ReviewNeurochemical research
Cellular stress reactions as putative cholinergic links in Alzheimer's disease.
Review in Neurochemical research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 25 citations in OpenAlex.
- Overcoming the blood-brain barrier in Alzheimer's disease: translational perspectives on advanced drug delivery platforms.Frontiers in neuroscience · 2026Review
- Neuroprotective effects of multifaceted hybrid agents targeting MAO, cholinesterase, iron and β-amyloid in ageing and Alzheimer's disease.British journal of pharmacology · 2016Review
- Sucralose induces biochemical responses in Daphnia magna.PloS one · 2014Article
- Neuronal AChE splice variants and their non-hydrolytic functions: redefining a target of AChE inhibitors?British journal of pharmacology · 2013Review
- Calcium signaling-induced Smad3 nuclear accumulation induces acetylcholinesterase transcription in apoptotic HeLa cells.Cellular and molecular life sciences : CMLS · 2009Article
- Multifunctional neuroprotective derivatives of rasagiline as anti-Alzheimer's disease drugs.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2009Review
- Article
- Senataxin, defective in ataxia oculomotor apraxia type 2, is involved in the defense against oxidative DNA damage.The Journal of cell biology · 2007Article
- Interleukin-1 mediates Alzheimer and Lewy body pathologies.Journal of neuroinflammation · 2006Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease involves normal cellular aging and chronic cellular stress events, leading to interrelated changes in gene expression and subsequent neurodegeneration. Premature death of cholinergic neurons and the formation of amyloid fibrils separately initiated the cholinergic and amyloid hypotheses of Alzheimer's disease. Here, we present evidence to the fact that these two distinct phenomena both associate with specific changes in acetylcholinesterase (AChE) gene expression within cholinergic neurons. For example, calcium misregulation promotes aberrant transcription and pro-apoptotic events, as well as AChE-induced modifications in cellular signal cascades. These reciprocally intercept with AChE regulation at the Endoplasmic Reticulum, modifying AChE gene expression, folding and signaling. Altered AChE properties may reflect changes in the enzymatic and/or non-enzymatic features of the multiple AChE splice variants. Under chronic cellular stress, aberrant AChE regulation may thus facilitate apoptotic pathways, promoting plaque formation, cognitive impairments and degeneration of cholinergic nerve cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.