Parishin A ameliorates cognitive decline by promoting PS1 autophagy in Alzheimer's disease
Alzheimer's disease (AD) is the most common form of progressive dementia characterized by amyloid beta (Aβ) accumulation and Tau hyperphosphorylation.Parishin A (PA), a phenolic acid-like tannin compound derived from the traditional Chinese
Alzheimer's disease (AD) is the most common form of progressive dementia characterized by amyloid beta (Aβ) accumulation and Tau hyperphosphorylation.Parishin A (PA), a phenolic acid-like tannin compound derived from the traditional Chinese medicinal herb Gastrodia elata, has been reported to possess anti-inflammatory properties. However, its potential neuroprotective effects in AD have not been fully elucidated. Here, we reported that PA decreased PS1 expression by promoting PS1 degradation through enhanced autophagy, rather than by inhibiting PS1 synthesis, thereby alleviating APP amyloidogenic processes in N2A APP cells. Additionally, we found that PA could counteract Chloroquine (CQ)-induced autophagy inhibition, as evidenced by an increase in autophagic flux. Furthermore, PA has the capability to reduce Tau hyperphosphorylation. Most importantly, PA improved cognitive impairment in Aβ1-42 -induced AD model mice by reducing oxidative stress and enhancing the anti-inflammatory response. Taken together, our study suggests that PA ameliorates cognitive dysfunction by promoting autophagy and reducing oxidative stress, underscoring its potential as a therapeutic candidate for AD..
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