دورية أكاديمية
أعرض في EDS

Neuroinflammation is associated with Alzheimer's disease co-pathology in dementia with Lewy bodies.

التفاصيل البيبلوغرافية
العنوان: Neuroinflammation is associated with Alzheimer's disease co-pathology in dementia with Lewy bodies.
المؤلفون: Wetering JV; Department of Anatomy and Neurosciences, Section Clinical Neuroanatomy and Biobanking and Life Sciences O|2 building 13e55, Amsterdam UMC location Vrije Universiteit Amsterdam, De Boelelaan 1118, Amsterdam, 1081 HV, The Netherlands.; Neurodegeneration, Amsterdam Neuroscience, Amsterdam, The Netherlands., Geut H; Department of Anatomy and Neurosciences, Section Clinical Neuroanatomy and Biobanking and Life Sciences O|2 building 13e55, Amsterdam UMC location Vrije Universiteit Amsterdam, De Boelelaan 1118, Amsterdam, 1081 HV, The Netherlands.; Neurodegeneration, Amsterdam Neuroscience, Amsterdam, The Netherlands., Bol JJ; Department of Anatomy and Neurosciences, Section Clinical Neuroanatomy and Biobanking and Life Sciences O|2 building 13e55, Amsterdam UMC location Vrije Universiteit Amsterdam, De Boelelaan 1118, Amsterdam, 1081 HV, The Netherlands., Galis Y; Department of Anatomy and Neurosciences, Section Clinical Neuroanatomy and Biobanking and Life Sciences O|2 building 13e55, Amsterdam UMC location Vrije Universiteit Amsterdam, De Boelelaan 1118, Amsterdam, 1081 HV, The Netherlands., Timmermans E; Department of Anatomy and Neurosciences, Section Clinical Neuroanatomy and Biobanking and Life Sciences O|2 building 13e55, Amsterdam UMC location Vrije Universiteit Amsterdam, De Boelelaan 1118, Amsterdam, 1081 HV, The Netherlands., Twisk JWR; Department of Epidemiology and Biostatistics, Amsterdam UMC location Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, The Netherlands., Hepp DH; Department of Neurology, Leiden University Medical Center, Albinusdreef 2, Leiden, 2333 ZA, The Netherlands., Morella ML; Department of Anatomy and Neurosciences, Section Clinical Neuroanatomy and Biobanking and Life Sciences O|2 building 13e55, Amsterdam UMC location Vrije Universiteit Amsterdam, De Boelelaan 1118, Amsterdam, 1081 HV, The Netherlands.; Neurodegeneration, Amsterdam Neuroscience, Amsterdam, The Netherlands., Pihlstrom L; Department of Neurology, Oslo University Hospital, Oslo, Norway., Lemstra AW; Neurodegeneration, Amsterdam Neuroscience, Amsterdam, The Netherlands.; Department of Neurology, Amsterdam UMC location Vrije Universiteit Amsterdam, Amsterdam, De Boelelaan 1117, The Netherlands.; Alzheimer Center, Department of Neurology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands., Rozemuller AJM; Neurodegeneration, Amsterdam Neuroscience, Amsterdam, The Netherlands.; Department of Pathology, Amsterdam UMC location Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, The Netherlands., Jonkman LE; Department of Anatomy and Neurosciences, Section Clinical Neuroanatomy and Biobanking and Life Sciences O|2 building 13e55, Amsterdam UMC location Vrije Universiteit Amsterdam, De Boelelaan 1118, Amsterdam, 1081 HV, The Netherlands.; Neurodegeneration, Amsterdam Neuroscience, Amsterdam, The Netherlands., van de Berg WDJ; Department of Anatomy and Neurosciences, Section Clinical Neuroanatomy and Biobanking and Life Sciences O|2 building 13e55, Amsterdam UMC location Vrije Universiteit Amsterdam, De Boelelaan 1118, Amsterdam, 1081 HV, The Netherlands. wdj.vandeberg@amsterdamumc.nl.; Neurodegeneration, Amsterdam Neuroscience, Amsterdam, The Netherlands. wdj.vandeberg@amsterdamumc.nl.
