title: 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 beta-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 beta-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.
authors.affiliation: Center for Brain Research, Medical University of Vienna, Austria.
authors.forename: Assunta
authors.initials: A
authors.lastname: Dal Bianco
authors.forename: Monika
authors.initials: M
authors.lastname: Bradl
authors.forename: Josa
authors.initials: J
authors.lastname: Frischer
authors.forename: Alexandra
authors.initials: A
authors.lastname: Kutzelnigg
authors.forename: Kurt
authors.initials: K
authors.lastname: Jellinger
authors.forename: Hans
authors.initials: H
authors.lastname: Lassmann
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000453:epidemiology / Q000276:immunology / Q000473:pathology*; D015415:Biomarkers / Q000032:analysis; D001921:Brain / Q000473:pathology*; D002536:Cerebral Arteries / Q000473:pathology; D002634:Chemotaxis, Leukocyte / Q000276:immunology; D015897:Comorbidity; D018450:Disease Progression; D004660:Encephalitis / Q000453:epidemiology / Q000276:immunology / Q000473:pathology*; D005260:Female; D005911:Gliosis / Q000453:epidemiology / Q000276:immunology / Q000473:pathology; D006801:Humans; D008297:Male; D008578:Meninges / Q000473:pathology; D017628:Microglia / Q000473:pathology; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000453:epidemiology / Q000276:immunology / Q000473:pathology*; D009186:Myelin Sheath / Q000473:pathology; D016874:Neurofibrillary Tangles / Q000473:pathology; D058225:Plaque, Amyloid / Q000473:pathology
chemical_list: D015415:Biomarkers