Retinoids as Potential Therapeutic Approach in Prevention of Alzheimer's Disease

Studies revealed that neuroinflammation is main factor in Alzheimer's disease pathogenesis (AD). Synaptic dysfunction and neuronal death are caused by neuroinflammation. Proinflammatory mediators over expression directed nerve cells to Aβ peptide synthesis, hyper phosphorylated tau protein and up regulated inflammatory metabolites and cytokines. These inflammatory factors interrupt blood-brain barrier integrity and provide Aβ42 oligomers fabrication. Retinoids and carotenoids are effective antioxidants and anti-inflammatory mediators having neuroprotective effects. They suppress cognitive performance imperfection via several mechanisms such as repression of Aβ peptide synthesis, oxidative stress, and pro-inflammatory mediator’s. Retinoids, have significant consequences on central nervous system (CNS) development. Through this review we consider retinoids biology, underlining on their neuroprotective mechanisms that will beneficial to clarify their effect in AD pathology. Consequently, Retinoids is considered as a potent approach for AD prevention. Keywords: Retinoids; Central nervous system; Alzheimer's disease; Amyloid beta; Retinolbinding proteins; Cytosolic retinol-binding proteins. Abbreviations: AD: Alzheimer's Disease; ATRA: All-trans Retinoic Acid; RBP: RetinolBinding Proteins; Aβ: Amyloid Beta; CNS: Central Nervous System; RA: Retinoic Acid; LTP/ LTD: Long-Term Potentiation/Depression; IL-6: Interleukin; ChAT: Choline Acetyltransferase; SOD: Superoxide Dismutase; NF-Κb: Signaling Pathway In Inflammation; CRABP1: Cytosolic Retinol-Binding Proteins 1; RXR: Retinoid X Receptor; CRABP2: Cytosolic Retinol-Binding Proteins Cytosolic 2; Fos: Proto-Oncogene; LXRs: Liver X Receptors; PPARs: Peroxisome Proliferator-Activated Receptors; OGD: Oxygen Glucose Deprivation; PC12: Model for Neural Differentiation.