title: Apolipoprotein E in cerebrospinal fluid in 85-year-old subjects. Relation to dementia, apolipoprotein E polymorphism, cerebral atrophy, and white matter lesions.
abstract: OBJECTIVE
  To further elucidate the pathogenetic role of apolipoprotein E (Apo E) in degenerative brain disorders, we analyzed cerebrospinal fluid (CSF) levels of Apo E in 85-year-old subjects with dementia disorders.
  
  
  METHODS
  Survey.
  
  
  METHODS
  Community.
  
  
  METHODS
  Population-based sample of 27 demented (12 with Alzheimer disease [AD]; 13, vascular dementia [VAD]; and 2, other types of dementia) and 35 nondemented individuals.
  
  
  METHODS
  Cerebrospinal fluid levels of Apo E, Apo E polymorphism, and brain atrophy and white matter lesions (WMLs) measured by computed tomography (CT) of the brain. Dementia was defined according to Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised criteria; AD, National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association criteria; and VAD, National Institute of Neurological Disorders and Stroke and the Association Internationale pour la Recherche et l'Enseignement en Neuroscience criteria.
  
  
  RESULTS
  The mean (+/- SD) CSF levels of Apo E were lower in the AD (2.6 +/- 1.5 mg/L; P < .02) and VAD groups (2.5 +/- 0.9 mg/L; P < .002) than in the nondemented group (3.8 +/- 1.7 mg/L). Cerebrospinal fluid levels of Apo E decreased with increasing severity of dementia and with increasing temporal cortical and central frontal atrophy. In nondemented individuals, CSF levels of Apo E decreased with increasing degree of WMLs. Cerebrospinal fluid levels of Apo E were not influenced by the Apo E4 isoform.
  
  
  CONCLUSIONS
  Whether our finding of an association between low CSF levels of Apo E and dementia disorders (both degenerative, such as AD, and vascular, such as VAD) is related to the pathogenesis of these disorders or is a secondary consequence of the disease process remains to be established. Although statistical correlations do not give direct evidence of causal relations, the correlations between CSF level of Apo E and severity of dementia and cortical atrophy suggest that CSF level of Apo E follows the disease process.
authors.affiliation: Department of Psychiatry, Sahlgrenska Hospital, Göteborg, Sweden.
authors.forename: I
authors.initials: I
authors.lastname: Skoog
authors.forename: C
authors.initials: C
authors.lastname: Hesse
authors.forename: P
authors.initials: P
authors.lastname: Fredman
authors.forename: L A
authors.initials: LA
authors.lastname: Andreasson
authors.forename: B
authors.initials: B
authors.lastname: Palmertz
authors.forename: K
authors.initials: K
authors.lastname: Blennow
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000134:cerebrospinal fluid* / Q000235:genetics; D001057:Apolipoproteins E / Q000134:cerebrospinal fluid* / Q000235:genetics; D001284:Atrophy; D001921:Brain / Q000473:pathology; D001927:Brain Diseases / Q000134:cerebrospinal fluid / Q000473:pathology; D003704:Dementia / Q000134:cerebrospinal fluid* / Q000235:genetics; D006801:Humans; D011110:Polymorphism, Genetic
chemical_list: D001057:Apolipoproteins E