Evidences path(MESH:D000544) to p(HGNC:ACHE)

Specifically, progressive phenotypic downregulation of markers within CBF neurons as well as frank CBF cell loss has been observed consistently, along with an associated reduction of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activity within the cortex in AD [16]. Most researchers presumed that progressive disruption of cholinergic function underlies much of the short-term memory loss seen in AD

Butyrylcholinesterase (BChE) is a serine hydrolase similar to AChE that is widely distributed throughout the CNS and also catalyzes the hydrolysis of ACh. BChE is localized to neurons and glia, and is associated with NFTs and senile plaques (SPs) in AD brain [32]. Interestingly, population-based genetic studies of AD have identified a point mutation that changes Ala539 to threonine in the K variant of BChE, which effectively reduces serum BChE concentrations, and may be associated with cognitive decline [33]. BChE activity also increases in AD brain whereas AChE activity remains unchanged or declines [34,35].

For example, the vesicular ACh transporter (VAChT), which is co-expressed with ChAT in human CBF neurons and participates in loading ACh into synaptic vesicles in cholinergic terminals, is not severely altered in AD [40]. In this regard, pharmacological studies of VAChT in postmortem AD tissue or in vivo imaging studies using vesamicol and its analogs, suggest that VAChT levels remain steady or are minimally decreased coincident with a severe decline in ChAT activity in cortical areas [41].

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.