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This review synthesizes current evidence on COVID-19–AD interactions and evaluates PROTACs as an emerging protein-degradation strategy targeting tau-driven pathology via the ubiquitin–proteasome 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Therapy: A Comprehensive Review  \nTeesta Bhowmick1 | Ritojo Basu1 | Arup Kumar Mitra1  | Sk Asfaque Ali2 | Ajoy Kumer3  | Bikram Dhara4   \n1Post Graduate and Research Department of Microbiology, St. Xavier's College (Autonomous), Kolkata, West Bengal, India | 2Saroj Gupta Cancer Center and Research Institute, Thakurpukur, West Bengal, India | 3Department of Chemistry, IUBAT—International University of Business Agriculture & Technology,  \nDhaka, Bangladesh | 4Center for Global Health Research, Saveetha Institute of Medical and Technical Sciences, Chennai, Tamil Nadu, India Correspondence: Ajoy Kumer ([kumarajoy.cu@gmail.com](kumarajoy.cu@gmail.com)) | Bikram Dhara ([bikramdhara.smc@saveetha.com](bikramdhara.smc@saveetha.com))  \nReceived: 6 June 2025 | Revised: 19 November 2025 | Accepted: 30 November 2025  \nKeywords: Alzheimer's disease | amyloid‐β | COVID‐19 | neurodegeneration | PROTAC | SARS‐CoV‐2 | tau | ubiquitin–proteasome system  \nABSTRACT  \nBackground and Aims: Alzheimer's disease (AD) is a progressive neurodegenerative disorder of aging characterized by memory loss and cognitive decline, associated with amyloid‐β toxicity, tau hyperphosphorylation, and neurofibrillary tangle formation. Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) affects the central nervous system and has been linked to neurological manifestations and accelerated neurodegeneration, including in individuals without pre‐existing AD. Emerging evidence suggests COVID‐19 may increase levels of hyperphosphorylated tau, potentially worsening AD severity. This review synthesizes current knowledge on COVID‐19–AD interactions and evaluates proteolysis‐targeting chimeras (PROTACs) as an emerging therapeutic strategy.  \nMethods: Narrative synthesis of recent literature on SARS‐CoV‐2–related neuropathology, tau pathology in AD, and the design and preclinical development of PROTACs targeting disease‐relevant proteins via the ubiquitin–proteasome system.  \nResults: Reports indicate COVID‐19 can precipitate or exacerbate neurodegenerative processes and is associated with increased tau phosphorylation and other biomarkers of neuronal injury. Conventional AD therapies remain limited in efficacy. PROTACs—heterobifunctional molecules that recruit target proteins to E3 ligases for proteasomal degradation—do not require classical active‐site binding and have demonstrated preclinical potential for degrading pathogenic proteins, supporting their exploration against tau‐driven pathology in AD.  \nConclusions: COVID‐19 may intensify AD pathogenesis through mechanisms that include tau hyperphosphorylation, underscoring the need for targeted interventions. PROTACs offer a mechanistically distinct, protein‐degradation–based approach with promise for modifying tau‐mediated disease; rigorous preclinical and clinical studies are warranted to establish feasibility, safety, and therapeutic impact in AD.  \n1 | Understanding Alzheimer's Disease: An Introduction  \nAlzheimer's is a neurodegenerative disease which leads to decline in learning, memory, behavior, and cognitive functions of the diseased individual. The Hippocampus region within the brain, responsible for maintaining learning and memory, is affected by deposition of β‐amyloid or tangling of neurofibrils  \n[1] . Symptoms of Alzheimer's disease generally appear in patients who are more than 60 years old. Figure 1 depicts how the brain of a diseased person differs from that of a non‐diseased person. There is marked shrinkage in the areas that involve learning, memory and other cognitive functions.  \nEarlier therapies for Alzheimer's disease were targeted towards β‐amyloid. These included βγ secretase inhibitors which  \nThis is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is pro","cbCaid57VAJgXWIr","https://ap.wps.com/l/cbCaid57VAJgXWIr","pdf",2514147,"English","# Understanding Alzheimer's Disease: An Introduction\n# COVID-19 and Alzheimer’s Disease Interactions\n# PROTACs-Based Remediation Approach","[{\"question\":\"What mechanisms link COVID-19 to worsened Alzheimer’s disease pathology?\",\"answer\":\"COVID-19 can precipitate or exacerbate neurodegenerative processes and is associated with increased tau phosphorylation and neuronal injury biomarkers.\"},{\"question\":\"Why are conventional Alzheimer’s therapies considered limited?\",\"answer\":\"Conventional therapies show limited efficacy, partly because they do not adequately modify disease-relevant pathogenic processes.\"},{\"question\":\"How do PROTACs potentially remediate Alzheimer’s disease?\",\"answer\":\"PROTACs recruit target proteins to E3 ligases for proteasomal degradation and do not rely on classical active-site binding, showing preclinical potential for degrading pathogenic proteins such as tau.\"}]","Post-Covid Alzheimer and Its Remediation via PROTACs Therapy - A Comprehensive Review | PDF",1790565927,28]