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31st January 2024
A simple blood test to diagnose Alzheimer’s disease could be as accurate as a lumbar puncture or expensive brain scans, according to a new study.
It raises the potential for early diagnosis to make best use of new medicines that slow the rate of cognitive decline but also could help doctors distinguish between different types of dementia in order to direct treatment.
The test, which is commercially available, measures levels of p-tau217 in plasma samples – a biomarker that can be used to detect a build-up of amyloid and tau proteins in the brain.
Research done in three separate groups of patients over eight years found the precision of the blood test was comparable to cerebrospinal fluid biomarkers.
It was particularly effective in detecting longitudinal changes, even in preclinical stages of the disease, the researchers reported in the journal JAMA Neurology.
The test could also significantly reduce the need for additional confirmatory tests patients have to have to verify their diagnosis, the international team of researchers said.
Study author Dr Daniel Alcolea, researcher at the Dementia Neurobiology Group at the Sant Pau Research Institute in Barcelona and head of the biomarkers platform at Hospital Sant Pau’s Memory Unit, said: ‘This biomarker has shown very high performance in detecting Alzheimer’s in blood, with an accuracy between 90 and 95%.
‘Of all the biomarkers currently being studied for diagnosing Alzheimer’s disease, this one has shown the best results.’
Dr Richard Oakley, associate director of research and innovation at Alzheimer’s Society, said there were potentially ground-breaking new drugs which can slow the progression of early-stage Alzheimer’s disease in the development pipeline.
‘But for people to be eligible for them if they’re approved in the UK, they will need an early, accurate diagnosis. This study is a hugely welcome step in the right direction,’ he said.
Professor David Curtis, honorary professor at the UCL Genetics Institute, said the test potentially had huge implications for screening, diagnosis and developing better treatments.
‘When effective treatments to prevent the progression of Alzheimer’s disease become available it will be essential to be able to identify people who are at high risk before they begin to deteriorate.
‘This study shows that a simple blood test might be able to do this by measuring levels of tau protein in the blood which has been phosphorylated in a specific way.’
The only way to prove someone has a build-up of Alzheimer’s-related proteins in the brain currently is through a lumbar puncture or an amyloid PET scan, which are only available in around one in 20 memory clinics, said Professor Charles Marshall, professor of clinical neurology at Queen Mary University of London.
‘Before these tests become widely used in the NHS, we will need further evidence to show that the blood test can accurately diagnose who is in the process of developing dementia, and that it can identify who is likely to benefit from treatments to slow down the disease’, he said.
‘We will also need to ensure that the blood test performs equally well in more diverse populations, so that it does not worsen existing health inequalities in access to diagnosis and treatment for dementia.’
A version of this article was originally published by our sister publication Pulse.
17th July 2023
Diagnosing Alzheimer’s disease through the use of blood biomarkers could transform care for patients after new proposed guidelines were presented at the International Alzheimer’s Congress in Amsterdam.
Developed by clinicians and researchers from around the world, the proposed guidelines incorporate blood-based biomarkers, which offer a low cost and easily accessible alternative to more traditional routes of diagnosis.
A blood test has been developed for this purpose in recent years, which has shown good results, and this can be used outside of specialist clinics, meaning underserved and rural populations can also benefit.
Charlotte Teunissen, professor of neurochemistry at Amsterdam University Medical Centre, who was involved in drafting the new guidelines, said: ‘A new generation of biomarkers is now available to detect Alzheimer’s disease more and more effectively. We have already gained a lot of experience with this in our Alzheimer’s centre, but in the long term the test can also be successfully implemented after a GP’s referral.‘
Currently, Alzheimer’s is diagnosed through the analysis of cerebrospinal fluid, acquired through an invasive lumbar puncture, or via an expensive PET scan. The proposed diagnostic criteria would prove less stressful to patients as well as speeding up diagnosis, offering a gateway to earlier treatment and allowing patients to make more informed decisions about their treatment and disease management.
Defining neurodegenerative diseases biologically, rather than based on syndromic presentation, has become a unifying concept common to all neurodegenerative diseases, not just Alzheimer’s.
While many biomarkers have shown promise and performance in the ability to detect Alzheimer’s disease, some of the biomarkers described in the proposal have not yet been extensively tested in broadly representative populations, and further analysis in these groups is urgently needed, the Alzheimer’s Association said.
The draft proposal will be open for consultation for 30 days, and the working group invites comments from scientific and clinical audiences.
Maria C. Carrillo, chief science officer, Alzheimer’s Association, said: ‘Care has to evolve with the science. Our understanding of Alzheimer’s disease has advanced, in particular our understanding of biomarkers, and this needs to be reflected in how we describe and diagnose the disease.
‘We look forward to input from the scientific and clinical community on these proposed revisions. The Alzheimer’s Association is proud to lead this important effort, which will ultimately enable people to get a more accurate diagnosis earlier, as well as help those diagnosed enrol in research trials and, if appropriate, get access to approved treatments.‘
17th May 2023
An early amyloid PET scan provides a high certainty diagnosis in memory clinic patients three months after their diagnosis, according to a new study.
