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https://www.selleckchem.com/mTOR.html We discuss the cellular control of protein palmitoylation and depalmitoylation, the relationship between lipid microdomains and lipidated and phospholipid binding proteins, and highlight the important unanswered questions in this emerging field.Despite fundamental differences in disease course and outcomes, neurodevelopmental (autism spectrum disorders - ASD) and neurodegenerative disorders (Alzheimer's disease - AD and Parkinson's disease - PD) present surprising, common traits in their molecular pathomechanisms. Uncontrolled oligomerization and aggregation of amyloid β (Aβ), microtubule-associated protein (MAP) tau, or α-synuclein (α-syn) contribute to synaptic impairment and the ensuing neuronal death in both AD and PD. Likewise, the pathogenesis of ASD may be attributed, at least in part, to synaptic dysfunction; attention has also been recently paid to irregularities in the metabolism and function of the Aβ precursor protein (APP), tau, or α-syn. Commonly affected elements include signaling pathways that regulate cellular metabolism and survival such as insulin/insulin-like growth factor (IGF) - PI3 kinase - Akt - mammalian target of rapamycin (mTOR), and a number of key synaptic proteins critically involved in neuronal communication. Understanding how these shared pathomechanism elements operate in different conditions may help identify common targets and therapeutic approaches.Despite the prevalence of neuroinflammation in psychiatric disorders, molecular mechanism underlying it remains elusive. Translocator protein 18 kDa (TSPO), also known as peripheral benzodiazepine receptor, is a mitochondrial protein implicated in the synthesis of steroids in a variety of tissues. Multiple reports have shown increased expression of TSPO in the activated microglia in the CNS. Radioactive probes targeting TSPO have been developed and used for imaging assessment in neurological and psychiatric disorders to examine neuroinflammation. Re

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