Overview: A new study could not only determine the risk of Alzheimer’s disease before symptoms appear, but also determine who will get worse in the next few years.
sauce: Lund University
Alzheimer’s patients can now be identified before symptoms appear, according to a large study led by Lund University in Sweden. It has also made it possible to predict who will get worse in the next few years.
This research natural medicineis very timely in light of the recent development of new drugs for Alzheimer’s disease.
It has long been known that there are two proteins associated with Alzheimer’s disease: beta-amyloid, which forms plaques in the brain, and tau, which accumulates in brain cells at a later stage. Elevated levels of these proteins in combination with cognitive impairment previously formed the basis for diagnosing Alzheimer’s disease.
“Brain changes occur 10 to 20 years before patients experience definite symptoms, neurons die, and the person in question experiences their first cognitive impairment when tau begins to spread. This is why it is so difficult to diagnose Alzheimer’s disease in its early stages, ”explains Oskar Hansson, senior physician in neurology at Skåne University Hospital and professor at Lund University.
He is currently leading a large international research study of 1,325 participants from Sweden, USA, Netherlands and Australia. Participants had no cognitive impairment at the start of the study. Using PET scans, we were able to visualize the presence of tau and amyloid in the brains of participants.
People in whom the two proteins were found had a 20- to 40-fold higher risk of developing the disease at follow-up several years later, compared to participants who had no biological changes.
“When beta-amyloid and tau are both present in the brain, it can be considered a diagnosis rather than a risk factor. will diagnose,” says Rick Ossenkoppele, lead author of the study and a senior researcher at Lund University and the University of Amsterdam Medical Center.
He explains that Alzheimer’s researchers belong to two schools of thought. On the one hand, there are those who believe that Alzheimer’s disease cannot be diagnosed until cognitive impairment sets in. Some groups he and his colleagues belong to say the diagnosis could be based purely on biology and what we can see in the brain.
“For example, we can compare our results to prostate cancer. If a biopsy is done and cancer cells are found, the cancer is diagnosed even if the person has not yet developed symptoms,” he said. says Rik Ossenkoppele.
Recently, a clinical trial of lecanemab, a new drug for Alzheimer’s disease, was evaluated in Alzheimer’s patients with positive results. On this basis, the researchers say the Lund University study is of particular interest.
“If we can diagnose the disease before cognitive impairment appears, we may eventually be able to use this drug at a very early stage to slow the progression of the disease.” , are more likely to prevent or delay future cognitive impairment.
“However, more research is needed before recommending treatment to people who have not yet developed memory loss,” concludes Oscar Hanson.
About this Alzheimer’s Disease Research News
author: press office
sauce: Lund University
contact: Press Office – Lund University
image: image is public domain
Original research: open access.
“Amyloid- and Tau-PET-Positive Cognitively Unimpaired Individuals Are at High Risk for Future Cognitive DeclineRick Ossenkoppele and others natural medicine
See also
Overview
Amyloid- and Tau-PET-Positive Cognitively Unimpaired Individuals Are at High Risk for Future Cognitive Decline
A major unresolved question in the dementia field is that cognitively unimpaired individuals with both neuropathological hallmarks of Alzheimer’s disease (i.e., amyloid-β plaques and tau neurofibrillary tangles) may lose cognitive ability over time. Is it sustainable or is it doomed to decline?
This large, multicenter amyloid and tau positron emission tomography (PET) study (n= 1,325), amyloid PET positive (A+) and tau PET positive (T+) medial temporal lobe (A+T.MTL+) and/or temporal neocortex (A+T.Neo T+), and compared them with A+T.− and A−T.− group.
Cox proportional hazards models showed a significantly increased risk of progression to mild cognitive impairment in A.+T.Neo T+ (hazard ratio (HR) = 19.2, 95% confidence interval (CI) = 10.9–33.7), A+T.MTL+ (HR = 14.6, 95% CI = 8.1–26.4) and A+T.− (HR = 2.4, 95% CI = 1.4–4.3) Group vs. A−T.− (Reference) Group.both+T.MTL+ (HR = 6.0, 95% CI = 3.4–10.6) and A+T.Neo T+ (HR = 7.9, 95% CI = 4.7–13.5) The group also showed faster clinical progression to mild cognitive impairment than the A group.+T.− group.
The linear mixed-effects model is A+T.Neo T+ (β= −0.056 ± 0.005, T.= −11.55, P.< 0.001), A+T.MTL+ (β= −0.024 ± 0.005, T.= −4.72, P.< 0.001) and A+T.− (β= −0.008 ± 0.002, T.= −3.46, P.< 0.001) group showed significantly faster longitudinal global cognitive decline compared to the A group.−T.− (Reference) Group (everyone) P.< 0.001).both+T.Neo T+ (P.< 0.001) and A+T.MTL+ (P.= 0.002) group also progressed faster than A+T.− group.
In summary, the evidence for pathological changes in advanced Alzheimer’s disease provided by the combination of abnormal amyloid and tau PET studies is associated with short-term (i.e., 3–5 years) cognitive decline in individuals without cognitive impairment. and is therefore of high clinical relevance. .