Amyloid-β is the predominant pathologic protein in Alzheimer’s disease (AD) and which affects disease progression and prognosis. Moreover, an amyloid-imaging PET tracer, provides quantitative information on the extent of these protein deposits in living subjects. Despite this, other work suggests the current appropriate use criteria for imaging cannot effectively identify patients who will benefit from such imaging.
In the current study, researchers sought to assess the value of amyloid scanning in patients from a memory clinic. They wondered if a PET scan performed soon after the patient’s diagnosis, enabled a more confident aetiological diagnosis. Patients had either subjective cognitive decline with symptoms of preclinical AD, mild cognitive impairment or dementia.
Researchers randomly placed individuals into three arms. Arm one (early scan), arm two (scan after eight months) and arm three (scan at the physician’s discretion). The aetiological diagnoses were grouped into three main categories: AD; non-AD and undetermined. The primary outcome was the proportion of participants receiving a high confidence (>90%) etiological diagnosis in arms one and two after three months.
The study included 840 patients with a similar proportion in each of the three arms. The prevalence of amyloid positivity was higher in those with a baseline diagnosis of AD versus participants with non-AD (69% vs 36%, p < 0.001) at baseline.
After three months, 40% of arm one patients and 11% in arm two, had high confidence diagnosis (p < 0.001). This effect was consistent across cognitive stages.
The findings led to authors to conclude that an early amyloid PET allowed memory clinic patients to receive an aetiological diagnosis with very high confidence after only three months. The findings supported the implementation of amyloid PET early in the diagnostic workup of memory clinic patients.
8th December 2022
The cognitive decline present in patients with early Alzheimer’s disease (AD) as well as the amyloid burden are significantly reduced compared to placebo, in those treated with lecanemab according to the results of a randomised, double-blind, phase 3 trial by US researchers.
There are an estimated 55 million across the world living with dementia of whom, approximately 60 to 70% have the most common form, Alzheimer’s disease. Currently available treatments such as cholinesterase inhibitors and memantine, do not alter disease progression but can help with some symptoms. Current thinking the pathophysiology of Alzheimer’s disease is based on the amyloid β-protein (Aβ peptides) theory which purports that in the early stages, there is an imbalance between production and clearance of Aβ peptides and which is a very early, often initiating factor in Alzheimer’s disease (AD). This leads to a build-up of Aβ peptides, and one therapeutic approach gaining interest is the use of monoclonal antibodies directed against amyloid-β (Aβ). In a 2021 systematic review of such antibodies directed against Aβ, there were clinical improvements but with small effect sizes.
In the current study, researchers examined the value of one such monoclonal antibody, lecanemab. Although in a phase 2b proof of concept trial in patients with early Alzheimer’s disease, the drug did not change clinical progression of the disease, it did demonstrate a reduction in brain amyloid accompanied by a consistent reduction of clinical decline in several endpoints. The current study was designed to evaluate the efficacy of lecanemab in patients with early Alzheimer’s disease, i.e., either mild cognitive impairment or mild dementia due to AD and with evidence of amyloid protein as assessed by either PET scan or CSF fluid measurement. Participants were randomised 1:1 to either intravenous lecanemab (10 mg/kg every two weeks) or placebo. The primary endpoint was the change from baseline after 18 months in the Clinical Dementia Rating Sum of Boxes (CDR-SB) which ranges from 0 to 18 and for which higher scores indicate greater cognitive impairment. There were several secondary endpoints, one of which was the change in amyloid burden on PET scanning whereas others assessed changes in cognition.
Early Alzheimer’s disease and change in cognition
A total of 1734 participants with a mean age of 71.2 years (52.3% women) were included and randomised to lecanemab (859) or placebo. The mean baseline CDR-SB score was approximately 3.2 in both groups.
The adjusted mean change from baseline in CDR-SB score was less with lecanemab (1.21) compared to placebo (1.66), i.e., there was less decline in cognition and the mean difference of -0.45 (95% CI -0.67 to -0.23) was statistically significant (p < 0.001).
In a subgroup of 698 participants, the mean amyloid level reduced by -55.48 centiloids in the lecanemab group and by 3.64 in the placebo group (mean difference = -59.12, 95% CI -62.64 to -55.60, p < 0.001).
There were also significant and positive changes favouring lecanemab in the cognition-related outcomes.
The overall incidence of adverse effects was similar between the two groups although lecanemab use resulted in a higher incidence of infusion-related reactions compared to placebo (26.4% vs 7.4%).
The authors concluded that the use of lecanemab reduced markers of amyloid in early Alzheimer’s disease and gave rise to moderately less decline on measures of cognition compared to placebo. They called for longer trials to determine the efficacy and safety of lecanemab in early Alzheimer’s disease.
Citation
van Dyck CH et al. Lecanemab in Early Alzheimer’s Disease. N Eng J Med 2022 DOI: 10.1056/NEJMoa2212948
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