神经退行性变
胰岛素
疾病
血脂异常
糖尿病
胰岛素受体
神经科学
β淀粉样蛋白
炎症
生物信息学
内科学
医学
胰岛素抵抗
生物
内分泌学
作者
Mayur B. Kale,Harshavardhan M Bhondge,Nitu L. Wankhede,Prajwali V Shende,Rushikesh P Thanekaer,Manish M. Aglawe,Sandip R. Rahangdale,Brijesh G. Taksande,Sunil Pandit,Aman B. Upaganlawar,Milind J. Umekar,Spandana Rajendra Kopalli,Sushruta Koppula
标识
DOI:10.1016/j.arr.2024.102415
摘要
Alzheimer's disease (AD) and Diabetes mellitus (DM) exhibit comparable pathophysiological pathways. Genetic abnormalities in APP, PS-1, and PS-2 are linked to AD, with diagnostic aid from CSF and blood biomarkers. Insulin dysfunction, termed "type 3 diabetes mellitus" in AD, involves altered insulin signalling and neuronal shrinkage. Insulin influences beta-amyloid metabolism, exacerbating neurotoxicity in AD and amyloid production in DM. Both disorders display impaired glucose transporter expression, hastening cognitive decline. Mitochondrial dysfunction and Toll-like receptor 4-mediated inflammation worsen neurodegeneration in both diseases. ApoE4 raises disease risk, especially when coupled with dyslipidemia common in DM. Targeting shared pathways like insulin-degrading enzyme activation and HSP60 holds promise for therapeutic intervention. Recognizing these interconnected mechanisms underscores the imperative for developing tailored treatments addressing the overlapping pathophysiology of AD and DM, offering potential avenues for more effective management of both conditions.
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