Multiple sclerosis and Alzheimer's disease
Abstract
Objective: Chronic inflammation with microglia activation is thought to play a major role in the formation or clearance of Alzheimer's disease (AD) lesions, as well as in the induction of demyelination in multiple sclerosis (MS). In MS, the cortex is severely affected by chronic, long‐lasting inflammation, microglia activation, and demyelination. To what extent chronic inflammation in the cortex of MS patients influences the development of AD lesions is so far unresolved. Methods: The study was performed on autopsy tissue of 45 MS cases, 9 AD cases, and 15 control subjects. We analyzed lymphocyte and plasma cell infiltration in relation to microglia activation, to the presence of β‐amyloid plaques and (AT8 + ) neurofibrillary tangles, and to myelin pathology. Results: Profound microglia activation, determined by a broad spectrum of markers, was found in both MS and AD cortices, and the patterns of microglia activation were closely similar. Microglia activation in MS cortex, in contrast with that in AD and control cortex, correlated with lymphocyte and plasma‐cell infiltrates in the meninges. MS cases older than 64 years experienced development of AD pathology in comparable incidence as seen in the course of normal aging. The density of β‐amyloid plaques and neurofibrillary tangles did not differ between demyelinated and nondemyelinated cortical areas. Conclusions: Our data suggest that microglia activation in the MS cortex alone has little or no influence on the development of cortical AD pathology. Ann Neurol 2007
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Cluster of differentiation 68 was higher in Alzheimer's disease relative to controls in 17 of 21 studies.
“cluster of differentiation 68 (17/21 studies)”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Ionized calcium-binding adaptor molecule 1 was not consistently elevated in Alzheimer's disease relative to controls; 10 of 20 studies identified increases.
“ionized calcium-binding adaptor molecule 1 (10/20 studies)”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Increased major histocompatibility complex II staining, counts or expression was noted in the entorhinal cortex, frontal and temporal gyri, hippocampus, and frontal, temporal and occipital cortices.
“Increased MHCII staining, counts or expression was noted in: the entorhinal cortex,7, 18, 20, 35, 43, 47 frontal and temporal gyri,7, 19, 24, 32, 33, 39, 45, 56 hippocampus20, 25, 27, 30, 32, 33, 34, 35, 36, 37, 38, 40, 42, 43, 44, 47 and frontal,18, 21, 25, 40, 41, 44, 46, 48, 49, 52 temporal16, 17, 18, 28, 30, 35, 43, 44, 48, 52 and occipital cortices.25, 35, 41, 43, 44”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Higher Iba1 was noted in the Alzheimer's disease frontal cortex in four studies, was the same as control in three others, and was lower in the white matter of the frontal lobe in one study.
“Higher Iba1 was noted in the AD frontal cortex in four studies,20, 63, 64, 68 but was the same as control in three others32, 70, 74 and lower in the white matter of the frontal lobe in one study.32”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Iba1 was higher in the entorhinal cortex and inferior parietal cortex in Alzheimer's disease compared with control, but this is based on a limited number of studies.
“Iba1 was higher in the entorhinal cortex20, 62 and inferior parietal cortex65 in AD compared with control, but this is based on a limited number of studies.”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Elevations in CD68 were reported in the temporal cortex, olfactory bulb, calcarine cortex, superior temporal sulcus, orbitofrontal cortex, parahippocampal gyrus and temporal association isocortex.
“Elevations in CD68 were also reported in the temporal cortex,20, 28 the olfactory bulb,80 the calcarine cortex,69, 86 the superior temporal sulcus,83 the orbitofrontal cortex,86 parahippocampal gyrus76 and temporal association isocortex.84”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Seventeen studies identified an increase in CD68 expression, staining or positive cell counts in Alzheimer's disease relative to control samples in at least one region.
“Seventeen identified an increase in CD68 expression, staining or positive cell counts in AD relative to control samples in at least one region,17, 18, 20, 28, 41, 56, 69, 76, 78, 79, 80, 81, 82, 83, 84, 85, 86”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Iba1 was higher in Alzheimer's disease than control in the hippocampus in three studies, unchanged in five studies, and reduced in one study.
“Similarly, although Iba1 was higher in AD than control in the hippocampus in three studies,20, 62, 67 it was unchanged in five studies32, 69, 71, 73, 75 and reduced in one study.76”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Ten studies identified increases in Iba1 cell counts, staining intensity or expression in Alzheimer's disease compared with control samples in at least one brain region.
“Ten studies identified increases in Iba1 cell counts, staining intensity or expression in AD compared with control samples in at least one brain region,20, 60, 61, 62, 63, 64, 65, 66, 67, 68”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
In the hippocampus, six of eight studies identified higher CD68 in Alzheimer's disease and two identified no differences.
“CD68-positive cell counts, staining area or gene expression were measured in the hippocampus in eight studies: six identified higher levels in AD20, 69, 76, 78, 79, 86 and two identified no differences.69, 87”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Iba1-positive cell density and gene expression was the same in Alzheimer's disease and control in the temporal cortex in two studies, but greater by western blot or immunocytochemistry in three other studies.
“Iba1-positive cell density72 and gene expression74 was the same in AD and control in the temporal cortex in two studies, but greater by western blot or immunocytochemistry in three other studies.20, 61, 66”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Four studies reported no difference in CD68 in at least one of the brain regions measured.
“and four reported no difference in at least one of the brain regions measured.20, 41, 69, 80”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Dal Bianco et al. identified a greater number of CD163-positive cells in the cortical areas of the temporal lobe, including the hippocampus and entorhinal and temporal cortices.
“Dal Bianco et al.20 identified a greater number of CD163-positive cells in the cortical areas of the temporal lobe, including the hippocampus and entorhinal and temporal cortices.”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [20]
Microglial activation is significantly higher within Aβ plaques compared with plaque-free cortical areas in AD brains.
“microglial activation was significantly higher within Aβ plaques compared with plaque-free cortical areas.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [125]
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References 54 · Cited by 123
- Authors
- Dal Bianco, A., Bradl, M., Frischer, J., Kutzelnigg, A., Jellinger, K., & Lassmann, H.
- Affiliations
- Medical University of Vienna (AT)
- Corresponding author
- Lassmann, Hans
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2008-02
- Volume
- 63
- Issue
- 2
- Pages
- 174-183
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2067644826
- Cited by
- 123
- References
- 54
- Citations by year
- 2026: 3 · 2025: 12 · 2024: 7 · 2023: 8 · 2022: 9 · 2021: 8 · 2020: 7 · 2019: 1 · 2018: 4 · 2017: 5 · 2016: 4 · 2015: 5 · 2014: 7 · 2013: 5 · 2012: 8
- FWCI
- 4.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- multiple sclerosis, Alzheimer's disease, microglial activation, chronic inflammation, demyelination, cortical lesions, lymphocyte infiltration, plasma cell infiltration, meningeal inflammation, amyloid plaques, neurofibrillary tangles, myelin pathology, aging
- MeSH terms
- Adult, Aged, Aged, 80 and over, Alzheimer Disease, Brain, Cerebral Arteries, Chemotaxis, Leukocyte, Encephalitis, Female, Gliosis, Humans, Male, Meninges, Middle Aged, Multiple Sclerosis, Myelin Sheath, Biomarkers, Comorbidity, Neurofibrillary Tangles, Microglia, Disease Progression, Plaque, Amyloid
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