Erlotinib as a Potential Therapeutic Agent for Alzheimer’s Disease: A Review of its Mechanism of action and Preclinical evidence

Authors

  • Jyoti Chauhan Assistant Professor, Himalayan Institute of Pharmacy, Kala Amb-173030, Himachal Pradesh, India
  • Gourav Thakur Himalayan Institute of Pharmacy, Kala Amb-173030, Himachal Pradesh, India
  • Manish Kumar Himalayan Institute of Pharmacy, Kala Amb-173030, Himachal Pradesh, India
  • Amardeep Kaur Himalayan Institute of Pharmacy, Kala Amb-173030, Himachal Pradesh, India
  • Swati Kaushal Himalayan Institute of Pharmacy, Kala Amb-173030, Himachal Pradesh, India
  • Khushboo Kishore Himalayan Institute of Pharmacy, Kala Amb-173030, Himachal Pradesh, India
  • RB Sharma Himalayan Institute of Pharmacy, Kala Amb-173030, Himachal Pradesh, India

Keywords:

Alzheimer's disease, Erlotinib, EGFR signaling, Beta-amyloid, Tau protein, Neurodegeneration, Tyrosine kinase inhibitor, Neuroprotection.

Abstract

Beta-amyloid peptide buildup and hyperphosphorylated tau protein are two hallmarks of Alzheimer's disease (AD), a complex and multifaceted neurodegenerative illness. Although our understanding of the molecular pathways behind AD has advanced significantly, effective treatment approaches are still elusive. Tyrosine kinase inhibitor erlotinib has demonstrated promise as a possible treatment for AD in preclinical research. This study offers a thorough analysis of the current understanding of erlotinib's mode of action in modifying EGFR signaling, as well as its impacts on tau protein phosphorylation and beta-amyloid formation. Along with its possible neuroprotective benefits, we also go over the preclinical and clinical data that support the use of erlotinib in AD. Erlotinib may be a viable treatment for AD, according to our study, and it merits more clinical research. We also point out that more research is necessary to completely understand the processes by which Erlotinib affects AD pathology and to ascertain whether it has the potential to be used as a treatment for this debilitating illness.

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Published

2025-05-08

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