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There is currently no cure for Alzheimer's disease (AD), with more than 100 million people expected to fall ill
worldwide by 2050.
Current research focuses on two key neurotoxic proteins: β amyloid (Aβ) and tau.
While these proteins have been shown to be associated with AD, levels of Aβ and tau proteins are not always explained or correlated
with the severity of cognitive decline for some people with the disease 。 To identify other proteins that may be directly related to fundamental aspects of AD, such as synapse loss and neurodegeneration, researchers at Brigham and Women's Hospital exposed lab neurons to brain extracts from about 40 people with AD who either had higher levels of Aβ and tau proteins but were protected by AD or had little or no β Aβ and tau proteins in their brains but were protected
by AD.
The researchers identified and verified that the ganglioside GM2 activator (GM2A) is a protein
capable of reducing neuronal firing and inducing loss of neurite integrity.
These protein signatures may contribute to the etiology of AD, the progression of the disease, or both
.
"Our data help identify a new, potentially important protein that may be involved in the pathogenesis of Alzheimer's," said
senior author Tracy Young-Pearse, Ph.
D.
, from the Department of Neurology.
"Interestingly, GM2A was previously thought to be the causative agent of lysosomal storage disorders, a disease very similar to Ty-Sachs disease and a disease
that destroys neurons like AD.
"
levated ganglioside GM2 activator (GM2A) in human brain tissue reduces neurite integrity and spontaneous neuronal activity