ArticleFrontiers in cellular neuroscience2018
NGF-Dependent Changes in Ubiquitin Homeostasis Trigger Early Cholinergic Degeneration in Cellular and Animal AD-Model.
Article in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
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- Role of Cholinergic Signaling in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2022Review
- Epigenetic regulation of synaptic disorder in Alzheimer's disease.Frontiers in neuroscience · 2022Review
- A fiber-deprived diet causes cognitive impairment and hippocampal microglia-mediated synaptic loss through the gut microbiota and metabolites.Microbiome · 2021Article
- Synaptic tau: A pathological or physiological phenomenon?Acta neuropathologica communications · 2021Review
- Overexpression of α-Synuclein Reorganises Growth Factor Profile of Human Astrocytes.Molecular neurobiology · 2021Article
- A comprehensive p75 neurotrophin receptor gene network and pathway analyses identifying new target genes.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Basal forebrain cholinergic neurons (BFCNs) depend on nerve growth factor (NGF) for their survival/differentiation and innervate cortical and hippocampal regions involved in memory/learning processes. Cholinergic hypofunction and/or degeneration early occurs at prodromal stages of Alzheimer's disease (AD) neuropathology in correlation with synaptic damages, cognitive decline and behavioral disability. Alteration(s) in ubiquitin-proteasome system (UPS) is also a pivotal AD hallmark but whether it plays a causative, or only a secondary role, in early synaptic failure associated with disease onset remains unclear. We previously reported that impairment of NGF/TrkA signaling pathway in cholinergic-enriched septo-hippocampal primary neurons triggers "dying-back" degenerative processes which occur prior to cell death in concomitance with loss of specific vesicle trafficking proteins, including synapsin I, SNAP-25 and α-synuclein, and with deficit in presynaptic excitatory neurotransmission. Here, we show that in this
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