ReviewMolecular neurobiology2025
Advancements in Proteolysis Targeting Chimeras for Targeted Therapeutic Strategies in Alzheimer's Disease.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed.
- Reimagining GSK-3β Therapeutics in Alzheimer's Disease: From Inhibition to Activity Normalization and Targeted Degradation.Journal of molecular neuroscience : MN · 2026Review
- Experimental Models and Translational Strategies in Neuroprotective Drug Development with Emphasis on Alzheimer's Disease.Molecules (Basel, Switzerland) · 2026Review
- Antioxidant Natural Compounds Integrated with Targeted Protein Degradation: A Multi-Modal Strategy for Alzheimer's Disease Therapy.Antioxidants (Basel, Switzerland) · 2025Review
- Nanoplatforms Targeting Intrinsically Disordered Protein Aggregation for Translational Neuroscience Applications.Nanomaterials (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The presence of hyperphosphorylated Tau proteins, which mislocalize and form neurofibrillary tangles, and the accumulation of amyloid-β plaques are hallmark features of Alzheimer's disease (AD). These toxic protein aggregates contribute to synaptic impairment and neuronal dysfunction, underscoring the need for strategies aimed at effectively clearing or reducing these aggregates in the treatment of AD. In recent years, proteolysis targeting chimera (PROTAC) technology has emerged as a promising approach for selectively degrading dysfunctional proteins rather than merely inhibiting their function. This approach holds great potential for developing more effective interventions that could slow AD progression and improve patient outcomes. In this review, we first examine the pathological mechanisms underlying AD, focusing on abnormal protein degradation and accumulation. We then explore the evolution of PROTAC technology, its mechanisms of action, and the current status of drug development. Finally, we discuss the latest findings regarding the application of PROTACs in AD therapy, highlighting the potential benefits and limitations of this technology. Although promising, further clinical research is necessary to fully assess the safety and efficacy of PROTAC-based therapies for AD treatment.
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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.