ArticleMolecular neurodegeneration2022
Upregulation of Ca
Article in Molecular neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- Targeting C/EBPβ/ Calbindin 1 pathway bolsters the neural resilience to tau pathology and improves tau-impaired episodic memory.Molecular psychiatry · 2026Article
- Targeting the dopaminergic midbrain in Alzheimer's disease: Therapeutic potential of focusing on specific neural circuits rather than single molecular pathways.Neural regeneration research · 2026Article
- Cell-Type-Selective Cortical Pathology and Functional Deficits in Synucleinopathy.bioRxiv : the preprint server for biology · 2026Article
- Alzheimer's Pathology Enhances Excitatory Synaptic Input and Integration in VTA Dopamine Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Microglial clearance, neuroprotection and cognitive recovery via a novel synthetic sulfolipid in Alzheimer's disease.Journal of neuroinflammation · 2025Article
- Brain region-specific dopamine receptor changes and astrocyte activation influence tau pathology through CDK5 in Alzheimer's disease models.Journal of Alzheimer's disease : JAD · 2025Article
- Midbrain degeneration triggers astrocyte reactivity and tau pathology in experimental Alzheimer's Disease.Molecular neurodegeneration · 2025Article
- Optogenetic stimulation of midbrain dopaminergic neurons rescues hippocampal synaptic plasticity deficits in a mouse model of Alzheimer's disease.Translational psychiatry · 2025Article
- PKC-dependent enhancement of glutamate input to VTA dopamine neurons in 3xTg-AD mice.bioRxiv : the preprint server for biology · 2025Article
- Microbial Metabolomes in Alzheimer's Disease: From Pathogenesis to Therapeutic Potential.Current issues in molecular biology · 2025Review
- Therapeutic potential of melatonin-induced mitophagy in the pathogenesis of Alzheimer's disease.Inflammopharmacology · 2025Review
- Tau conveys intrinsic hyperactivity of VTA dopamine neurons but an inability to sustain burst firing.bioRxiv : the preprint server for biology · 2025Article
- Temporal Changes in Mitochondria-Centric Excitotoxic Responses Following Severe Penetrating Traumatic Brain Injury.Biomedicines · 2025Article
- Melatonin protects against sarcopenia in middle-aged mice.Histology and histopathology · 2025Article
- Repetitive prefrontal tDCS activates VTA dopaminergic neurons, resulting in attenuation of Alzheimer's Disease-like deficits in Tg2576 mice.Alzheimer's research & therapy · 2025Article
- VTA dopamine neurons are hyperexcitable in 3xTg-AD mice due to casein kinase 2-dependent SK channel dysfunction.Nature communications · 2024Article
- Advanced Immunolabeling Method for Optical Volumetric Imaging Reveals Dystrophic Neurites of Dopaminergic Neurons in Alzheimer's Disease Mouse Brain.Molecular neurobiology · 2024Article
- Dopamine neuron degeneration in the Ventral Tegmental Area causes hippocampal hyperexcitability in experimental Alzheimer's Disease.Molecular psychiatry · 2024Article
- GUCY2C signaling limits dopaminergic neuron vulnerability to toxic insults.NPJ Parkinson's disease · 2024Article
- Cerebellum Purkinje cell vulnerability in aged rats with memory impairment.The Journal of comparative neurology · 2024Article
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent clinical and experimental studies have highlighted the involvement of Ventral Tegmental Area (VTA) dopamine (DA) neurons for the early pathogenesis of Alzheimer's Disease (AD). We have previously described a progressive and selective degeneration of these neurons in the Tg2576 mouse model of AD, long before amyloid-beta plaque formation. The degenerative process in DA neurons is associated with an autophagy flux impairment, whose rescue can prevent neuronal loss. Impairments in autophagy can be the basis for accumulation of damaged mitochondria, leading to disturbance in calcium (Ca
methodsIn Tg2576 mice, we performed amperometric recordings of DA levels and analysis of dopaminergic fibers in the Nucleus Accumbens - a major component of the ventral striatum precociously affected in AD patients - together with retrograde tracing, to identify the most vulnerable DA neuron subpopulations in the VTA. Then, we focused on these neurons to analyze mitochondrial integrity and Apoptosis-inducing factor (AIF) localization by electron and confocal microscopy, respectively. Stereological cell count was also used to evaluate degeneration of DA neuron subpopulations containing the Ca
resultsWe found a progressive degeneration of mesolimbic DA neurons projecting to the ventral striatum, located in the paranigral nucleus and parabrachial pigmented subnucleus of the VTA. At the onset of degeneration (3 months of age), the vulnerable DA neurons in the Tg2576 accumulate damaged mitochondria, while AIF translocates from the mitochondria to the nucleus. Although we describe an age-dependent loss of the DA neurons expressing Calbindin-D28K or Calretinin, we observed that the remaining cells upregulate the levels of Ca
conclusionOverall, our results suggest that the overexpression of Ca
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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 Socratic graph.