Patterns of Microglial Cell Activation in Alzheimer Disease and Frontotemporal Lobar DegenerationCitation formats

  • External authors:
  • Ricardo Taipa
  • Paulo Brochado
  • Inês Reis
  • Patrício Costa
  • David M Mann
  • Manuel Melo Pires
  • Nuno Sousa

Standard

Patterns of Microglial Cell Activation in Alzheimer Disease and Frontotemporal Lobar Degeneration. / Taipa, Ricardo; Brochado, Paulo; Robinson, Andrew; Reis, Inês; Costa, Patrício; Mann, David M; Melo Pires, Manuel; Sousa, Nuno.

In: Neurodegenerative Diseases, Vol. 17, No. 4-5, 2017, p. 145-154.

Research output: Contribution to journalArticle

Harvard

Taipa, R, Brochado, P, Robinson, A, Reis, I, Costa, P, Mann, DM, Melo Pires, M & Sousa, N 2017, 'Patterns of Microglial Cell Activation in Alzheimer Disease and Frontotemporal Lobar Degeneration', Neurodegenerative Diseases, vol. 17, no. 4-5, pp. 145-154. https://doi.org/10.1159/000457127

APA

Taipa, R., Brochado, P., Robinson, A., Reis, I., Costa, P., Mann, D. M., ... Sousa, N. (2017). Patterns of Microglial Cell Activation in Alzheimer Disease and Frontotemporal Lobar Degeneration. Neurodegenerative Diseases, 17(4-5), 145-154. https://doi.org/10.1159/000457127

Vancouver

Taipa R, Brochado P, Robinson A, Reis I, Costa P, Mann DM et al. Patterns of Microglial Cell Activation in Alzheimer Disease and Frontotemporal Lobar Degeneration. Neurodegenerative Diseases. 2017;17(4-5):145-154. https://doi.org/10.1159/000457127

Author

Taipa, Ricardo ; Brochado, Paulo ; Robinson, Andrew ; Reis, Inês ; Costa, Patrício ; Mann, David M ; Melo Pires, Manuel ; Sousa, Nuno. / Patterns of Microglial Cell Activation in Alzheimer Disease and Frontotemporal Lobar Degeneration. In: Neurodegenerative Diseases. 2017 ; Vol. 17, No. 4-5. pp. 145-154.

Bibtex

@article{ad622b426a754457a57e5cf0c3ace56e,
title = "Patterns of Microglial Cell Activation in Alzheimer Disease and Frontotemporal Lobar Degeneration",
abstract = "AIMS: Microglia-driven neuroinflammation can play an important role in the pathophysiology of neurodegenerative disorders. In this study, we sought to characterize the distribution of microglial cell activation in 2 neurodegenerative dementias with distinct protein signatures, Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD) of the TDP subtype, and to determine if there was an anatomical correlation with the phenotypes most commonly associated with these conditions.METHODS: The distribution and extent of microglial cell activation was assessed semiquantitatively in the hippocampal formation, cortical gray matter, and subcortical white matter of CD68-immunostained sections of the frontal, temporal, parietal, and occipital cortices from 15 pathologically confirmed cases of AD, 13 cases of FTLD, and 18 controls.RESULTS: Significantly higher levels of microglial cell activation occurred in the subiculum in AD and FTLD than in controls. Additionally, AD had higher microglial activation in the CA1 and FTLD in the hippocampal white matter than the controls. Microglial activation was greater in the dentate gyrus molecular layer in AD than in FTLD. In the cortical regions, the 2 pathological groups differed only in frontal white matter, with the FTLD group showing higher microglial scores. FTLD showed higher microglial activation in the white matter compared to the respective gray matter in the entorhinal, temporal, and frontal regions.CONCLUSIONS: Our work expands the knowledge of the distribution and magnitude of microglial activation in these disorders. Additionally, we found some microglial circuit-specific patterns that could help to explain some of the clinical overlap between AD and FTLD-TDP, namely in memory deficits.",
keywords = "Journal Article",
author = "Ricardo Taipa and Paulo Brochado and Andrew Robinson and In{\^e}s Reis and Patr{\'i}cio Costa and Mann, {David M} and {Melo Pires}, Manuel and Nuno Sousa",
note = "{\circledC} 2017 S. Karger AG, Basel.",
year = "2017",
doi = "10.1159/000457127",
language = "English",
volume = "17",
pages = "145--154",
journal = "Neurodegenerative Diseases",
issn = "1660-2854",
publisher = "S. Karger AG",
number = "4-5",

