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Tau-Targeting Nanoparticles for Treatment of Alzheimer's Disease
  • +1
  • Shreya Pawar,
  • MOHDAHMAR RAUF,
  • Arun Iyer,
  • Hosam Abdelhady
Shreya Pawar
Wayne State University School of Medicine
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MOHDAHMAR RAUF
University of Michigan Michigan Medicine
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Arun Iyer

Corresponding Author:[email protected]

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Hosam Abdelhady
Sam Houston State University
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Abstract

Alzheimer’s Disease (AD) is a neurodegenerative disorder that causes loss of neural connections in the cells, and brain tissue volume. The disease first affects the hippocampus and entorhinal complex, which produce memories, then the cerebral cortex, which controls language, logic, and social conduct. Genetic mutations and environmental factors may cause AD, but the exact reason is unknown. AD is diagnosed using CT scans, MRIs, PET scans, and lumbar punctures to detect brain abnormalities, aberrant protein deposits, and cerebrospinal fluid biomarkers. Beta-amyloid plaques and neurofibrillary tau tangles impede neuronal transmission and function in AD. AD also causes chronic inflammation, blood-brain barrier impairment, brain atrophy, and neuronal death. AD has no cure, and current medications mainly manage symptoms and halt cognitive loss. Genetic, cellular, and molecular pathways are being studied to develop targeted medicines to stop disease progression. Extensive studies have shown that tau tangle accumulation and pathogenic changes to tau protein mechanics are correlated with AD pathogenesis. Thus, investigating the potential for therapies focused on restoring normal tau pathways and preventing tau accumulation is critical. Nanoparticulate drug delivery technologies may improve investigational medicines and lead to AD therapy breakthroughs.
20 Sep 2023Submitted to Exploration
27 Sep 2023Submission Checks Completed
27 Sep 2023Assigned to Editor
01 Oct 2023Reviewer(s) Assigned
26 Oct 2023Review(s) Completed, Editorial Evaluation Pending
31 Oct 2023Editorial Decision: Revise Major
16 Nov 20231st Revision Received
22 Nov 2023Submission Checks Completed
22 Nov 2023Assigned to Editor