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Scientists have developed a small molecule that disrupts the mechanism through which neurons become dysfunctional in Alzheimer’s disease (AD)
The novel drug candidate TGR63 developed by the JNCASR team has potential as a promising drug candidate for AD treatment.
Alzheimer’s disease
- In the Alzheimer's brain, abnormal levels of naturally forming protein clump together to form plaques that collect between neurons and disrupt cell function.
- This is caused by production and deposition of the amyloid peptide (Aβ) that accumulates in the central nervous system.
- The multifactorial nature of Alzheimer’s disease (AD) attributed to multifaceted amyloid toxicity has kept researchers from developing effective treatment
- AD severely affects the patients, families, caregivers and hence is a major societal and economic burden globally.
About the study
- The detailed studies established the molecule called TGR63 as the lead candidate to rescue neuronal cells from amyloid toxicity.
- The molecule was also found to reduced amyloid burden in the cortex and hippocampus, or a complex part embedded deep into the temporal lobe, thereby reversing cognitive decline.
- This research has been published recently in the journalAdvanced Therapeutics.
Source: PIB
