A group of scientists from Jawaharlal Nehru Centre for Advanced Scientific Research (JNCASR) have designed a set of novel small molecules that could disrupt the mechanism through which neurons become dysfunctional in Alzheimer’s disease (AD).
The molecule could reduce the toxicity of Amyloid Beta (Aβ) toxicity and be a potential drug candidate to halt or cure the leading cause of dementia (70-80%) worldwide.
• In Alzheimer’s disease , usually abnormal levels of naturally forming protein accumulate to form plaques that collect between neurons and disrupt cell function.
• This is caused due to production and deposition of the amyloid peptide (Aβ), which collects in the central nervous system.
• However, detailed studies have established the TGR63 molecule as a potential candidate to rescue neuronal cells from amyloid toxicity.
• The molecule is found to reduce amyloid burden in the cortex and hippocampus, a complex part embedded deep into the temporal lobe, thereby reversing cognitive decline.
• The research was published recently in the journal Advanced Therapeutics.
• When mice with Alzheimer’s disease were treated with TGR63, their brain showed a significant reduction of amyloid deposits.
• The mice also showed a reduction in memory impairment, learning deficiency and cognitive decline.
• These attributes validate the potential of TGR63 as a promising drug candidate for the treatment of Alzheimer’s Disease.
There is no particular drug that can directly act on the disease mechanisms of Alzheimer’s disease to cure or halt it. The current available treatments only provide temporary relief.
The disease severely affects the patients, caregivers and families and hence is a major societal and economic burden globally.