ArticleHealth science reports2026
Post-Covid Alzheimer and Its Remediation via PROTACs Therapy: A Comprehensive Review.
Article in Health science reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Sphenoid sinus pneumatization types, extensions and adjacent neurovascular structures: a systematic review with meta-analysis and meta-regression.Anatomical science international · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background 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. Methods: 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. Results: 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. Conclusions: 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.