title: Medial temporal lobe atrophy and APOE genotype do not predict cognitive improvement upon treatment with rivastigmine in Alzheimer's disease patients.
abstract: BACKGROUND
  Only a subgroup of subjects with probable AD shows cognitive improvement after treatment with cholinesterase inhibitors.
  
  
  OBJECTIVE
  To investigate whether atrophy of the medial temporal lobe and the apolipoprotein E (APOE) genotype could predict cognitive improvement in subjects with probable AD treated with rivastigmine.
  
  
  METHODS
  121 subjects with mild to moderate probable AD were treated for 26 weeks with escalating doses of rivastigmine. Outcome measures were change on the MMSE and the ADAS-Cog between baseline and follow-up and treatment response defined as at least 2 points improvement on the MMSE or at least 4 points improvement on the ADAS-Cog. The study was an open-label multi-centre study in The Netherlands.
  
  
  RESULTS
  Subjects with medial temporal lobe atrophy (MTLA) tended to show more decline on the MMSE after correction for age, sex, education, baseline cognitive score, and dosage at week 26 compared with subjects without MTLA (p = 0.08). A significant interaction between MTLA and dosage at week 26 existed for change on the MMSE and ADAS-Cog: subjects with MTLA showed more cognitive decline than subjects without MTLA only in the group of patients who received a low dosage at week 26. MTLA was not associated with treatment response. The APOE genotype was not associated with change on the MMSE or ADAS-Cog or with treatment response.
  
  
  CONCLUSIONS
  MTLA and the APOE genotype are not clinically useful predictors of cognitive response in subjects with probable AD who are treated with rivastigmine.
authors.affiliation: Department of Neurology, Alzheimer Centre, VU Medisch Centrum, Amsterdam, The Netherlands. pj.visser@vumc.nl
authors.forename: Pieter Jelle
authors.initials: PJ
authors.lastname: Visser
authors.forename: Philip
authors.initials: P
authors.lastname: Scheltens
authors.forename: Esther
authors.initials: E
authors.lastname: Pelgrim
authors.forename: Frans R J
authors.initials: FR
authors.lastname: Verhey
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000175:diagnosis / Q000188:drug therapy*; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics*; D001284:Atrophy; D002800:Cholinesterase Inhibitors / Q000008:administration & dosage* / Q000009:adverse effects; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D005260:Female; D005500:Follow-Up Studies; D005823:Genetics; D005838:Genotype; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008609:Mental Status Schedule / Q000706:statistics & numerical data; D009426:Netherlands; D018696:Neuroprotective Agents / Q000008:administration & dosage* / Q000009:adverse effects; D048448:Phenylcarbamates / Q000008:administration & dosage* / Q000009:adverse effects; D011379:Prognosis; D011594:Psychometrics / Q000706:statistics & numerical data; D000068836:Rivastigmine; D013702:Temporal Lobe / Q000473:pathology*; D016896:Treatment Outcome
chemical_list: D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D002800:Cholinesterase Inhibitors; D018696:Neuroprotective Agents; D048448:Phenylcarbamates; D000068836:Rivastigmine