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• W4310671731 startingPage "795" @default.
• W4310671731 abstract "Down Syndrome (DS), caused by triplication of human chromosome 21 (Hsa21) is the most common form of intellectual disability worldwide. Recent progress in healthcare has resulted in a dramatic increase in the lifespan of individuals with DS. Unfortunately, most will develop Alzheimer's disease like dementia (DS-AD) as they age. Understanding similarities and differences between DS-AD and the other forms of the disease - i.e., late-onset AD (LOAD) and autosomal dominant AD (ADAD) - will provide important clues for the treatment of DS-AD. In addition to the APP gene that codes the precursor of the main component of amyloid plaques found in the brain of AD patients, other genes on Hsa21 are likely to contribute to disease initiation and progression. This review focuses on SYNJ1, coding the phosphoinositide phosphatase synaptojanin 1 (SYNJ1). First, we highlight the function of SYNJ1 in the brain. We then summarize the involvement of SYNJ1 in the different forms of AD at the genetic, transcriptomic, proteomic and neuropathology levels in humans. We further examine whether results in humans correlate with what has been described in murine and cellular models of the disease and report possible mechanistic links between SYNJ1 and the progression of the disease. Finally, we propose a set of questions that would further strengthen and clarify the role of SYNJ1 in the different forms of AD." @default.
• W4310671731 created "2022-12-15" @default.
• W4310671731 creator A5016050187 @default.
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• W4310671731 creator A5048818823 @default.
• W4310671731 creator A5064327348 @default.
• W4310671731 creator A5065916490 @default.
• W4310671731 date "2022-10-01" @default.
• W4310671731 modified "2023-10-15" @default.
• W4310671731 title "Triplication of Synaptojanin 1 in Alzheimer’s Disease Pathology in Down Syndrome" @default.
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