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INPP5D/SHIP1: Expression, Regulation and Roles in Alzheimer's Disease Pathophysiology.

Edward O Olufunmilayo1,2, R M Damian Holsinger1,3

  • 1Laboratory of Molecular Neuroscience and Dementia, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2050, Australia.

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|October 28, 2023
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Summary

Genetic variations in the INPP5D gene, which produces the SHIP1 protein in brain immune cells, are linked to increased Alzheimer's disease risk. Targeting INPP5D/SHIP1 may offer new Alzheimer's therapies.

Keywords:
Alzheimer’s disease risk geneSHIP1microgliasingle-nucleotide polymorphism

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Alzheimer's disease (AD) is a leading cause of dementia, disproportionately affecting low- and middle-income countries.
  • Microglial cells, the brain's immune cells, are crucial for neuroprotection and homeostasis.
  • The Src Homology 2 (SH2) domain-containing Inositol 5' Phosphatase 1 (SHIP1) protein, encoded by the INPP5D gene, is expressed in microglia.

Purpose of the Study:

  • To review the current understanding of INPP5D/SHIP1 expression controllers and its role in microglial signaling.
  • To explore the relevance of INPP5D/SHIP1 in Alzheimer's disease pathophysiology.
  • To discuss the therapeutic potential of targeting INPP5D/SHIP1 for AD.

Main Methods:

  • Literature review of studies on INPP5D/SHIP1 in microglia and peripheral immune cells.
  • Analysis of gene-environment interactions and genetic polymorphisms associated with AD.
  • Synthesis of current knowledge on SHIP1's signaling pathways and AD relevance.

Main Results:

  • Polymorphisms in the INPP5D gene are significantly associated with an increased risk of Alzheimer's disease.
  • SHIP1 influences signaling pathways in peripheral immune cells, but its specific roles in microglia and AD are not fully elucidated.
  • Limited knowledge exists regarding the regulation of INPP5D/SHIP1 and its precise impact on microglial function in AD.

Conclusions:

  • INPP5D/SHIP1 represents a potential therapeutic target for Alzheimer's disease.
  • Further research is needed to understand INPP5D/SHIP1 regulation and its specific functions in microglia for AD treatment.
  • Targeting INPP5D/SHIP1 could offer novel therapeutic strategies for Alzheimer's disease.