What question did this study set out to answer?

To assess the therapeutic effects of pterostilbene on neuroinflammation and tau phosphorylation in an Alzheimer's disease model.

March 22, 2026

Pterostilbene Intervenes in Neuroinflammation and Abnormal Phosphorylation of Tau Protein in Alzheimer's Disease by Inhibiting Bace 1

Puntos clave

To assess the therapeutic effects of pterostilbene on neuroinflammation and tau phosphorylation in an Alzheimer's disease model.
Used an Aβ1-42-induced Alzheimer's mouse model
Administered pterostilbene, donepezil, and a BACE1 upregulating agent
Conducted cognitive performance assessments through behavioral tests
Evaluated AD-related pathology using ELISA, immunofluorescence, RT-qPCR, and Western blotting
Pterostilbene significantly improved cognitive performance in behavioral tests
Reduced hippocampal Aβ deposition and lowered soluble and insoluble Aβ40/42 levels
Inhibited tau phosphorylation at Ser396 and Thr231
Suppressed neuroinflammatory responses indicated by lower TNF-α, IL-1β, and IL-6 levels
Downregulated BACE1-related proteins and inhibited NF-κB pathway, restoring IκBα expression

Resumen

Background: Alzheimer's disease (AD) is characterized by neuroinflammation, amyloid-β (Aβ) accumulation, and abnormal microtubule-associated protein tau (Tau) phosphorylation. This study evaluates the therapeutic potential of pterostilbene (PTS), a natural compound with anti-inflammatory activity, in an Aβ1-42-induced AD mouse model. Methods: AD mice were established by intraperitoneal injection of aggregated Aβ1-42 and were subsequently treated with PTS, donepezil, or PTS combined with a β-site amyloid precursor protein–cleaving enzyme 1 (BACE1) upregulating agent. Cognitive performance was assessed through behavioral tests, and AD-related pathology was evaluated using Enzyme-linked immunosorbent assay (ELISA), immunofluorescence, reverse transcription quantitative polymerase chain reaction (RT-qPCR), and Western blotting. Results: Compared with AD mice, PTS treatment significantly improved cognitive performance in behavioral tests (p p p p p < 0.01). Co-treatment with the BACE1 upregulation–associated agent partially attenuated the protective effects of PTS. Conclusion: PTS exerts significant neuroprotective effects in an Aβ1-42-induced AD mouse model by alleviating cognitive impairment, amyloidogenic pathology, neuroinflammation, and Tau hyperphosphorylation, potentially through modulation of BACE1-related processes and NF-κB signaling. PTS may represent a promising multi-target therapeutic candidate for AD.

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