The DOI matches its Crossref record; 199 of the 202 references it cites were found in a registry or an index.
Neuroprotective and neurotoxic properties of glial cells in the pathogenesis of Alzheimer's disease
Open accessAbstract
• Introduction • Innate immune response in the AD brain - Microglia - Astrocyte • Glial cells mediate the peripheral immune response in AD - Glial cell interaction with endothelial cells - Glial cell interaction with T cells • Glial cell activation as a therapeutic target in AD • Conclusion 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-β (Aβ), 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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“T-helper 1 cells can promote microglial cell activation through the secretion of IFN-γ, which also up-regulates the expression major histocompatibility complex class II molecules by microglial cells, thereby enhancing the interaction between T cells and microglial cells [164, 165].”
From PKR, the double stranded RNA‐dependent protein kinase as a critical target in Alzheimer's disease (2009) · cites this paper as [164]
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“T-helper 1 cells can promote microglial cell activation through the secretion of IFN-γ, which also up-regulates the expression major histocompatibility complex class II molecules by microglial cells, thereby enhancing the interaction between T cells and microglial cells [164, 165].”
From PKR, the double stranded RNA‐dependent protein kinase as a critical target in Alzheimer's disease (2009) · cites this paper as [164]
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“It is also known that glial cells can mediate the permeability of blood brain barrier to recruit specialized immune cells from the periphery such as T cells [164].”
From PKR, the double stranded RNA‐dependent protein kinase as a critical target in Alzheimer's disease (2009) · cites this paper as [164]
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Cites
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BackgroundImmunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse
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Cited by
Sorted by citations
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Interactions Between Neurons and Microglia During Neuroinflammation
Suzumura, A. (2013) · Advances in neurobiology · doi:10.1007/978-1-4614-8313-7_4
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Cerebral small vessel disease: cerebrospinal fluid aspects
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“Activation of glial cells can trigger inflammatory pathways(29).”
BackgroundMethodSelf-citationNeurons and Plasticity: What Do Glial Cells Have to Do with This?
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21116 基礎浮き上がり構造物の地震応答に及ぼす入力地震動位相特性の影響(相互作用(4):モデル化と応答,構造II)
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Kuruvilla, J., Yong, Y. T., Lee, W. J., Yap, K., Deng, X., Tan, E., & Xiao, B. (2025) · Research Square · doi:10.21203/rs.3.rs-5954887/v1
A Hybrid Deep Neural Network for Early Diagnosis of Alzheimer’s Disease
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Farfara, D., Sooliman, M., Avrahami, L., Royal, T. G., Amram, S., Rozenstein‐Tsalkovich, L., Trudler, D., Blanga‐Kanfi, S., Eldar-Finkelman, H., Pahnke, J., et al. (2023) · Figshare · doi:10.6084/m9.figshare.26606671
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Self-citationSilk fibroin@polydopamine for acupoint catgut-embedding therapy in Alzheimer’s disease
Wang, C., Liu, X., Fan, Y., Liu, G.-Y., Wu, P., Li, S.-C., & Du, Y. (2026) · Journal of Chinese Integrative Medicine · doi:10.1016/j.joim.2026.01.010
Neutrophils and aortic medial amyloid: mutually beneficial or a dangerous combination?
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Novel cell markers with altered expression in brain aging and Alzheimer's disease: A review
Alobu, E. J., Uchewa, O. O., & Ibegbu, A. O. (2026) · IBRO Neuroscience Reports · doi:10.1016/j.ibneur.2026.08.010
“These cellular associations render neuroinflammation both a consequence and an inducer within AD, thereby highlighting glial states as essential determinants of disease prognosis, from A β formation to massive neuronal cell death in AD patients (Farfara et al., 2008; Goel et al., 2022).”
Peshdary, V. (2012) · uO Research (University of Ottawa) · doi:10.20381/ruor-5394
Metadata
- Authors
- Farfara, D., Lifshitz, V., & Frenkel, D.
- Affiliations
- Tel Aviv University (IL)
- Corresponding author
- Frenkel, D.
- Venue
- Journal of Cellular and Molecular Medicine
- Publisher
- Wiley
- Published
- 2008-05-21
- Volume
- 12
- Issue
- 3
- Pages
- 762-780
- ISSN
- 1582-1838 (ISSN-L)
- 1582-4934
- PMC
- PMC4401126
- OpenAlex
- W2022388884
- Cited by
- 216
- References
- 202
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 8 · 2023: 7 · 2022: 7 · 2021: 10 · 2020: 13 · 2019: 5 · 2018: 7 · 2017: 9 · 2016: 7 · 2015: 8 · 2014: 15 · 2013: 15 · 2012: 20
- FWCI
- 2.12
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Cellular and Molecular Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, glial cells, microglia, astrocytes, neuroinflammation, innate immune response, amyloid-beta, neurofibrillary tangles, amyloid plaques, complement system, cytokines and chemokines, neuroprotection, neurotoxicity, neurodegeneration, anti-inflammatory therapy
- MeSH terms
- Alzheimer Disease, Amyloid, Animals, Astrocytes, Brain, Disease Models, Animal, Humans, Models, Neurological, Synaptic Transmission, Synapses, T-Lymphocytes, Amyloid beta-Peptides, Microglia, Endothelial Cells, Plaque, Amyloid
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