ReviewJournal of cellular and molecular medicine2008
Neuroprotective and neurotoxic properties of glial cells in the pathogenesis of Alzheimer's disease.
Review in Journal of cellular and molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 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
101 citing papers in PubMed, 218 citations in OpenAlex.
- Novel cell markers with altered expression in brain aging and Alzheimer's disease: A review.IBRO neuroscience reports · 2026Article
- Neuroprotective Potential ofInternational journal of molecular sciences · 2026Article
- Neutrophils and aortic medial amyloid: mutually beneficial or a dangerous combination?Frontiers in immunology · 2026Article
- Alterations in the inflammatory homeostasis of aging-related cardiac dysfunction and Alzheimer's diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Recent advances in potential enzymes and their therapeutic inhibitors for the treatment of Alzheimer's disease.Heliyon · 2024Review
- Differential Glial Response and Neurodegenerative Patterns in CA1, CA3, and DG Hippocampal Regions of 5XFAD Mice.International journal of molecular sciences · 2024Article
- An insight into the concept of neuroinflammation and neurodegeneration in Alzheimer's disease: targeting molecular approach Nrf2, NF-κB, and CREB.Inflammopharmacology · 2024Review
- Engineered Antibodies to Improve Efficacy against Neurodegenerative Disorders.International journal of molecular sciences · 2024Review
- Neuropathological changes in the TASTPM mouse model of Alzheimer's disease and their relation to hyperexcitability and cortical spreading depolarization.Scientific reports · 2024Article
- Effects of anti-tau immunotherapy on reactive microgliosis, cerebral endotheliopathy, and cognitive function in an experimental model of cerebral malaria.Journal of neurochemistry · 2023Article
- Physiological expression of mutated TAU impaired astrocyte activity and exacerbates β-amyloid pathology in 5xFAD mice.Journal of neuroinflammation · 2023Article
- Enhancement of Cholinesterase Inhibition ofMolecules (Basel, Switzerland) · 2022Article
- Significant Therapeutic Effects of Adult Human Neural Stem Cells for Spinal Cord Injury Are Mediated by Monocyte Chemoattractant Protein-1 (MCP-1).International journal of molecular sciences · 2022Article
- SARS-CoV-2 spike protein induces cognitive deficit and anxiety-like behavior in mouse via non-cell autonomous hippocampal neuronal death.Scientific reports · 2022Article
- The significance of glycolysis index and its correlations with immune infiltrates in Alzheimer's disease.Frontiers in immunology · 2022Article
- Effects of Atipamezole Preconditioning on Cognitive Function and Protein Expression in Related Brain Regions of Aged Rats after General Anesthesia.Disease markers · 2022Article
- Mitochondrial Dynamics in SARS-COV2 Spike Protein Treated Human Microglia: Implications for Neuro-COVID.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- Implications of exosomes derived from cholesterol-accumulated astrocytes in Alzheimer's disease pathology.Disease models & mechanisms · 2021Article
- Microglia modulation with 1070-nm light attenuates Aβ burden and cognitive impairment in Alzheimer's disease mouse model.Light, science & applications · 2021Article
- Endosomal-lysosomal dysfunctions in Alzheimer's disease: Pathogenesis and therapeutic interventions.Metabolic brain disease · 2021Review
41 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) affects more than 18 million people worldwide and is characterized by progressive memory deficits, cognitive impairment and personality changes. The main cause of AD is generally attributed to the increased production and accumulation of amyloid-beta (Abeta), in association with neurofibrillary tangle (NFT) formation. Increased levels of pro-inflammatory factors such as cytokines and chemokines, and the activation of the complement cascade occurs in the brains of AD patients and contributes to the local inflammatory response triggered by senile plaque. The existence of an inflammatory component in AD is now well known on the basis of epidemiological findings showing a reduced prevalence of the disease upon long-term medication with anti-inflammatory drugs, and evidence from studies of clinical materials that shows an accumulation of activated glial cells, particularly microglia and astrocytes, in the same areas as amyloid plaques. Glial cells maintain brain plasticity and protect the brain for functional recovery from injuries. Dysfunction of glial cells may promote neurodegeneration and, eventually, the retraction of neuronal synapses, which leads to cognitive deficits. The focus of this review is on glial cells and their diversity properties 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.