New research suggests that targeting proteins essential to neurotransmission could be a promising alternative to treat Alzheimer's disease
New research published today in Alzheimer's & Dementia: The Journal of the Alzheimer's Association could explain why neurons fail to communicate effectively in people with Alzheimer's disease (AD). The study conducted by researchers in the laboratory of Christophe Mulle at the Interdisciplinary Institute of Neuroscience in Bordeaux opens a new research path to establish the molecular mechanism causing AD.
Despite intense efforts in clinical research, there is no treatment to cure or even slow down the progression of AD. Current clinical interventions are typically based on the ‘amyloid cascade’ hypothesis, postulating that neurodegeneration in AD is caused by the abnormal accumulation of amyloid plaques in the brain. However, these interventions have failed to demonstrate clinical efficacy. Recently, the European Medicines Agency did not approve a controversial new drug for AD that targets plaques, concluding that the benefits do not outweigh the risks. The decision leaves an estimated 8 million people living with dementia in the EU with no treatment options, highlighting the urgent need for an alternative target for AD research.
The new study reveals that the amyloid peptide composing the plaques is not the only offender accumulating in the human AD brain. Its precursor, the amyloid precursor protein (APP), was found to surround amyloid plaques in intense microscopic staining.