Document Detail


Microglia cells are the driving force in fibrillar plaque formation, whereas astrocytes are a leading factor in plague degradation.
MedLine Citation:
PMID:  10985692     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ultrastructural three-dimensional reconstruction of human classical plaques in different stages of development shows that microglial cells are the major factor driving plaque formation by fibrillar amyloid-beta (Abeta) deposition. The amount of fibrillar Abeta released by microglial cells and the area of direct contact between amyloid and neuron determine the extent of dystrophic changes in neuronal processes and synapses. The volume of hypertrophic astrocytic processes separating fibrillar amyloid from neuron is a measure of the protective activation of astrocytes. On the bases of the volume of amyloid star, microglial cells, dystrophic neurites, and hypertrophic astrocytic processes, and spatial relationships between plaque components, three stages in classical plaque development have been distinguished: early, mature, and late. In early plaque, the leading pathology is fibrillar Abeta deposition by microglial cells with amyloid star formation. The mature plaque is characterized by a balance between amyloid production, neuronal dystrophy, and astrocyte hypertrophy. In late classical plaque, microglial cells retract and expose neuropil on direct contact with amyloid star, enhancing both dystrophic changes in neurons and hypertrophic changes in astrocytes. In late plaques, activation of astrocytes predominates. They degrade amyloid star and peripheral amyloid wisps. The effect of these changes is classical plaque degradation to fibrillar primitive and finally to nonfibrillar, diffuse-like plaques.
Authors:
J Wegiel; K C Wang; M Tarnawski; B Lach
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Acta neuropathologica     Volume:  100     ISSN:  0001-6322     ISO Abbreviation:  Acta Neuropathol.     Publication Date:  2000 Oct 
Date Detail:
Created Date:  2000-12-21     Completed Date:  2001-02-01     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0412041     Medline TA:  Acta Neuropathol     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  356-64     Citation Subset:  IM    
Affiliation:
Department of Pathological Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314, USA. J_Wegiel@email.msn.com
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MeSH Terms
Descriptor/Qualifier:
Aged
Alzheimer Disease / pathology*
Amyloid beta-Protein / analysis
Astrocytes / pathology*
Disease Progression
Female
Humans
Hypertrophy
Male
Microglia / pathology*
Neurites / pathology
Neurofibrillary Tangles / pathology*
Senile Plaques / pathology*
Grant Support
ID/Acronym/Agency:
P0Q-HD3897/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Amyloid beta-Protein

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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