Literature DB >> 29679378

Prominent microglial activation in cortical white matter is selectively associated with cortical atrophy in primary progressive aphasia.

D T Ohm1, G Kim1, T Gefen1,2, A Rademaker1,3, S Weintraub1,2, E H Bigio1,4, M-M Mesulam1,5, E Rogalski1, C Geula1.   

Abstract

AIMS: Primary progressive aphasia (PPA) is a clinical syndrome characterized by selective language impairments associated with focal cortical atrophy favouring the language dominant hemisphere. PPA is associated with Alzheimer's disease (AD), frontotemporal lobar degeneration (FTLD) and significant accumulation of activated microglia. Activated microglia can initiate an inflammatory cascade that may contribute to neurodegeneration, but their quantitative distribution in cortical white matter and their relationship with cortical atrophy remain unknown. We investigated white matter activated microglia and their association with grey matter atrophy in 10 PPA cases with either AD or FTLD-TDP pathology.
METHODS: Activated microglia were quantified with optical density measures of HLA-DR immunoreactivity in two regions with peak cortical atrophy, and one nonatrophied region within the language dominant hemisphere of each PPA case. Nonatrophied contralateral homologues of the language dominant regions were examined for hemispheric asymmetry.
RESULTS: Qualitatively, greater densities of activated microglia were observed in cortical white matter when compared to grey matter. Quantitative analyses revealed significantly greater densities of activated microglia in the white matter of atrophied regions compared to nonatrophied regions in the language dominant hemisphere (P < 0.05). Atrophied regions of the language dominant hemisphere also showed significantly more activated microglia compared to contralateral homologues (P < 0.05).
CONCLUSIONS: White matter activated microglia accumulate more in atrophied regions in the language dominant hemisphere of PPA. While microglial activation may constitute a response to neurodegenerative processes in white matter, the resultant inflammatory processes may also exacerbate disease progression and contribute to cortical atrophy.
© 2018 British Neuropathological Society.

Entities:  

Keywords:  zzm321990PPAzzm321990; Alzheimer's disease; Cortical atrophy; TDP-43; White matter pathology; activated microglia

Year:  2018        PMID: 29679378      PMCID: PMC6196127          DOI: 10.1111/nan.12494

Source DB:  PubMed          Journal:  Neuropathol Appl Neurobiol        ISSN: 0305-1846            Impact factor:   8.090


  56 in total

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Journal:  Ann Neurol       Date:  2003-02       Impact factor: 10.422

3.  Primary progressive aphasia: reversed asymmetry of atrophy and right hemisphere language dominance.

Authors:  M Mesulam; S Weintraub; T Parrish; D Gitelman
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Review 4.  Inflammation, autotoxicity and Alzheimer disease.

Authors:  P L McGeer; E G McGeer
Journal:  Neurobiol Aging       Date:  2001 Nov-Dec       Impact factor: 4.673

Review 5.  Primary progressive aphasia.

Authors:  M M Mesulam
Journal:  Ann Neurol       Date:  2001-04       Impact factor: 10.422

Review 6.  Microglia and inflammation-mediated neurodegeneration: multiple triggers with a common mechanism.

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Authors:  Emma Schofield; Cindy Kersaitis; Claire E Shepherd; Jillian J Kril; Glenda M Halliday
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  8 in total

1.  Neuropathologic basis of in vivo cortical atrophy in the aphasic variant of Alzheimer's disease.

Authors:  Daniel T Ohm; Angela J Fought; Alfred Rademaker; Garam Kim; Jaiashre Sridhar; Christina Coventry; Tamar Gefen; Sandra Weintraub; Eileen Bigio; Marek Marsel Mesulam; Emily Rogalski; Changiz Geula
Journal:  Brain Pathol       Date:  2019-09-12       Impact factor: 6.508

2.  Primary Progressive Aphasia has a Unique Signature Distinct from Dementia of the Alzheimer's Type and Behavioral Variant Frontotemporal Dementia Regardless of Pathology.

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Journal:  J Neuropathol Exp Neurol       Date:  2020-12-04       Impact factor: 3.685

3.  Cerebrospinal Fluid YKL-40 and Chitotriosidase Levels in Frontotemporal Dementia Vary by Clinical, Genetic and Pathological Subtype.

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4.  Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD.

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Journal:  Acta Neuropathol       Date:  2019-02-09       Impact factor: 17.088

5.  The relationship between TLR4/NF-κB/IL-1β signaling, cognitive impairment, and white-matter integrity in patients with stable chronic schizophrenia.

Authors:  Hongna Li; Wenjin Chen; Mengzhuang Gou; Wei Li; Jinghui Tong; Yanfang Zhou; Ting Xie; Ting Yu; Wei Feng; Yanli Li; Song Chen; Baopeng Tian; Shuping Tan; Zhiren Wang; Shujuan Pan; Na Li; Xingguang Luo; Ping Zhang; Junchao Huang; Li Tian; Chiang-Shan R Li; Yunlong Tan
Journal:  Front Psychiatry       Date:  2022-08-16       Impact factor: 5.435

6.  Microglial burden, activation and dystrophy patterns in frontotemporal lobar degeneration.

Authors:  Ione O C Woollacott; Christina E Toomey; Catherine Strand; Robert Courtney; Bridget C Benson; Jonathan D Rohrer; Tammaryn Lashley
Journal:  J Neuroinflammation       Date:  2020-08-10       Impact factor: 8.322

7.  Distribution of microglial phenotypes as a function of age and Alzheimer's disease neuropathology in the brains of people with Down syndrome.

Authors:  Alessandra C Martini; Alex M Helman; Katie L McCarty; Ira T Lott; Eric Doran; Frederick A Schmitt; Elizabeth Head
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8.  Accumulation of neurofibrillary tangles and activated microglia is associated with lower neuron densities in the aphasic variant of Alzheimer's disease.

Authors:  Daniel T Ohm; Angela J Fought; Adam Martersteck; Christina Coventry; Jaiashre Sridhar; Tamar Gefen; Sandra Weintraub; Eileen Bigio; M-Marsel Mesulam; Emily Rogalski; Changiz Geula
Journal:  Brain Pathol       Date:  2020-11-05       Impact factor: 6.508

  8 in total

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