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Molecular Targets in Alzheimer’s Disease: From Mechanisms to Therapeutic Strategies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 September 2026 | Viewed by 1174

Special Issue Editor


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Guest Editor
Department of Neurology, Henry Ford Health System, Detroit, MI 48202, USA
Interests: Alzheimer’s disease; cerebral stroke; neuroprotection

Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, characterized by loss of memory and cognition. Understanding, the molecular mechanism underlying the progression of AD is essential to understanding the potential cause of disease. Investigating this mechanism can provide valuable insight into the development of targeted therapeutic strategy.

Aim: 1) To explain molecular mechanism behind Aβ deposition and Tau phosphorylation; 2) To study the potential role of inflammation in progression of AD pathology; 3) To identify early biomarkers for the diagnosis of AD.

Potential topic:

  • The role of Amyloid-beta and Tau Interactions in AD associated neurodegeneration.
  • Microglial in Alzheimer’s disease and its role in neuroinflammation.
  • Mitochondrial fission and fusion in Alzheimer’s disease.
  • Role of inflammation in early and late onset of Alzheimer’s disease and therapeutic implication.
  • Neurovascular dysfunction and amyloid angiopathy in Alzheimer’s disease.

Dr. Mohammad Ejaz Ahmed
Guest Editor

Manuscript Submission Information

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Keywords

  • amyloid beta
  • neurodegeneration
  • neuroinflammation
  • microglia
  • mitochondrial dysfucntion
  • oxidative stress
  • molecular pathway
  • biomarkers of AD

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Published Papers (1 paper)

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Review

21 pages, 1000 KB  
Review
Taurine as an Early-Phase Disease-Modifying Candidate for Alzheimer’s Disease
by Muhammad Kamal Hossain and Hyung-Ryong Kim
Int. J. Mol. Sci. 2026, 27(4), 1871; https://doi.org/10.3390/ijms27041871 - 15 Feb 2026
Viewed by 745
Abstract
Alzheimer’s disease is driven by converging pathological processes, including amyloid-β accumulation, tau dysfunction, synaptic failure, and chronic neuroinflammation, which emerge decades before clinical onset. Growing evidence supports the concept that early, upstream neuroprotective interventions may meaningfully alter disease trajectory in both sporadic and [...] Read more.
Alzheimer’s disease is driven by converging pathological processes, including amyloid-β accumulation, tau dysfunction, synaptic failure, and chronic neuroinflammation, which emerge decades before clinical onset. Growing evidence supports the concept that early, upstream neuroprotective interventions may meaningfully alter disease trajectory in both sporadic and familial AD. Taurine, an endogenously abundant and clinically safe neuromodulator, has re-emerged as a promising multi-target regulator of AD-relevant pathways. Accumulating mechanistic data indicate that taurine modulates Aβ aggregation, attenuates oxidative and endoplasmic reticulum stress, preserves mitochondrial homeostasis, suppresses neuroinflammatory signaling, and stabilizes synaptic function, positioning it as a promising upstream intervention strategy in AD. This review synthesizes current evidence supporting taurine’s pleiotropic neuroprotective actions and discusses its translational potential as an early-stage, low-risk intervention to delay or prevent AD progression. Full article
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