The Use of Dimethyl Biguanide as a Potential Treatment for Alzheimer's Disease in Rats
Hamed A. Abosharaf, Yasmin Elsonbaty, Ehab Tousson, Tarek Mostafa Mohamed
Abstract
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Hamed A. Abosharaf, Yasmin Elsonbaty, Ehab Tousson, Tarek Mostafa Mohamed
Abstract
Open-access reader
Amis: Alzheimer’s disease (AD) is one of the most rapidly growing diseases in recent times. Despite extensive research to find an appropriate medicine, there has been no effective drug until now. Study Design: The present study was designated to investigate the therapeutic impact of antihyperglycemic dimethyl biguanide on Alzheimer’s disease symptoms. Methodology: Alzheimer’s disease was induced in male rats by AlCl3 and D-galactose at doses of 50 and 120 mg/kg daily for one month. Then, for the next four weeks, rats were given oral dimethyl biguanide (200 mg/kg daily). Results: The obtained data indicated an increase in the arrival time of the AD rat group (G2) compared to the control group (G1). In addition, the AD rat group showed an elevation in glucose level, oxidative stress, liver, and kidney function. Importantly, dimethyl biguanide was able to ameliorate these unpleasant outcomes in G3. Interestingly, dimethyl biguanide was able to reduce GFAB immunoreactivity in the dimethyl biguanide -treated group (G3) compared to the AD group (G2). Conclusion: In fact, dimethyl biguanide can delay the symptomatology of AD.
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Amis: Alzheimer’s disease (AD) is one of the most rapidly growing diseases in recent times. Despite extensive research to find an appropriate medicine, there has been no effective drug until now. Study Design: The present study was designated to investigate the therapeutic impact of antihyperglycemic dimethyl biguanide on Alzheimer’s disease symptoms. Methodology: Alzheimer’s disease was induced in male rats by AlCl3 and D-galactose at doses of 50 and 120 mg/kg daily for one month. Then, for the next four weeks, rats were given oral dimethyl biguanide (200 mg/kg daily). Results: The obtained data indicated an increase in the arrival time of the AD rat group (G2) compared to the control group (G1). In addition, the AD rat group showed an elevation in glucose level, oxidative stress, liver, and kidney function. Importantly, dimethyl biguanide was able to ameliorate these unpleasant outcomes in G3. Interestingly, dimethyl biguanide was able to reduce GFAB immunoreactivity in the dimethyl biguanide -treated group (G3) compared to the AD group (G2). Conclusion: In fact, dimethyl biguanide can delay the symptomatology of AD.
Key concepts: Biguanide, Medicine, Disease, Pharmacology, Internal medicine, Metformin, Insulin