title: Statins, incident Alzheimer disease, change in cognitive function, and neuropathology.
abstract: OBJECTIVE
  To examine the relation of statins to incident Alzheimer disease (AD) and change in cognition and neuropathology.
  
  
  METHODS
  Participants were 929 older Catholic clergy (68.7% women, mean baseline age 74.9 years, education 18.2 years, Mini-Mental State Examination 28.5) free of dementia, enrolled in the Religious Orders Study, a longitudinal clinical-pathologic study of AD. All agreed to brain autopsy at time of death and underwent annual structured clinical evaluations, allowing for classification of AD and assessment of cognition (based on 19 neuropsychological tests). Statins were identified by direct medication inspection. Neuropathologic data were available on 262 participants. All macroscopic chronic cerebral infarctions were recorded. A measure of global AD pathology was derived from silver stain, and separate measures of amyloid and tangles were based on immunohistochemistry. We examined the relation of statins to incident AD using Cox proportional hazards, change in cognition using mixed effects models, and pathologic indices using logistic and linear regression.
  
  
  RESULTS
  Statin use at baseline (12.8%) was not associated with incident AD (191 persons, up to 12 follow-up years), change in global cognition, or five separate cognitive domains (all p values > 0.20). Statin use any time prior to death (17.9%) was not related to global AD pathology. Persons taking statins were less likely to have amyloid (p = 0.02). However, among those with amyloid, there was no relation of statins to amyloid load. Statins were not related to tangles or infarction.
  
  
  CONCLUSIONS
  Overall, statins were not related to incident Alzheimer disease (AD) or change in cognition, or continuous measures of AD pathology or infarction.
authors.affiliation: Rush Alzheimer's Disease Center, Department of Neurological Sciences, 600 S. Paulina, Suite 1020, Rush University Medical Center, Chicago, IL 60612, USA.
authors.forename: Z
authors.initials: Z
authors.lastname: Arvanitakis
authors.forename: J A
authors.initials: JA
authors.lastname: Schneider
authors.forename: R S
authors.initials: RS
authors.lastname: Wilson
authors.forename: J L
authors.initials: JL
authors.lastname: Bienias
authors.forename: J F
authors.initials: JF
authors.lastname: Kelly
authors.forename: D A
authors.initials: DA
authors.lastname: Evans
authors.forename: D A
authors.initials: DA
authors.lastname: Bennett
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000188:drug therapy* / Q000453:epidemiology / Q000517:prevention & control; D001921:Brain / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D003072:Cognition Disorders / Q000188:drug therapy* / Q000453:epidemiology / Q000517:prevention & control; D015331:Cohort Studies; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000188:drug therapy; D015994:Incidence; D020300:Intracranial Hemorrhages / Q000139:chemically induced; D008137:Longitudinal Studies; D008297:Male; D018696:Neuroprotective Agents / Q000009:adverse effects / Q000627:therapeutic use; D058225:Plaque, Amyloid / Q000187:drug effects / Q000378:metabolism / Q000473:pathology
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018696:Neuroprotective Agents