title: Injection of β-amyloid into the hippocampus induces metabolic disturbances and involuntary weight loss which may be early indicators of Alzheimer's disease.
abstract: BACKGROUND
  Alzheimer's disease (AD) and type 2 diabetes, two diseases that contribute considerable morbidity and mortality in middle-age and elderly people, coexist and progress in parallel, leading to the presumption that one may cause the other. However, a causative link has not yet been established.
  
  
  METHODS
  This study used non-diabetic and diabetic rats injected with β-amyloid (25-35) into the CA1 of the hippocampus to induce AD like plaques as a model of early-stage AD to evaluate the effects of AD on energy metabolism. AD like cognitive dysfunction was confirmed using passive avoidance tests and Morris water maze tests.
  
  
  RESULTS
  Diabetic and non-diabetic rats with experimental AD exhibited memory deficits by β-amyloid (25-35) accumulation in the hippocampus, but diabetes exacerbated memory impairment. All rats, diabetic and non-diabetic, infused with β-amyloid had profound decreases in energy intake, activity and fat oxidation and increased carbohydrate oxidation and energy expenditure. Energy expenditure was increased by 8-10 % and energy intake decreased by approximately 20 % in the rats injected with β-amyloid regardless of diabetic status.
  
  
  CONCLUSIONS
  These results suggest that AD type plaques in the brain may induce metabolic disturbances and cachexia in early AD, which may be an early warning sign of AD in humans.
authors.affiliation: Daily Manufacturing, Inc, Rockwell, NC, USA.
authors.forename: Daily
authors.initials: D
authors.lastname: James
authors.forename: Suna
authors.initials: S
authors.lastname: Kang
authors.forename: Sunmin
authors.initials: S
authors.lastname: Park
mesh_terms: D000544:Alzheimer Disease / Q000139:chemically induced / Q000503:physiopathology*; D016229:Amyloid beta-Peptides / Q000009:adverse effects* / Q000494:pharmacology*; D000818:Animals; D003072:Cognition Disorders / Q000139:chemically induced / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology; D004195:Disease Models, Animal; D002149:Energy Intake / Q000187:drug effects / Q000502:physiology; D004734:Energy Metabolism / Q000187:drug effects* / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects / Q000503:physiopathology*; D008569:Memory Disorders / Q000139:chemically induced / Q000503:physiopathology; D010446:Peptide Fragments / Q000009:adverse effects* / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015431:Weight Loss / Q000187:drug effects* / Q000502:physiology
chemical_list: D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C074636:amyloid beta-protein (25-35)