ArticleJournal of neuroinflammation2018
Neuroinflammation is increased in the parietal cortex of atypical Alzheimer's disease.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Transcriptomics Meta-Analysis Reveals Phagosome and Innate Immune System Dysfunction as Potential Mechanisms in the Cortex of Alzheimer's Disease Mouse Strains.Journal of molecular neuroscience : MN · 2023Pooled it
- Presynaptic accumulation of APP-CTFβ may contribute to synaptic dysfunction in Alzheimer's disease.The EMBO journal · 2026Article
- Immunotherapy with B28, an antibody to Aβ oligomers, potently decreases amyloid plaques, microgliosis, and memory decline in APP knock-in mice.Cell reports · 2026Article
- Clinical and pathologic correlations of machine learning quantification of Aβ deposits across 3 brain regions of decedents with Alzheimer disease.Journal of neuropathology and experimental neurology · 2026Article
- The Role and Molecular Mechanism of Icaritin in the Treatment of Alzheimer's Disease.Current medicinal chemistry · 2026Review
- Neuroinflammation in Alzheimer disease.Nature reviews. Immunology · 2025Review
- Pathological Characterisation of Posterior Cortical Atrophy in Comparison With Amnestic Alzheimer's Disease.Neuropathology and applied neurobiology · 2025Article
- Neurodegenerative diseases and neuroinflammation-induced apoptosis.Open life sciences · 2025Review
- Alzheimer's disease clinical variants show distinct neuroinflammatory profiles with neuropathology.Neuropathology and applied neurobiology · 2024Article
- Neuroinflammation is associated with Alzheimer's disease co-pathology in dementia with Lewy bodies.Acta neuropathologica communications · 2024Article
- Inflammation, Autoimmunity and Neurodegenerative Diseases, Therapeutics and Beyond.Current neuropharmacology · 2024Article
- Hesperetin attenuates cognitive dysfunction via SIRT6/NLRP3 pathway in scopolamine-induced mice.Metabolic brain disease · 2023Article
- Neuroprotective Effect of Nosustrophine in a 3xTg Mouse Model of Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Temporal lobe epilepsy with GAD antibodies: neurons killed by T cells not by complement membrane attack complex.Brain : a journal of neurology · 2023Article
- Expanding the spectrum of amyloid-β plaque pathology: the Down syndrome associated 'bird-nest plaque'.Acta neuropathologica · 2022Article
- Targeting innate immunity to protect and cure Alzheimer's disease: opportunities and pitfalls.Molecular psychiatry · 2021Review
- Astrogliosis and episodic memory in late life: higher GFAP is related to worse memory and white matter microstructure in healthy aging and Alzheimer's disease.Neurobiology of aging · 2021Article
- Multimodal, label-free fluorescence and Raman imaging of amyloid deposits in snap-frozen Alzheimer's disease human brain tissue.Communications biology · 2021Article
- New insights into atypical Alzheimer's disease in the era of biomarkers.The Lancet. Neurology · 2021Review
- Amyloid-β, p-tau and reactive microglia are pathological correlates of MRI cortical atrophy in Alzheimer's disease.Brain communications · 2021Article
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8 authors.
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Abstract
backgroundWhile most patients with Alzheimer's disease (AD) present with memory complaints, 30% of patients with early disease onset present with non-amnestic symptoms. This atypical presentation is thought to be caused by a different spreading of neurofibrillary tangles (NFT) than originally proposed by Braak and Braak. Recent studies suggest a prominent role for neuroinflammation in the spreading of tau pathology.
methodsWe aimed to explore whether an atypical spreading of pathology in AD is associated with an atypical distribution of neuroinflammation. Typical and atypical AD cases were selected based on both NFT distribution and amnestic or non-amnestic clinical presentation. Immunohistochemistry was performed on the temporal pole and superior parietal lobe of 10 typical and 9 atypical AD cases. The presence of amyloid-beta (N-terminal; IC16), pTau (AT8), reactive astrocytes (GFAP), microglia (Iba1, CD68, and HLA-DP/DQ/DR), and complement factors (C1q, C3d, C4b, and C5b-9) was quantified by image analysis. Differences in lobar distribution patterns of immunoreactivity were statistically assessed using a linear mixed model.
resultsWe found a temporal dominant distribution for amyloid-beta, GFAP, and Iba1 in both typical and atypical AD. Distribution of pTau, CD68, HLA-DP/DQ/DR, C3d, and C4b differed between AD variants. Typical AD cases showed a temporal dominant distribution of these markers, whereas atypical AD cases showed a parietal dominant distribution. Interestingly, when quantifying for the number of amyloid-beta plaques instead of stained surface area, atypical AD cases differed in distribution pattern from typical AD cases. Remarkably, plaque morphology and localization of neuroinflammation within the plaques was different between the two phenotypes.
conclusionsOur data show a different localization of neuroinflammatory markers and amyloid-beta plaques between AD phenotypes. In addition, these markers reflect the atypical distribution of tau pathology in atypical AD, suggesting that neuroinflammation might be a crucial link between amyloid-beta deposits, tau pathology, and clinical symptoms.
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