TL;DR
Serum DLX6-AS1 is a potential biomarker for early diagnosis and assessment of AD, and regulates Aβ-induced neuronal damage and tau phosphorylation by targeting miR-204-5p, offering a new mechanism target for AD molecular therapy.
FBXL19-AS1 appears to interact with and modulate miR-650, thereby affecting ITGB3 expression and potentially participating in the pathological progression of AD.
This study is the first to elucidate that SNHG3 could regulate microglial polarization and neuroinflammation through the SNHG3/miR-128-3p/UBR5 axis.
SNHG16 is highly expressed in pediatric TLE and has certain diagnostic potential and exacerbates epilepsy-related neuronal damage by binding to and suppressing miR-485-5p function, which provides novel insights into understanding the disease mechanism.
Let-7d-5p alleviates cognitive deficits in AD by inhibiting Aβ deposition and neuronal apoptosis through targeting bach1, and bach1 upregulation counteracted the inhibitory effects of let-7d-5p overexpression on Aβ1-42-induced cellular injury.
The present review aims to delve into the potential mechanism of action of Dalbergia sissoo in Alzheimer’s disease, focusing on the interaction between the P2X7 receptor and NLRP3 inflammasome.
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