المصدر: Acta neuropathologica communications [Acta Neuropathol Commun] 2024 May 07; Vol. 12 (1), pp. 73. Date of Electronic Publication: 2024 May 07.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 101610673 Publication Model: Electronic Cited Medium: Internet ISSN: 2051-5960 (Electronic) Linking ISSN: 20515960 NLM ISO Abbreviation: Acta Neuropathol Commun Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London : BioMed Central, [2013]-
مواضيع طبية MeSH: Lewy Body Disease*/pathology , Lewy Body Disease*/metabolism , Alzheimer Disease*/pathology , Alzheimer Disease*/metabolism , Neuroinflammatory Diseases*/pathology , Neuroinflammatory Diseases*/metabolism , Microglia*/pathology , Microglia*/metabolism , Astrocytes*/pathology , Astrocytes*/metabolism, Humans ; Female ; Male ; Aged ; Aged, 80 and over ; alpha-Synuclein/metabolism ; tau Proteins/metabolism ; Antigens, CD/metabolism ; Amyloid beta-Peptides/metabolism ; Middle Aged ; Antigens, Differentiation, Myelomonocytic/metabolism ; Brain/pathology ; Brain/metabolism ; CD68 Molecule
مستخلص: Background: Neuroinflammation and Alzheimer's disease (AD) co-pathology may contribute to disease progression and severity in dementia with Lewy bodies (DLB). This study aims to clarify whether a different pattern of neuroinflammation, such as alteration in microglial and astroglial morphology and distribution, is present in DLB cases with and without AD co-pathology.
Methods: The morphology and load (% area of immunopositivity) of total (Iba1) and reactive microglia (CD68 and HLA-DR), reactive astrocytes (GFAP) and proteinopathies of alpha-synuclein (KM51/pser129), amyloid-beta (6 F/3D) and p-tau (AT8) were assessed in a cohort of mixed DLB + AD (n = 35), pure DLB (n = 15), pure AD (n = 16) and control (n = 11) donors in limbic and neocortical brain regions using immunostaining, quantitative image analysis and confocal microscopy. Regional and group differences were estimated using a linear mixed model analysis.
Results: Morphologically, reactive and amoeboid microglia were common in mixed DLB + AD, while homeostatic microglia with a small soma and thin processes were observed in pure DLB cases. A higher density of swollen astrocytes was observed in pure AD cases, but not in mixed DLB + AD or pure DLB cases. Mixed DLB + AD had higher CD68-loads in the amygdala and parahippocampal gyrus than pure DLB cases, but did not differ in astrocytic loads. Pure AD showed higher Iba1-loads in the CA1 and CA2, higher CD68-loads in the CA2 and subiculum, and a higher astrocytic load in the CA1-4 and subiculum than mixed DLB + AD cases. In mixed DLB + AD cases, microglial load associated strongly with amyloid-beta (Iba1, CD68 and HLA-DR), and p-tau (CD68 and HLA-DR), and minimally with alpha-synuclein load (CD68). In addition, the highest microglial activity was found in the amygdala and CA2, and astroglial load in the CA4. Confocal microscopy demonstrated co-localization of large amoeboid microglia with neuritic and classic-cored plaques of amyloid-beta and p-tau in mixed DLB + AD cases.
Conclusions: In conclusion, microglial activation in DLB was largely associated with AD co-pathology, while astrocytic response in DLB was not. In addition, microglial activity was high in limbic regions, with prevalent AD pathology. Our study provides novel insights into the molecular neuropathology of DLB, highlighting the importance of microglial activation in mixed DLB + AD.
(© 2024. The Author(s).)
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معلومات مُعتمدة: Health~Holland Health~Holland; Stichting Woelse Waard Stichting Woelse Waard
فهرسة مساهمة: Keywords: Alpha-synuclein; Alzheimer’s disease; Amyloid-beta; Astroglia; Co-pathology; Dementia with Lewy bodies; Immunohistochemistry; Lewy body disease; Microglia; Neuroinflammation; Phosphorylated-tau; Post-mortem
المشرفين على المادة: 0 (alpha-Synuclein)
0 (tau Proteins)
0 (Antigens, CD)
0 (Amyloid beta-Peptides)
0 (Antigens, Differentiation, Myelomonocytic)
0 (CD68 antigen, human)
0 (CD68 Molecule)
تواريخ الأحداث: Date Created: 20240507 Date Completed: 20240508 Latest Revision: 20240624
رمز التحديث: 20240624
مُعرف محوري في PubMed: PMC11075309
DOI: 10.1186/s40478-024-01786-z
PMID: 38715119
قاعدة البيانات: MEDLINE
الوصف
تدمد:2051-5960
DOI:10.1186/s40478-024-01786-z