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Updated: Jan 7, 2026

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Basic Science and Pathogenesis.

Aryan Malik1

  • 1MMCP, Ambala, Haryana, India.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease involves uncontrolled neuronal cell death and neuroinflammation, impacting memory impairments. Understanding these mechanisms is key to developing new dementia treatments beyond symptom management.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Alzheimer's disease (AD) is a major cause of dementia and a global health concern.
  • The exact causes of AD remain largely unknown.
  • AD is characterized by progressive neurodegeneration and cognitive decline.

Purpose of the Study:

  • To review the molecular mechanisms driving Alzheimer's disease progression.
  • To explore the roles of specific pathways like RIPK/MLKL, autophagy, necroptosis, and neuroinflammation in AD.
  • To highlight the need for novel therapeutic strategies targeting disease modification.

Main Methods:

  • Literature review of molecular mechanisms in AD.
  • Analysis of the RIPK/MLKL axis, autophagy, and necroptosis.

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  • Examination of neuroinflammation and associated signaling pathways (NFκB, p38 MAPK).

    • Main Results:

    • Uncontrolled neuronal cell death contributes to synaptic dysfunction and AD progression.
    • The RIPK/MLKL axis, autophagy, and necroptosis are critical in AD pathogenesis.
    • Neuroinflammation, driven by pro-inflammatory cytokines, exacerbates AD via pathways like NFκB and p38 MAPK.

    Conclusions:

    • Understanding the interplay of these molecular pathways is vital for effective AD therapeutics.
    • Current AD treatments primarily manage symptoms.
    • Novel therapeutic approaches are urgently needed to modify AD progression.