ArticleNeurobiology of aging2016
Protein homeostasis gene dysregulation in pretangle-bearing nucleus basalis neurons during the progression of Alzheimer's disease.
Article in Neurobiology of aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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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Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- Global brain activity links subcortical degeneration to cortical tau progressively across Braak regions over early Alzheimer's disease stages.bioRxiv : the preprint server for biology · 2026Article
- Pretangle tau pathology accrual in the default mode network during the progression of Alzheimer's disease.Molecular neurodegeneration advances · 2026Article
- Neuronal gene profiling of tau oligomer-bearing cholinergic nucleus basalis neurons during the onset of Alzheimer's disease.Acta neuropathologica communications · 2025Article
- Potential Role of Membrane Contact Sites in the Dysregulation of the Crosstalk Between Mitochondria and Lysosomes in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Cholinotrophic basal forebrain connectome dysfunction in Down syndrome with and without dementia.iScience · 2025Article
- Article
- TTC3-Mediated Protein Quality Control, A Potential Mechanism for Cognitive Impairment.Cellular and molecular neurobiology · 2022Review
- Posterior cingulate cortex reveals an expression profile of resilience in cognitively intact elders.Brain communications · 2022Article
- Visualization of neurofibrillary tangle maturity in Alzheimer's disease: A clinicopathologic perspective for biomarker research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Review
- Clearance of intracellular tau protein from neuronal cells via VAMP8-induced secretion.The Journal of biological chemistry · 2020Article
- Expression profiling of precuneus layer III cathepsin D-immunopositive pyramidal neurons in mild cognitive impairment and Alzheimer's disease: Evidence for neuronal signaling vulnerability.The Journal of comparative neurology · 2020Article
- Brain-derived neurotrophic factor (BDNF) and TrkB hippocampal gene expression are putative predictors of neuritic plaque and neurofibrillary tangle pathology.Neurobiology of disease · 2019Article
- Peri-Infarct Upregulation of the Oxytocin Receptor in Vascular Dementia.Journal of neuropathology and experimental neurology · 2019Article
- Article
- Modulation of the p75 neurotrophin receptor suppresses age-related basal forebrain cholinergic neuron degeneration.Scientific reports · 2019Article
- Frontal cortex and striatal cellular and molecular pathobiology in individuals with Down syndrome with and without dementia.Acta neuropathologica · 2019Article
- Pathogenic tau modifications occur in axons before the somatodendritic compartment in mossy fiber and Schaffer collateral pathways.Acta neuropathologica communications · 2019Article
- Nerve Growth Factor Pathobiology During the Progression of Alzheimer's Disease.Frontiers in neuroscience · 2019Review
- Tau Secretion: Good and Bad for Neurons.Frontiers in neuroscience · 2019Review
- Selective vulnerability in neurodegenerative diseases.Nature neuroscience · 2018Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Conformational phosphorylation and cleavage events drive the tau protein from a soluble, monomeric state to a relatively insoluble, polymeric state that precipitates the formation of neurofibrillary tangles (NFTs) in projection neurons in Alzheimer's disease (AD), including the magnocellular perikarya located in the nucleus basalis of Meynert (NBM) complex of the basal forebrain. Whether these structural changes in the tau protein are associated with pathogenic changes at the molecular and cellular level remains undetermined during the onset of AD. Here, we examined alterations in gene expression within individual NBM neurons immunostained for pS422, an early tau phosphorylation event, or dual labeled for pS422 and TauC3, a later stage tau neoepitope, from tissue obtained postmortem from subjects who died with an antemortem clinical diagnosis of no cognitive impairment, mild cognitive impairment, or mild/moderate AD. Specifically, pS422-positive pretangles displayed an upregulation of select gene transcripts subserving protein quality control. On the other hand, late-stage TauC3-positive NFTs exhibited upregulation of messenger RNAs involved in protein degradation but also cell survival. Taken together, these results suggest that molecular pathways regulating protein homeostasis are altered during the evolution of NFT pathology in the NBM. These changes likely contribute to the disruption of protein turnover and neuronal survival of these vulnerable NBM neurons during the progression of AD.
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Registered trials
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