ArticleActa neuropathologica communications2019
Microglial motility in Alzheimer's disease and after Aβ42 immunotherapy: a human post-mortem study.
Article in Acta neuropathologica communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Regulatory role of the endocannabinoid system on glial cells toward cognitive function in Alzheimer's disease: A systematic review and meta-analysis of animal studies.Frontiers in pharmacology · 2023Pooled it
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- Emerging directions in tauopathy research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Alzheimer's disease: from molecular pathways to therapies.Molecular biomedicine · 2026Review
- Targeting Microglial Activation to Modulate Neuroinflammation in Alzheimer's Disease.Neuromolecular medicine · 2025Review
- Neuroinflammation in Alzheimer disease.Nature reviews. Immunology · 2025Review
- Divergent actions of physiological and pathological amyloid-β on synapses in live human brain slice cultures.Nature communications · 2025Article
- Volatile oil ofFrontiers in pharmacology · 2025Review
- Primary cortical cell tri-culture to study effects of amyloid-β on microglia function and neuroinflammatory response.Journal of Alzheimer's disease : JAD · 2024Article
- Cellular and pathological functions of tau.Nature reviews. Molecular cell biology · 2024Review
- Human Umbilical Cord-Mesenchymal Stem Cells Promote Extracellular Matrix Remodeling in Microglia.Cells · 2024Article
- Human brain organoids containing microglia that have arisen innately adapt to a β-amyloid challenge better than those in which microglia are integrated by co-culture.Stem cell research & therapy · 2024Article
- Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer's disease.Acta neuropathologica · 2024Article
- Glial reactivity and T cell infiltration in frontotemporal lobar degeneration with tau pathology.Brain : a journal of neurology · 2024Article
- Chuanxiong Renshen Decoction Inhibits Alzheimer's Disease Neuroinflammation by Regulating PPARγ/NF-κB Pathway.Drug design, development and therapy · 2024Article
- Saponin components inFrontiers in pharmacology · 2024Review
- Neuroinflammation in comorbid depression in Alzheimer's disease: A pilot study using post-mortem brain tissue.Neuroscience applied · 2024Article
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- Cerebellar degeneration in gluten ataxia is linked to microglial activation.Brain communications · 2024Article
- The mitochondrial protein TSPO in Alzheimer's disease: relation to the severity of AD pathology and the neuroinflammatory environment.Journal of neuroinflammation · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Microglial function is highly dependent on cell motility, with baseline motility required for homeostatic surveillance activity and directed motility to migrate towards a source of injury. Experimental evidence suggests impaired microglial motility in Alzheimer's disease (AD) and therefore we have investigated whether the expression of proteins associated with motility is altered in AD and affected by the Aβ immunotherapy using post-mortem brain tissue of 32 controls, 44 AD cases, and 16 AD cases from our unique group of patients immunised against Aβ42 (iAD).Sections of brain were immunolabelled and quantified for (i) the motility-related microglial proteins Iba1, cofilin 1 (CFL1), coronin-1a (CORO1A) and P2RY12, and (ii) pan-Aβ, Aβ42 and phosphorylated tau (ptau). The neuroinflammatory environment was characterised using Meso Scale Discovery multiplex assays. The expression of all four motility-related proteins was unmodified in AD compared with controls, whereas Iba1 and P2RY12, the homeostatic markers, were increased in the iAD group compared with AD. Iba1 and P2RY12 showed significant positive correlations with Aβ in controls but not in the AD or iAD groups. Pro- and anti-inflammatory proteins were increased in AD, whereas immunotherapy appears to result in a slightly less pro-inflammatory environment.Our findings suggest that as Aβ appears during the ageing process, the homeostatic Iba1 and P2RY12 -positive microglia respond to Aβ, but this response is absent in AD. Aβ-immunisation promoted increased Iba1 and P2RY12 expression, likely reflecting increased baseline microglial motility but without restoring the profile observed in controls.
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