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Summary: A new study shows that not only is it possible to determine who is at risk for Alzheimer’s before symptoms appear, but also who will become worse over the next few years.
Source: Lund University
A large study led by Lund University in Sweden has shown that people with Alzheimer’s disease can now be identified before they show any symptoms. It is now also possible to predict who will deteriorate over the next few years.
The study was published in naturopathyand is very timely given the recent development of new drugs for Alzheimer’s disease.
It has long been known that there are two proteins associated with Alzheimer’s – beta-amyloid, which forms plaques in the brain, and tau, which accumulates in brain cells at a later stage. Elevated levels of these proteins combined with cognitive impairment previously formed the basis of the diagnosis of Alzheimer’s.
“Changes in the brain occur between ten and twenty years before the patient feels any clear symptoms, and it is only when the dew spreads that the nerve cells die and the affected person has the first cognitive problems. This is why Alzheimer’s disease is so difficult to diagnose in its early stages,” explains Oskar Hansson, senior physician in neurology at Skåne University Hospital and professor at Lund University.
He has now led a large international research study conducted with 1,325 participants from Sweden, the US, the Netherlands and Australia. Participants had no cognitive impairment at the start of the study. PET scans were used to visualize the presence of tau and amyloid in the participants’ brains.
It was found that the people who had the two proteins detected had a 20 to 40 times greater risk of developing the disease at follow-up a few years later compared to the participants who had neither exhibited biological changes.
“When both beta amyloid and tau are present in the brain, this can no longer be considered a risk factor, but rather a diagnosis. A pathologist examining such brain samples would immediately diagnose Alzheimer’s in the patient,” says Rik Ossenkupplunge, the study’s first author and principal investigator at Lund University and University Medical Center Amsterdam.
He explains that Alzheimer’s researchers belong to two schools of thought – on the one hand, those who believe that Alzheimer’s disease can only be diagnosed once cognitive impairment begins. There’s also the group that he and his colleagues belong to – who say that a diagnosis can be purely biological and what you can see in the brain.
“You can compare our results with prostate cancer, for example. If you take a biopsy and you find cancer cells, the diagnosis is cancer, even if the person concerned has not yet developed symptoms,” says Rik Ossenkupplunge.
Positive results in clinical trials of a new drug for Alzheimer’s, lecanemab, studied in Alzheimer’s patients were recently published. Based on this, the Lund University study is particularly interesting, the researchers say:
“If we can diagnose the disease before cognitive challenges arise, we may be able to use the drug to slow the disease down at a very early stage. When combined with physical activity and good nutrition, one would then have a greater chance of preventing or slowing down future cognitive decline.
“However, more research is needed before a treatment can be recommended for people who have not yet developed memory loss,” Oskar Hansson concludes.
About this news from Alzheimer’s research
Author: press office
Source: Lund University
Contact: Press Office – Lund University
Picture: The image is in the public domain
Original research: Open access.
“Amyloid and tau PET positive non-cognitive individuals are at high risk for future cognitive decline” by Rik Ossenkupplunge et al. naturopathy
See also
abstract
Amyloid and tau PET positive non-cognitive individuals are at high risk for future cognitive decline
A major unanswered question in the field of dementia is whether or not cognitively unimpaired individuals who share both neuropathological features of Alzheimer’s disease (i.e., amyloid β plaques and tau neurofibrillary tangles) retain their cognition over time are intended to be removed.
In this large multicenter amyloid and tau positron emission tomography (PET) study (n= 1,325) we assessed the risk of future progression to mild cognitive impairment and the rate of cognitive decline over time in cognitively unimpaired individuals who were amyloid PET positive (A+) and tau PET positive (T+) in the medial temporal lobe (A+TMTL+) and/or in the temporal neocortex (A+TNEO T+) and compared them to A+T− and a−T− Groups.
Cox proportional hazards models showed a substantially increased risk of progression to mild cognitive impairment in A+TNEO T+ (Hazard ratio (HR) = 19.2, 95% confidence interval (CI) = 10.9-33.7), A+TMTL+ (HR = 14.6, 95% CI = 8.1-26.4) and A+T− (HR = 2.4, 95% CI = 1.4-4.3) groups versus A−T− (Reference group. BothA+TMTL+ (HR = 6.0, 95% CI = 3.4-10.6) and A+TNEO T+ (HR = 7.9, 95% CI = 4.7-13.5) groups also showed faster clinical progression to mild cognitive impairment than the A+T− Group.
Linear mixed-effects models showed that the A+TNEO T+ (β= −0.056 ± 0.005, T= -11.55, P< 0.001), A+TMTL+ (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) groups showed compared to the A−T− (Reference) group (all P< 0.001). BothA+TNEO T+ (P< 0.001) and A+TMTL+ (P= 0.002) also progressed faster than the A+T− Group.
In conclusion, evidence of advanced pathologic changes in Alzheimer’s disease provided by a combination of abnormal amyloid and tau PET studies is strongly associated with short-term (i.e., 3–5 years) cognitive decline in the cognitively unimpaired people and is therefore of high clinical relevance.
