ReviewCNS & neurological disorders drug targets2013
Innate immunity in Alzheimer's disease: a complex affair.
Review in CNS & neurological disorders drug targets, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 73 citations in OpenAlex.
- Normal-Tension Glaucoma and Potential Clinical Links to Alzheimer's Disease.Journal of clinical medicine · 2024Review
- Amyloid-β and caspase-1 are indicators of sepsis and organ injury.ERJ open research · 2024Article
- Association between the neutrophil to lymphocyte ratio and mild cognitive impairment in patients with type 2 diabetes.Aging clinical and experimental research · 2023Article
- Investigation of the peripheral inflammation (neutrophil-lymphocyte ratio) in two neurodegenerative diseases of the central nervous system.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Article
- Human iPSC-Derived Neural Models for Studying Alzheimer's Disease: from Neural Stem Cells to Cerebral Organoids.Stem cell reviews and reports · 2022Review
- Impact of Anti-amyloid-β Monoclonal Antibodies on the Pathology and Clinical Profile of Alzheimer's Disease: A Focus on Aducanumab and Lecanemab.Frontiers in aging neuroscience · 2022Review
- Astrocytes and microglia in neurodegenerative diseases: Lessons from human in vitro models.Progress in neurobiology · 2021Review
- Physical Exercise and Alzheimer's Disease: Effects on Pathophysiological Molecular Pathways of the Disease.International journal of molecular sciences · 2021Review
- Ultrasound Combined With Microbubbles Loading BDNF Retrovirus to Open BloodBrain Barrier for Treatment of Alzheimer's Disease.Frontiers in pharmacology · 2021Article
- Fibrillar Aβ triggers microglial proteome alterations and dysfunction in Alzheimer mouse models.eLife · 2020Article
- Biological Hallmarks of Cancer in Alzheimer's Disease.Molecular neurobiology · 2019Review
- TNFα and IL-1β but not IL-18 Suppresses Hippocampal Long-Term Potentiation Directly at the Synapse.Neurochemical research · 2019Article
- Regulatory Effects of Neuroinflammatory Responses Through Brain-Derived Neurotrophic Factor Signaling in Microglial Cells.Molecular neurobiology · 2018Article
- RAGE-TLR Crosstalk Sustains Chronic Inflammation in Neurodegeneration.Molecular neurobiology · 2018Review
- Glial Draper Rescues Aβ Toxicity in aThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Dopaminergic Regulation of Innate Immunity: a Review.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Review
- Article
- Cytokines and cytokine networks target neurons to modulate long-term potentiation.Cytokine & growth factor reviews · 2017Article
- Young microglia restore amyloid plaque clearance of aged microglia.The EMBO journal · 2017Article
- IL-1β impairs retrograde flow of BDNF signaling by attenuating endosome trafficking.Journal of neuroinflammation · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is characterized by three major histopathological hallmarks: β-amyloid deposits, neurofibrillary tangles and gliosis. While neglected for decades, the neuroinflammatory processes coordinated by microglia are now accepted as etiologic events in AD evolution. Microglial cells are found in close vicinity to amyloid plaques and display various activation phenotypes determined by the expression of a wide range of cytokines, chemokines, and innate immune surface receptors. During the development of AD pathology, microglia fail to restrict amyloid plaques and may contribute to neurotoxicity and cognitive deficit. Nevertheless, under specific activation states, microglia can participate in cerebral amyloid clearance. This review focuses on the complex relationship between microglia and Aβ pathology, and highlights both deleterious and beneficial roles of microglial activation states in the context of AD. A deeper understanding of microglial biology will hopefully pave the way for next-generation AD therapeutic approaches aimed at harnessing these enigmatic innate immune cells of the central nervous system.
Indexed as
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What OpenQuestion holds
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.