scans, the team compared how the disease affected the brains of a subset of participants over an average followup of two to three years.
Among the patients with early-onset disease, 1 in 5 showed mainly non-memory symptoms, while more than 99% of the late-onset patients showed memory-dominant symptoms.
While current medications approved to slow Alzheimer's progression focus primarily on a different brain protein called amyloid, the dramatic differences in tau for patients with early-onset AD found in this study mean therapies designed to clear tau will be critical for younger patients, researchers said.
“Treatments that target tau may be particularly important in early-onset Alzheimer’s, and therefore younger patients may be good candidates for clinical trials combining treatments targeting both amyloid and tau,” said senior author Dr. Gil Rabinovici, a professor of neurology at UCSF.
While about 5% of early-onset cases are linked to specific gene mutations, most young patients do not carry them, researchers said in background notes. They hope that future studies of other genetic factors will unlock new ways to target tau in the brain and improve outcomes for families affected by early-onset cognitive decline.
The study was supported by funding from the National Institute on Aging. Findings were published Nov. 4 in Science Translational Medicine.
More information
Visit Alzheimer's.gov for more information on Alzheimer's disease.
SOURCE: University of California San Francisco, news release, Nov. 4, 2026
Copyright © 2026 HealthDay. All rights reserved.