Purposed potential Alzheimer’s Disease treatment based on the results from current primary research models

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Alzheimer’s Disease is one of the most known neurodegenerative diseases that causes over 100,000 deaths till now. The pathology of Alzheimer’s Disease is still not fully clear, but the most widely accepted pathology is the chronic endoplasmic reticulum (ER) stress caused by neurotoxicity via amyloid beta (Aß) plaques and intracellular tau tangles. In Alzheimer's patients, the abnormal Aß plaques and tau tangles cause oxidative stress and induce chronic ER stress, which can hardly be relieved by the normal UPR pathway. One potential treatment for rescuing the excessive ER stress caused by Aß accumulation in human neural cells is the Salubrinal (Sal) treatment. Amentoflavone (AF) treatment is a plausible treatment to alleviate cell death stress due to pyroptosis in Alzheimer's patients. Latrepirdine (LAT) is a treatment that can induce autophagy with the help of ATG5. Mitophagy is a special form of autophagy that degrades dysfunctional mitochondria and does not function well in Alzheimer's patients. Treatment like NMN, UA, and AC can effectively induce mitophagy, decrease memory loss, and relieve common Alzheimer’s pathology like Aß plaques and tau tangles. In this review, the primary research on four key mechanisms in Alzheimer's etiology - UPR pathway(apoptosis), pyroptosis, autophagy and mitophagy - will be discussed and some potential treatments targeting these four mechanisms will be briefly introduced with the primary research results.