The Alzheimer disease is a age related neurodegenerative disease. The factors causing alzheimer disease are numerous. Research on humans and rodent models predicted various causative factors involved in Alzheimer disease progression. Among them, neuroinflammation, oxidative stress and apoptosis play a major role because of accumulation of extracellular amyloid beta peptides. Here, the clearance of amyloid beta peptide plays a major role because of the imbalance in the
production and clearance of the amyloid beta peptide. Additionally, neuroinflammation by microglia, astrocytes, cytokines,
chemokines and the complement system also have a major role in Alzheimer disease. The physiological clearance pathways
involved in amyloid beta peptide are glymphatic, vascular and immune pathways. Amyloid precursor protein, low density
lipoprotein receptor-related protein 1, receptor for advanced glycation end product, apolipoprotein E, clusterin, aquaporin 4,
auto-antibodies, complement system, cytokines and microglia are involved in amyloid beta peptide clearance pathways across
the blood brain barrier. The plaque formation in the brain by alternative splicing of amyloid precursor protein and production
of misfolded protein results in amyloid beta agglomeration. This insoluble amyloid beta leads to neurodegenerative cascade
and neuronal cell death occurs. Studies had shown disturbed sleep may be a risk factor for dementia and cognitive decline. In
this review, the therapeutic targets for alzheimer disease via focussing on pathways for amyloid beta clearance are discussed.
Syntaxin 5 interacts with presenilin holoproteins, but not with their N- or C-terminal fragments, and affects β-amyloid peptide production
