Researchers from Brigham and Womens Hospital identified a new protein that may add to Alzheimers illness.
Alzheimers illness (AD) is a debilitating progressive health problem that begins with mild amnesia and slowly ruins cognitive function and memory. It currently has no remedy and is predicted to impact over 100 million people worldwide by 2050. In the United States, advertisement is the leading reason for dementia in older adults and the 7th most common cause of death, according to the National Institute on Aging.
Ongoing Alzheimers research is concentrated on 2 essential neurotoxic proteins: amyloid beta (Aβ) and tau. Although these proteins have actually been shown to be associated with advertisement, the levels of Aβ and tau do not consistently describe or correlate with the intensity of cognitive decrease for some individuals with the illness.
Investigators at Brigham and Womens Hospital, a founding member of the Mass General Brigham health care system, set out to identify other proteins that might be straight involved with fundamental aspects of AD, like synaptic loss and neurodegeneration. They exposed lab neurons to human brain extracts from about 40 individuals who either had AD, were protected from advertisement regardless of having high Aβ and tau levels, or were safeguarded from advertisement with little or no Aβ and tau in their brains.
The researchers determined and verified ganglioside GM2 activator (GM2A) as a protein able to reduce neuronal shooting and induce a loss of neurite integrity. These protein attributes may add to the reason for AD, progression of the illness, or both.
” Our data helps recognize a potentially important and new protein that might be connected with the pathogenesis of Alzheimers disease,” said senior author Tracy Young-Pearse, PhD, from the Department of Neurology. “Interestingly, GM2A has actually been formerly implicated as a causative agent in a lysosomal storage condition really comparable to Tay-Sachs illness, another condition like AD that destroys neurons.”
Reference: “Elevated ganglioside GM2 activator (GM2A) in human brain tissue lowers neurite stability and spontaneous neuronal activity” by Yi-Chen Hsieh, Joseph Negri, Amy He, Richard V. Pearse II, Lei Liu, Duc M. Duong, Lori B. Chibnik, David A. Bennett, Nicholas T. Seyfried and Tracy L. Young-Pearse, 21 September 2022, Molecular Neurodegeneration.DOI: 10.1186/ s13024-022-00558-4.