Genes, Vol. 14, Pages 1845: INPP5D/SHIP1: Expression, Regulation and Roles in Alzheimer & rsquo;s Disease Pathophysiology

Genes, Vol. 14, Pages 1845: INPP5D/SHIP1: Expression, Regulation and Roles in Alzheimer’s Disease Pathophysiology Genes doi: 10.3390/genes14101845 Authors: Edward O. Olufunmilayo R. M. Damian Holsinger Alzheimer’s disease (AD) is the most common form of dementia, accounting for approximately 38.5 million cases of all-cause dementia. Over 60% of these individuals live in low- and middle-income countries and are the worst affected, especially by its deleterious effects on the productivity of both patients and caregivers. Numerous risk factors for the disease have been identified and our understanding of gene–environment interactions have shed light on several gene variants that contribute to the most common, sporadic form of AD. Microglial cells, the innate immune cells of the central nervous system (CNS), have long been established as guardians of the brain by providing neuroprotection and maintaining cellular homeostasis. A protein with a myriad of effects on various important signaling pathways that is expressed in microglia is the Src Homology 2 (SH2) domain-containing Inositol 5′ Phosphatase 1 (SHIP1) protein. Encoded by the INPP5D (Inositol Polyphosphate-5-Phosphatase D) gene, SHIP1 has diminutive effects on most microglia signaling processes. Polymorphisms of the INPP5D gene have been found to be associated with a significantly increased risk of AD. Several studies have elucidated mechanistic processes by whic...
Source: Genes - Category: Genetics & Stem Cells Authors: Tags: Review Source Type: research