Model
Digital Document
Publisher
Florida Atlantic University
Description
This research investigated the relationship between exercise training and
cathepsin B expression in the 3xTg-AD murine model of Alzheimer’s disease. 3xTg-AD
mice were assigned to control (Tg, n=10), aerobic training (Tg+AT, n=10), or resistance
training (Tg+RT, n=10). RotaRod peak latency and grip strength were assessed as preand
post-measurements. Skeletal muscle was collected after training and analyzed for
cathepsin B protein. Tg+RT showed greater grip strength than Tg and Tg+AT at posttesting
(p ≤ 0.05). Only Tg+AT showed an improvement in RotaRod peak latency (p ≤
0.05). Gastrocnemius weight was greater in Tg+RT compared to Tg (p ≤ 0.05), and no
differences were observed in cathepsin B or procathepsin B expression (p > 0.05). This
data suggests that cathepsin B was not induced by either mode of exercise training,
however, physical function and muscle mass were improved, therefore inclusion of both
training modalities may address peripheral comorbidities in Alzheimer’s disease.
cathepsin B expression in the 3xTg-AD murine model of Alzheimer’s disease. 3xTg-AD
mice were assigned to control (Tg, n=10), aerobic training (Tg+AT, n=10), or resistance
training (Tg+RT, n=10). RotaRod peak latency and grip strength were assessed as preand
post-measurements. Skeletal muscle was collected after training and analyzed for
cathepsin B protein. Tg+RT showed greater grip strength than Tg and Tg+AT at posttesting
(p ≤ 0.05). Only Tg+AT showed an improvement in RotaRod peak latency (p ≤
0.05). Gastrocnemius weight was greater in Tg+RT compared to Tg (p ≤ 0.05), and no
differences were observed in cathepsin B or procathepsin B expression (p > 0.05). This
data suggests that cathepsin B was not induced by either mode of exercise training,
however, physical function and muscle mass were improved, therefore inclusion of both
training modalities may address peripheral comorbidities in Alzheimer’s disease.
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