Alzheimer's disease (AD) is the most common cause of dementia. An early feature of the AD pathology is the dysregulation of intracellular Ca signaling in neurons. In particular, increased Ca release from endoplasmic reticulum-located Ca channels, including inositol-1,4,5-trisphosphate type 1 receptors (IPR1) and ryanodine receptors type 2 (RyR2), have been extensively reported.
View Article and Find Full Text PDFAlzheimer's disease and cerebral ischemia are among the many causative neurodegenerative diseases that lead to disabilities in the middle-aged and elderly population. There are no effective disease-preventing therapies for these pathologies. Recent in vitro and in vivo studies have revealed the TRPC6 channel to be a promising molecular target for the development of neuroprotective agents.
View Article and Find Full Text PDFDespite decades of research and effort, there is still no effective disease-modifying treatment for Alzheimer's Disease (AD). Most of the recent AD clinical trials were targeting amyloid pathway, but all these trials failed. Although amyloid pathology is a hallmark and defining feature of AD, targeting the amyloid pathway has been very challenging due to low efficacy and serious side effects.
View Article and Find Full Text PDFAlzheimer's disease (AD) is the neurodegenerative disorder with no cure. Recent studies suggest that dysregulated postsynaptic store-operated calcium entry (nSOCE) may underlie mushroom spine loss that is related to AD pathology. In the present study we observed that PSEN1ΔE9 familial AD (FAD) mutation causes mushroom spine loss in hippocampal neuronal cultures.
View Article and Find Full Text PDFAlzheimer's disease (AD) is a neurodegenerative disorder that is the major cause of dementia in the elderly. There is no cure against AD. We have recently discovered a novel transient receptor potential canonical 6 (TRPC6)-mediated intracellular signaling pathway that regulates the stability of dendritic spines and plays a role in memory formation.
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