A recent study led by researchers at University College London (UCL) has found that the brain volume loss associated with new immunotherapies for Alzheimer’s disease may result from the removal of amyloid plaques rather than from the loss of neurons or brain tissue. The findings were published in Lancet Neurology and analyzed data from twelve clinical trials of amyloid-targeting immunotherapies, including lecanemab, which has recently received approval from the UK’s Medicines and Healthcare Products Regulatory Agency (MHRA).
Although brain shrinkage is typically viewed as a negative outcome, the research team observed that the extent of volume loss was consistent across various studies and correlated with the effectiveness of the therapy in eliminating amyloid plaques. Notably, this volume loss was not linked to any harmful effects, leading the researchers to conclude that the removal of amyloid plaques, which are prevalent in Alzheimer’s patients, could explain the observed brain volume changes. Consequently, they argue that this volume loss should not be a cause for alarm.
To describe this phenomenon, the researchers introduced the term “amyloid-removal-related pseudo-atrophy” (ARPA).
Amyloid-targeting monoclonal antibodies represent a significant advancement in Alzheimer’s treatment by binding to and facilitating the removal of amyloid plaques from the brain. However, the impact of these treatments on brain volume has sparked controversy. Brain volume loss is a hallmark of Alzheimer’s disease, primarily due to the progressive degeneration of neurons. Concerns have arisen in both media and medical literature regarding the potential toxicity of these drugs, given the consistent reports of increased brain volume loss associated with amyloid immunotherapy.
Professor Nick Fox, the senior author and director of the UCL Dementia Research Centre, stated, “Based on the available data, we believe that this excess volume change is an anticipated consequence of the removal of pathological amyloid plaques from the brains of patients with Alzheimer’s disease.”
Dr. Christopher Belder, the first author of the study from the UCL Dementia Research Centre and The University of Adelaide, emphasized the need for improved reporting of brain volume changes in clinical trials and further evaluation to better understand these effects as these therapies become more widely used.
In August, the MHRA licensed lecanemab for use in the early stages of Alzheimer’s disease in the UK. The drug targets beta-amyloid, a protein that accumulates in the brains of Alzheimer’s patients and is believed to trigger neuronal dysfunction and cell death.
The National Institute for Health and Care Excellence (NICE), which assesses whether drugs should be available on the NHS, has issued draft guidance stating that the benefits of lecanemab may not justify its cost. However, this decision is set to be reviewed following a public consultation and a second independent committee meeting later this year.
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