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A study published Nov. 4 in Science Translational Medicine found that tau accumulated at more than twice the rate in patients with early-onset Alzheimer’s as in those whose symptoms began at 65 or older. The study links faster tau accumulation with disease progression but did not test treatments or establish why the difference occurs.
People whose Alzheimer’s symptoms began before age 65 had more extensive tau deposits and accumulated the protein at more than twice the rate of patients with later-onset disease, according to a study published Nov. 4 in Science Translational Medicine. The findings may help explain differences in disease progression and symptoms, but the research did not test whether any treatment works better for either group.
Researchers compared 390 people with early-onset Alzheimer’s from the Longitudinal Early-Onset Alzheimer’s Disease Study with 211 people with late-onset disease from the Alzheimer’s Disease Neuroimaging Initiative. The groups had average ages of 59 and 78, respectively. Participants had mild cognitive impairment or mild dementia attributed to Alzheimer’s, and PET scans showed amyloid, an early disease biomarker.
A subset of participants had repeat tau PET scans over an average follow-up of two to three years, allowing the team to track changes in tau over time. The researchers reported that tau accumulation and spread were faster and more widespread in the early-onset group. They also found the differences between onset groups were greater for tau than for amyloid. The study was supported by the National Institute on Aging.
Among the early-onset participants, one in five had symptoms not dominated by memory problems. More than 99% of the late-onset participants whose symptom presentation was documented had a memory-dominant form. The study authors said the tau findings were associated with progression in memory loss, while the study design does not establish that tau alone causes the differences in symptoms or progression.
Tau Differences May Shape Disease Course
The results point to different patterns of tau pathology in Alzheimer’s depending on the age when symptoms begin. That matters because early-onset disease can involve language, visual-spatial or executive-function difficulties, not only memory loss. Recognizing those patterns may help researchers better characterize the disease and select participants for studies.
The findings also bear on treatment research. The two drugs approved to slow Alzheimer’s progression target amyloid, while this study found larger differences between the age groups in tau. Senior author Gil Rabinovici of the University of California, San Francisco, said tau-targeting approaches may be particularly relevant to early-onset disease and that younger patients may be candidates for clinical trials combining amyloid- and tau-targeting treatments. Those are research implications, not evidence that such combinations are effective.
Early-onset Alzheimer’s accounts for about 5% of Alzheimer’s cases, according to the report. A better understanding of this group could inform trials and clarify why some patients experience relatively rapid progression or symptoms that initially appear unlike typical memory-led disease.
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How Researchers Tracked Tau
Alzheimer’s is associated with abnormal deposits of both amyloid and tau. Amyloid can be detected early in the disease, while tau PET scans can help researchers examine where tau is present and how it changes. In this study, all participants had PET evidence of amyloid, and repeat tau scans in a subset provided a way to compare the protein’s development over time.
Early-onset Alzheimer’s refers to symptoms starting before age 65; late-onset disease begins at 65 or later. People with early-onset disease are more likely to have non-memory symptoms at first. Co-senior author Renaud La Joie, a UCSF professor in precision care for memory disorders, described possible difficulties with judging distances, reading, retrieving words, following long sentences, planning and adapting to changing situations. These examples describe patterns that can occur; they are not symptoms experienced by every patient.
The study, led by Konstantinos Chiotis and colleagues, was published as “Distinct tau PET dynamics in early versus late age-of-onset Alzheimer’s disease.” The authors excluded people with known disease-causing mutations from the analysis, according to the report.
“A key question is whether other genetic factors explain this more aggressive tau pathology.”
— Konstantinos Chiotis, first author
What the Study Cannot Establish
The findings do not explain why tau develops more rapidly in the early-onset group. Chiotis said researchers do not fully understand why Alzheimer’s begins early in some people and identified other genetic influences as one possibility to investigate. The study does not show that genetics account for the observed difference.
The research also did not test Alzheimer’s drugs, so it cannot determine whether people with early-onset disease respond differently to existing amyloid-targeting treatments or whether tau-targeting combinations would help. The report describes repeat scans for a subset over an average of two to three years, but does not give the subset’s size in the supplied material. The results should not be taken to mean every person with early-onset Alzheimer’s has faster progression or non-memory symptoms.
Research Into Tau and Treatment
Researchers will need to examine what biological or genetic factors may account for the difference in tau accumulation and whether the pattern holds across other patient groups and longer follow-up. Further work could also test whether tau measures help explain changes in symptoms and disease progression.
The study’s authors point to clinical trials as a way to investigate treatments that target tau, alone or alongside amyloid-targeting drugs. Whether younger patients benefit more from those approaches remains unknown; the current findings provide a rationale for research, not a treatment recommendation.
Key Questions
What did the study find about tau in early-onset Alzheimer’s?
The study found more extensive tau deposits and tau accumulation at more than twice the rate in people whose symptoms began before age 65 compared with those whose symptoms began at 65 or later.
How many people were included?
Researchers compared 390 early-onset patients with 211 late-onset patients. A subset had repeat tau PET scans over an average follow-up of two to three years.
Does this prove that tau causes faster progression?
No. The study reported an association between tau accumulation and disease progression, but it does not establish that tau alone causes faster progression or the differences in symptoms.
Did the researchers test Alzheimer’s treatments?
No. The study examined tau PET patterns, not treatment effectiveness. Its authors said the results raise questions for future trials, including studies of treatments targeting tau alongside amyloid.
Why can early-onset Alzheimer’s look different?
Some people with early-onset disease initially have difficulties involving language, visual-spatial skills or executive functions rather than memory being the main concern. The study does not establish why these patterns occur.
Source: news-medical.net
