ArticleNeurobiology of aging2014
Alterations of Ca²⁺-responsive proteins within cholinergic neurons in aging and Alzheimer's disease.
Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Associations between cerebrospinal fluid markers and cognition in ageing and dementia: A systematic review.The European journal of neuroscience · 2022Pooled it
- Pathological Calcium Signaling in Traumatic Brain Injury and Alzheimer's Disease: From Acute Neuronal Injury to Chronic Neurodegeneration.International journal of molecular sciences · 2025Review
- Article
- Research advances on CaMKs-mediated neurodevelopmental injury.Archives of toxicology · 2024Review
- Resistance of Basal Forebrain Cholinergic Neurons to TDP-43 Proteinopathy in Primary Progressive Aphasia.Journal of neuropathology and experimental neurology · 2022Article
- Effects of Specific Inhibitors for CaMK1D on a Primary Neuron Model for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2021Article
- Severity of Lesions Involving the Cortical Cholinergic Pathways May Be Associated With Cognitive Impairment in Subacute Ischemic Stroke.Frontiers in neurology · 2021Article
- Advances in transcriptome analysis of human brain aging.Experimental & molecular medicine · 2020Review
- Modulation of the p75 neurotrophin receptor suppresses age-related basal forebrain cholinergic neuron degeneration.Scientific reports · 2019Article
- Precuneus-Dominant Degeneration of Parietal Lobe Is at Risk of Epilepsy in Mild Alzheimer's Disease.Frontiers in neurology · 2019Article
- Elevated CSF GAP-43 is Alzheimer's disease specific and associated with tau and amyloid pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2019Article
- Transient increase in CSF GAP-43 concentration after ischemic stroke.BMC neurology · 2018Article
- Pretangle pathology within cholinergic nucleus basalis neurons coincides with neurotrophic and neurotransmitter receptor gene dysregulation during the progression of Alzheimer's disease.Neurobiology of disease · 2018Article
- Locus coeruleus cellular and molecular pathology during the progression of Alzheimer's disease.Acta neuropathologica communications · 2017Article
- Diabetes negatively affects cortical and striatal GABAergic neurons: an effect that is partially counteracted by exendin-4.Bioscience reports · 2016Article
- Olfactory Deprivation Hastens Alzheimer-Like Pathologies in a Human Tau-Overexpressed Mouse Model via Activation of cdk5.Molecular neurobiology · 2016Article
- Loss of calbindin-D28K is associated with the full range of tangle pathology within basal forebrain cholinergic neurons in Alzheimer's disease.Neurobiology of aging · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The molecular basis of selective neuronal vulnerability in Alzheimer's disease (AD) remains poorly understood. Using basal forebrain cholinergic neurons (BFCNs) as a model and immunohistochemistry, we have demonstrated significant age-related loss of the calcium-binding protein calbindin-D(28K) (CB) from BFCN, which was associated with tangle formation and degeneration in AD. Here, we determined alterations in RNA and protein for CB and the Ca(2+)-responsive proteins Ca(2+)/calmodulin-dependent protein kinase I (CaMKI), growth-associated protein-43 (GAP43), and calpain in the BF. We observed progressive downregulation of CB and CaMKI RNA in laser-captured BFCN in the normal-aged-AD continuum. We also detected progressive loss of CB, CaMKIδ, and GAP43 proteins in BF homogenates in aging and AD. Activated μ-calpain, a calcium-sensitive protease that degrades CaMKI and GAP43, was significantly increased in the normal aged BF and was 10 times higher in AD BF. Overactivation of μ-calpain was confirmed using proteolytic fragments of its substrate spectrin. Substantial age- and AD-related alterations in Ca(2+)-sensing proteins most likely contribute to selective vulnerability of BFCN to degeneration in AD.
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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.