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Appears in Networks 2

In-Edges 3

bp(GO:"GO:0008292") association path(MESH:D003704) View Subject | View Object

In fact, it has been demonstrated that decreasing levels of ACh synthesis are significantly correlated with increasing severity of dementia in patients with Alzheimer's disease (Table) PubMed:16273023

a(MESH:D059329) association path(MESH:D003704) View Subject | View Object

Notably, reports that physostigmine and oral anticholinesterases have beneficial effects for patients with AD suggest that the CBF system is somewhat preserved during the progression of dementia, despite well-documented loss of cholinergic biosynthetic machinery (including ChAT and AChE enzyme deficits) in patients with this disease. Interestingly, recent studies have shown that ChAT activity, which results in acetylcholine (ACh) synthesis, is preserved in the neocortex of people with MCI [18,19]. PubMed:18986241

path(HBP:aMCI) association path(MESH:D003704) View Subject | View Object

People with a clinical diagnosis of MCI comprise a heterogeneous cohort of which those with memory deficits only are classified as amnestic MCI (aMCI) and those with impairment in other cognitive domains lacking a clinical diagnosis of dementia are designated multidomain MCI (mdMCI) [3,4]. Many individuals characterized with aMCI progress steadily to greater stages of dementia severity, and in many instances exhibit the neuropathologic, molecular and biochemical hallmarks of AD [5–9]. These clinical pathobiologic studies suggest that MCI, in general, represents a prodromal or preclinical stage of AD. PubMed:18986241

Out-Edges 4

path(MESH:D003704) association bp(GO:"GO:0008292") View Subject | View Object

In fact, it has been demonstrated that decreasing levels of ACh synthesis are significantly correlated with increasing severity of dementia in patients with Alzheimer's disease (Table) PubMed:16273023

path(MESH:D003704) association path(HBP:aMCI) View Subject | View Object

People with a clinical diagnosis of MCI comprise a heterogeneous cohort of which those with memory deficits only are classified as amnestic MCI (aMCI) and those with impairment in other cognitive domains lacking a clinical diagnosis of dementia are designated multidomain MCI (mdMCI) [3,4]. Many individuals characterized with aMCI progress steadily to greater stages of dementia severity, and in many instances exhibit the neuropathologic, molecular and biochemical hallmarks of AD [5–9]. These clinical pathobiologic studies suggest that MCI, in general, represents a prodromal or preclinical stage of AD. PubMed:18986241

path(MESH:D003704) association a(MESH:D059329) View Subject | View Object

Notably, reports that physostigmine and oral anticholinesterases have beneficial effects for patients with AD suggest that the CBF system is somewhat preserved during the progression of dementia, despite well-documented loss of cholinergic biosynthetic machinery (including ChAT and AChE enzyme deficits) in patients with this disease. Interestingly, recent studies have shown that ChAT activity, which results in acetylcholine (ACh) synthesis, is preserved in the neocortex of people with MCI [18,19]. PubMed:18986241

path(MESH:D003704) decreases p(HGNC:ACHE) View Subject | View Object

The enzyme that hydrolyzes ACh at the synapse, AChE, does not show a decline in cortical areas until at least moderately severe levels of dementia [28]. PubMed:18986241

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.