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A study published Nov. 4 in Science Translational Medicine found that tau accumulated at more than twice the rate in people with early-onset Alzheimer’s than in older-onset patients. The findings are associated with faster progression and a greater range of symptoms, but the research did not test treatments or establish why tau changes more rapidly.
A study published Nov. 4 in Science Translational Medicine found that tau, a protein associated with Alzheimer’s disease, accumulated at more than twice the rate in patients whose symptoms began before age 65 than in patients with later-onset disease. The researchers also found more extensive tau deposits in the early-onset group, a difference that may help explain the group’s faster disease progression and broader range of symptoms.
The researchers compared 390 people with early-onset Alzheimer’s, whose average age was 59, with 211 people with late-onset disease, whose average age was 78. Participants had mild cognitive impairment or mild dementia due to Alzheimer’s, and PET scans showed amyloid accumulation. Some participants also had repeat tau PET scans, taken over an average follow-up of two to three years, so researchers could track changes over time.
About one in five early-onset patients had a presentation in which symptoms other than memory problems were prominent. By contrast, more than 99% of the late-onset patients with documented presentations had memory-dominant symptoms. Early-onset Alzheimer’s is generally defined as symptoms beginning before age 65; the study report says this group accounts for about 5% of Alzheimer’s patients.
The team reported that tau differences between the groups were greater than the differences in amyloid. The study did not test Alzheimer’s drugs or determine how patients in either group would respond to treatment. It was supported by the U.S. National Institute on Aging. The authors’ paper is titled “Distinct tau PET dynamics in early versus late age-of-onset Alzheimer’s disease.”
How Tau Findings Could Shape Research
The results add evidence that Alzheimer’s disease can differ by age of onset not only in the symptoms people first experience, but also in the measured course of a disease-related protein. The reported faster tau accumulation and wider spread in younger patients may help researchers investigate why early-onset disease often progresses more quickly and can affect abilities beyond memory.
The findings may also inform treatment research. The two drugs described in the report as approved to slow Alzheimer’s progression target amyloid, while this study found larger group differences for tau. Senior author Gil Rabinovici said the results support examining tau-targeting approaches, including trials that combine amyloid- and tau-directed treatments. That is a research implication, not evidence that any such treatment is effective for early-onset patients.
For patients and families, the symptom differences are relevant because early Alzheimer’s may initially affect language, visual-spatial skills or executive functions rather than memory alone. The study does not provide a diagnostic test or a prediction for any individual. Its findings describe patterns across research groups, and further work is needed to explain them and establish their clinical significance.
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Why Researchers Compared Onset Ages
Alzheimer’s disease is associated with amyloid and tau, but the two proteins are distinct and the study examined their patterns separately. Participants were drawn from two research cohorts: the Longitudinal Early-Onset Alzheimer’s Disease Study and the Alzheimer’s Disease Neuroimaging Initiative. The researchers focused on people with early or later symptom onset who had mild cognitive impairment or mild dementia attributed to Alzheimer’s.
Repeat tau scans were available for only a subset of participants. Those scans provided a way to estimate how tau changed over roughly two to three years, rather than relying only on a single comparison between groups. The research therefore combines information about the extent of tau deposits with observed changes over time. It does not, on its own, establish the biological cause of the difference.
The report says patients with early-onset disease are more likely to have non-memory symptoms at first. The study excluded people carrying a known disease-causing mutation, according to first author Konstantinos Chiotis. The authors raised the possibility that other genetic factors may contribute, but did not identify a genetic explanation in this research.
“We don’t fully understand why Alzheimer’s develops so early in some people.”
— Konstantinos Chiotis, first author and assistant professor at Karolinska Institutet
What the Study Cannot Establish
The study found differences between groups but did not explain why tau accumulates faster in early-onset Alzheimer’s. The authors raised genetics as one possible line of inquiry; the research does not show that genetic factors caused the observed pattern. Known disease-causing mutation carriers were excluded, according to the report.
The results also do not establish whether tau-targeting drugs, or combinations aimed at tau and amyloid, would slow disease in younger patients. No treatments were tested. The report does not provide enough information to determine how well the findings apply to people with more advanced disease, people without amyloid-positive scans, or every person diagnosed before age 65. Repeat tau imaging was conducted in a subset of participants, and individual outcomes may differ from group averages.
Further Study of Tau and Treatment
Researchers will need to investigate what drives the more rapid tau changes and whether the pattern holds in larger or different patient groups. The authors pointed to genetics as a potential area for follow-up, while the study’s findings also support further examination of tau as a treatment target in early-onset disease.
Clinical trials could test whether people with early-onset Alzheimer’s respond differently to tau-directed treatments or to combinations that target both tau and amyloid. Until such trials report results, the current findings should be understood as evidence about disease patterns, not a recommendation or proof of treatment benefit. The published study does not specify a next trial or a timeline for one.
Key Questions
What did the study find about tau in early-onset Alzheimer’s?
Researchers reported more extensive tau deposits and accumulation at more than twice the rate in patients whose symptoms began before age 65 compared with the later-onset group.
How did the researchers track tau changes?
Participants had PET scans, and a subset underwent repeat tau PET scans over an average follow-up of two to three years. This allowed researchers to estimate how tau changed over time.
Does the study prove tau causes early-onset Alzheimer’s to progress faster?
No. The study found an association between early onset, faster tau accumulation and disease progression. It did not establish why the differences occur or prove that tau alone causes faster progression.
Does this research show that tau-targeting treatment works?
No. The researchers did not test treatments. The findings may support future trials of tau-directed or combined treatments, but they do not show that these approaches benefit patients.
Can early-onset Alzheimer’s begin with symptoms other than memory loss?
Yes. The report says some patients initially experience difficulties with language, visual and spatial abilities, or executive functions such as planning and problem-solving. The study describes group patterns; symptoms vary between individuals.
Source: news-medical.net
