ReviewThe Journal of biological chemistry2018
Are N- and C-terminally truncated Aβ species key pathological triggers in Alzheimer's disease?
Review in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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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
59 citing papers in PubMed, 111 citations in OpenAlex.
- Association of CSF AβNeurology · 2022Trial
- Association of Human Gut Microbiota with Alzheimer's Disease Pathogenesis: An Exploratory Clinical Study.Brain sciences · 2026Article
- Amyloid Beta in Alzheimer's Disease: Mechanisms, Biomarker Potential, and Therapeutic Targets.CNS neuroscience & therapeutics · 2025Review
- Characterization of endothelin-converting enzyme 1 as a key enzyme in the multienzyme Aβ degradation pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Selegiline Improves Cognitive Impairment in the Rat Model of Alzheimer's Disease.Molecular neurobiology · 2025Article
- Mapping cellular stress and lipid dysregulation in Alzheimer-related progressive neurodegeneration using label-free Raman microscopy.Communications biology · 2024Article
- Amyloid-β peptide signature associated with cerebral amyloid angiopathy in familial Alzheimer's disease with APPdup and Down syndrome.Acta neuropathologica · 2024Article
- Profiling amyloid-β peptides as biomarkers for cerebral amyloid angiopathy.Journal of neurochemistry · 2024Article
- Pyroglutamylation modulates electronic properties and the conformational ensemble of the amyloid β-peptide.Proteins · 2024Article
- Chemical signatures delineate heterogeneous amyloid plaque populations across the Alzheimer's disease spectrum.bioRxiv : the preprint server for biology · 2024Article
- Variants in the MS4A cluster interact with soluble TREM2 expression on biomarkers of neuropathology.Molecular neurodegeneration · 2024Article
- Article
- Investigating the Potential Impact of Air Pollution on Alzheimer's Disease and the Utility of Multidimensional Imaging for Early Detection.ACS omega · 2024Review
- The structure of tyrosine-10 favors ionic conductance of Alzheimer's disease-associated full-length amyloid-β channels.Nature communications · 2024Article
- Cacao Ameliorates Amyloid Beta-Induced Cognitive and Non-Cognitive Disturbances.Neuroscience insights · 2024Article
- Cholinergic-like neurons and cerebral spheroids bearing the PSEN1 p.Ile416Thr variant mirror Alzheimer's disease neuropathology.Scientific reports · 2023Article
- Review
- Cascade autohydrolysis of Alzheimer's Aβ peptides.Chemical science · 2023Article
- The η-secretase-derived APP fragment ηCTF is localized in Golgi, endosomes and extracellular vesicles and contributes to Aβ production.Cellular and molecular life sciences : CMLS · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The histopathology of Alzheimer's disease (AD) is characterized by neuronal loss, neurofibrillary tangles, and senile plaque formation. The latter results from an exacerbated production (familial AD cases) or altered degradation (sporadic cases) of 40/42-amino acid-long β-amyloid peptides (Aβ peptides) that are produced by sequential cleavages of Aβ precursor protein (βAPP) by β- and γ-secretases. The amyloid cascade hypothesis proposes a key role for the full-length Aβ42 and the Aβ40/42 ratio in AD etiology, in which soluble Aβ oligomers lead to neurotoxicity, tau hyperphosphorylation, aggregation, and, ultimately, cognitive defects. However, following this postulate, during the last decade, several clinical approaches aimed at decreasing full-length Aβ42 production or neutralizing it by immunotherapy have failed to reduce or even stabilize AD-related decline. Thus, the Aβ peptide (Aβ40/42)-centric hypothesis is probably a simplified view of a much more complex situation involving a multiplicity of APP fragments and Aβ catabolites. Indeed, biochemical analyses of AD brain deposits and fluids have unraveled an Aβ peptidome consisting of additional Aβ-related species. Such Aβ catabolites could be due to either primary enzymatic cleavages of βAPP or secondary processing of Aβ itself by exopeptidases. Here, we review the diversity of N- and C-terminally truncated Aβ peptides and their biosynthesis and outline their potential function/toxicity. We also highlight their potential as new pharmaceutical targets and biomarkers.
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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.