Topic: Wnt/β-catenin signaling

Presenilin1 (PSEN1) E280A mutation causes early onset Alzheimer’s disease (AD) in the world’s largest familial AD kindred. We previously published a case report of a carrier from this kindred who was remarkably protected from cognitive decline for thirty years. Positron emission tomography (PET) brain analysis showed lower levels of Tau pathology relative to typical PSEN1 E280A carriers. Whole-genome sequencing revealed homozygosity for an Apolipoprotein E mutation (Christchurch, APOECh). As the ApoECh mutation is found within the heparan sulfate proteoglycan (HSPG) binding domain, we hypothes

Parkinson’s disease (PD) is a neurodegenerative disorder that is characterized by dopaminergic neuronal damage. We evaluated the neuroprotective effect of γ-amino butyric acid (GABA) in PD and the underlying mechanism focusing on WNT/β-catenin signaling mediated by the MAPK pathway. We treated MPTP-induced SH-SY5Y cells with GABA Low and High concentrations, and we also treated PD model mice with GABA. GABA treatment effectively reduced the expression of biomarkers associated with PD, particularly lewy’s bodies and α-synuclein, and increased the number of tyrosine hydroxylase positive cells. G

The deposition of amyloid-β (Aβ) peptides has been implicated as a one of pathological hallmark of Alzheimer's disease (AD). Increasing evidence indicates that Aβ initiates oxidative stress and a vicious cycle of mitochondrial damage, leading to apoptotic neuronal death. Pinocembrin (5,7-dihydroxyflavone), a major flavonoid found in honey and propolis, has shown significant neuroprotective property by suppressing Aβ cleaving enzyme in our previous study. The present study investigated a novel anti-AD effect of pinocembrin on mitochondrial dysfunction and apoptosis against Aβ injury. Neurotoxic