Aging clinical and experimental research · 2014
Injection of β-amyloid into the hippocampus induces metabolic disturbances and involuntary weight loss which may be early indicators of Alzheimer's disease.
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James Daily, Kang Suna, Park Sunmin
Аннотация
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.
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.