}

RIS

TY - JOUR

T1 - Patterns of Microglial Cell Activation in Alzheimer Disease and Frontotemporal Lobar Degeneration

AU - Taipa, Ricardo

AU - Brochado, Paulo

AU - Robinson, Andrew

AU - Reis, Inês

AU - Costa, Patrício

AU - Mann, David M

AU - Melo Pires, Manuel

AU - Sousa, Nuno

N1 - © 2017 S. Karger AG, Basel.

PY - 2017

Y1 - 2017

N2 - AIMS: Microglia-driven neuroinflammation can play an important role in the pathophysiology of neurodegenerative disorders. In this study, we sought to characterize the distribution of microglial cell activation in 2 neurodegenerative dementias with distinct protein signatures, Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD) of the TDP subtype, and to determine if there was an anatomical correlation with the phenotypes most commonly associated with these conditions.METHODS: The distribution and extent of microglial cell activation was assessed semiquantitatively in the hippocampal formation, cortical gray matter, and subcortical white matter of CD68-immunostained sections of the frontal, temporal, parietal, and occipital cortices from 15 pathologically confirmed cases of AD, 13 cases of FTLD, and 18 controls.RESULTS: Significantly higher levels of microglial cell activation occurred in the subiculum in AD and FTLD than in controls. Additionally, AD had higher microglial activation in the CA1 and FTLD in the hippocampal white matter than the controls. Microglial activation was greater in the dentate gyrus molecular layer in AD than in FTLD. In the cortical regions, the 2 pathological groups differed only in frontal white matter, with the FTLD group showing higher microglial scores. FTLD showed higher microglial activation in the white matter compared to the respective gray matter in the entorhinal, temporal, and frontal regions.CONCLUSIONS: Our work expands the knowledge of the distribution and magnitude of microglial activation in these disorders. Additionally, we found some microglial circuit-specific patterns that could help to explain some of the clinical overlap between AD and FTLD-TDP, namely in memory deficits.

AB - AIMS: Microglia-driven neuroinflammation can play an important role in the pathophysiology of neurodegenerative disorders. In this study, we sought to characterize the distribution of microglial cell activation in 2 neurodegenerative dementias with distinct protein signatures, Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD) of the TDP subtype, and to determine if there was an anatomical correlation with the phenotypes most commonly associated with these conditions.METHODS: The distribution and extent of microglial cell activation was assessed semiquantitatively in the hippocampal formation, cortical gray matter, and subcortical white matter of CD68-immunostained sections of the frontal, temporal, parietal, and occipital cortices from 15 pathologically confirmed cases of AD, 13 cases of FTLD, and 18 controls.RESULTS: Significantly higher levels of microglial cell activation occurred in the subiculum in AD and FTLD than in controls. Additionally, AD had higher microglial activation in the CA1 and FTLD in the hippocampal white matter than the controls. Microglial activation was greater in the dentate gyrus molecular layer in AD than in FTLD. In the cortical regions, the 2 pathological groups differed only in frontal white matter, with the FTLD group showing higher microglial scores. FTLD showed higher microglial activation in the white matter compared to the respective gray matter in the entorhinal, temporal, and frontal regions.CONCLUSIONS: Our work expands the knowledge of the distribution and magnitude of microglial activation in these disorders. Additionally, we found some microglial circuit-specific patterns that could help to explain some of the clinical overlap between AD and FTLD-TDP, namely in memory deficits.

KW - Journal Article

U2 - 10.1159/000457127

DO - 10.1159/000457127

M3 - Article

VL - 17

SP - 145

EP - 154

JO - Neurodegenerative Diseases

JF - Neurodegenerative Diseases

SN - 1660-2854

IS - 4-5

ER -