Regular ArticleFrom Acetylcholine to Amyloid: Neurotransmitters and the Pathology of Alzheimer's Disease
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Epigenetic plasticity and redox regulation of neural stem cell state and fate
2021, Free Radical Biology and MedicineGinsenosides attenuate D-galactose- and AlCl<inf>3</inf>-inducedspatial memory impairment by restoring the dysfunction of the neurotransmitter systems in the rat model of Alzheimer's disease
2016, Journal of EthnopharmacologyCitation Excerpt :Restoring the dysfunction of various neurotransmitters was a possible mechanism of the beneficial effect of ginsenosides in AD rats because the anti-AD effect of ginsenosides was proven by increasing learning and memory abilities and decreasing the damage of the hippocampus, deposition of Aβ, and expression of p-tau. AD is the most common neurodegenerative disorder that results in the failure of all but the most primitive cognitive functions, which is associated with the degeneration of many neurotransmitter systems (Nitsch, 1996). Meanwhile, in contrast to western medicine, which interacts with the human body via a single-compound drug representing a pattern of “point vs. system,” TCM interacts with the human body via a group of substances representing a pattern of “system vs. system” (Liang et al., 2008).
Describing Brain Activity of Persons With AD and Depressive Symptoms
2014, Archives of Psychiatric NursingOkadaic acid induced neurotoxicity: An emerging tool to study Alzheimer's disease pathology
2013, NeuroToxicologyCitation Excerpt :Pyramidal cells are lost in the disease, subject to tangle formation, represent a major source of APP and are regulated by a neurotransmitter ACh, affected early in the disease (Francis et al., 1999). Observations in cell lines and primary neuronal cultures it is evident that the activation of muscarinic, metabotropic glutamate and other phospholipase C-linked receptors favors the non-amyloidogenic processing of APP (Nitsch, 1996). Furthermore, β-amyloid neurotoxicity is attenuated by treatment with muscarinic agonists (Emmerling et al., 1997).
The history of the cholinergic hypothesis
2011, Behavioural Brain ResearchCitation Excerpt :These early developments of the cholinergic hypothesis had soon to confront with other ideas stemming from progress in the biochemistry of β-amyloid protein and of tau protein hyperphosphorylation, the two oldest stigmata associated with Alzheimer's disease since its early description from Alois Alzheimer [1,2] the senile plaques and the neurofibrillary tangles. These ideas gave rise to the amyloid cascade hypothesis for the pathogenesis of Alzheimer's disease [60,61,89]. In addition to the strong biochemical evidence, genetic studies of familial cases of Alzheimer's disease played an important role of support for this hypothesis, based on the demonstration that all main mutations found in these patients were related to genes involved in the production of the precursor of β-amyloid protein or in its processing to give final fragments [6].