ReviewFrontiers in cell and developmental biology2022
Key brain cell interactions and contributions to the pathogenesis of Alzheimer's disease.
Review in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 16 citations in OpenAlex.
- Peripheral blood DNA methylation partially reports on immune cell type composition in the frontal brain.Brain, behavior, & immunity - health · 2026Article
- From neuroinflammation to immune reprogramming: Nanozyme-Integrated nanoplatforms for neuroimmune modulation in Parkinson's disease.Materials today. Bio · 2026Article
- Therapeutic potential of melatonin-induced mitophagy in the pathogenesis of Alzheimer's disease.Inflammopharmacology · 2025Review
- Astrocyte-driven vasoconstriction impairs glymphatic clearance in a human tauopathy-on-chip model.APL bioengineering · 2025Article
- Single Nuclei Transcriptomics Reveals Obesity-Induced Endothelial and Neurovascular Dysfunction: Implications for Cognitive Decline.International journal of molecular sciences · 2024Article
- Interleukin-22 Contributes to Blood-Brain Barrier Disruption via STAT3/VEGFA Activation inACS infectious diseases · 2024Article
- Mitochondria in Alzheimer's Disease Pathogenesis.Life (Basel, Switzerland) · 2024Review
- Effect of age and sex differences on the abundances of neuronal, glial, and endothelial cells in non-diseased brain tissue.PloS one · 2024Article
- Microglia and the Blood-Brain Barrier: An External Player in Acute and Chronic Neuroinflammatory Conditions.International journal of molecular sciences · 2023Review
- Towards Novel BiomimeticBioengineering (Basel, Switzerland) · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common neurodegenerative disease worldwide, with the two major hallmarks being the deposition of extracellular β-amyloid (Aβ) plaques and of intracellular neurofibrillary tangles (NFTs). Additionally, early pathological events such as cerebrovascular alterations, a compromised blood-brain barrier (BBB) integrity, neuroinflammation and synaptic dysfunction, culminate in neuron loss and cognitive deficits. AD symptoms reflect a loss of neuronal circuit integrity in the brain; however, neurons do not operate in isolation. An exclusively neurocentric approach is insufficient to understand this disease, and the contribution of other brain cells including astrocytes, microglia, and vascular cells must be integrated in the context. The delicate balance of interactions between these cells, required for healthy brain function, is disrupted during disease. To design successful therapies, it is critical to understand the complex brain cellular connections in AD and the temporal sequence of their disturbance. In this review, we discuss the interactions between different brain cells, from physiological conditions to their pathological reactions in AD, and how this basic knowledge can be crucial for developing new therapeutic strategies.
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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.