Reactive Glia not only Associates with Plaques but also Parallels Tangles in Alzheimer’s Disease
Open accessAbstract
Senile plaques are a prominent pathological feature of Alzheimer's disease (AD), but little is understood about the association of glial cells with plaques or about the dynamics of glial responses through the disease course. We investigated the progression of reactive glial cells and their relationship with AD pathological hallmarks to test whether glial cells are linked only to amyloid deposits or also to tangle deposition, thus integrating both lesions as a marker of disease severity. We conducted a quantitative stereology-based post-mortem study on the temporal neocortex of 15 control subjects without dementia and 91 patients with AD, including measures of amyloid load, neurofibrillary tangles, reactive astrocytes, and activated microglia. We also addressed the progression of glial responses in the vicinity (≤50 μm) of dense-core plaques and tangles. Although the amyloid load reached a plateau early after symptom onset, astrocytosis and microgliosis increased linearly throughout the disease course. Moreover, glial responses correlated positively with tangle burden, whereas astrocytosis correlated negatively with cortical thickness. However, neither correlated with amyloid load. Glial responses increased linearly around existing plaques and in the vicinity of tangles. These results indicate that the progression of astrocytosis and microgliosis diverges from that of amyloid deposition, arguing against a straightforward relationship between glial cells and plaques. They also suggest that reactive glia might contribute to the ongoing neurodegeneration.
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Microglia become activated under conditions of stress or deterioration (e.g., Aβ amyloid fibrils and tau paired helical filaments) and are observed around senile plaques, with increased numbers in promotion to neuronal damage associated with NFTs and NT.
“Normally they play a role in synaptic monitoring and turnover, but under conditions of stress or deterioration (e.g., protein aggregates such as Aβ amyloid fibrils and tau paired helical filaments) they become activated and are observed around senile plaques, and their numbers increase in promotion to neuronal damage associated with NFTs and NT [86, 87].”
From The neuropathological diagnosis of Alzheimer's disease (2019) · cites this paper as [86]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredAstrocyte morphology changes near Aβ plaques and pTau NFTs.
“Because astrocyte morphology changes near Aβ plaques and pTau NFTs23,24”
From Astrocyte transcriptomic changes along the spatiotemporal progression of Alzheimer’s disease (2024) · cites this paper as [23]
The Spatial Relationships section (page unavailable) reports increased density of reactive astrocytes near dense-core plaques and NFTs. It does not report a change in astrocyte morphology near those lesions; the measured change was in reactive-cell density. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAstrocytes undergo a dynamic phenotypic change from homeostatic to reactive through an intermediate state in response to their microenvironment conditions, namely the presence of Aβ plaques and NFTs.
“These results are consistent with a dynamic phenotypic change of astrocytes from homeostatic to reactive through an intermediate state in response to their microenvironment conditions, namely the presence of Aβ plaques and NFTs23,54–57”
From Astrocyte transcriptomic changes along the spatiotemporal progression of Alzheimer’s disease (2024) · cites this paper as [23]
The Spatial Relationships section (page unavailable) reports increasing densities of reactive astrocytes near Aβ plaques and NFTs as disease progresses. It does not establish that individual astrocytes transition from homeostatic to reactive through an intermediate state, and the Discussion cautions that the study is cross-sectional. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPro-inflammatory microglia are closely associated with protein aggregate pathologies characteristic of most dementias.
“Immune involvement in neurodegenerative disease centres on findings that pro-inflammatory microglia are closely associated with protein aggregate pathologies characteristic of most dementias.”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [12]
Activated microglia are observed close to tau protein in neurofibrillary tangles.
“Activated microglia are also observed close to tau protein in neurofibrillary tangles [12].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [12]
In Alzheimer's disease, reactive microglia and astrocytes are associated with amyloid plaques and respond to Aβ with expression of pro-inflammatory cytokines.
“In AD, reactive microglia and astrocytes are associated with the amyloid plaques and respond to Aβ with the expression of pro-inflammatory cytokines [12,13,14].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [12]
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Self-citation
- Authors
- Serrano-Pozo, A., Mielke, M. L., Gómez-Isla, T., Betensky, R. A., Growdon, J. H., Frosch, M. P., & Hyman, B. T.
- Affiliations
- Massachusetts General Hospital (US)
- Harvard University (US)
- Corresponding author
- Hyman, Bradley T.
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2011-09
- Volume
- 179
- Issue
- 3
- Pages
- 1373-1384
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC3157187
- OpenAlex
- W2001618696
- Cited by
- 488
- References
- 56
- Citations by year
- 2026: 30 · 2025: 32 · 2024: 49 · 2023: 52 · 2022: 55 · 2021: 51 · 2020: 36 · 2019: 39 · 2018: 29 · 2017: 22 · 2016: 20 · 2015: 18 · 2014: 16 · 2013: 22 · 2012: 13
- FWCI
- 11.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal Of Pathology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- NIH (P50AG05134, AG08487)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, reactive glia, astrocyte activation, microglial activation, amyloid plaques, neurofibrillary tangles, temporal neocortex, cortical thickness, disease progression, neurodegeneration, stereology
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Astrocytes, Female, Gliosis, Humans, Immunohistochemistry, Male, Neurofibrillary Tangles, Microglia, Disease Progression, Neocortex, Plaque, Amyloid
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