No abstract

Alzheimer’s disease (AD) is the most common reason for progressive dementia in the elderly. It has been shown that disorders of the mammalian/mechanistic target of rapamycin (mTOR) signaling pathways are related to the AD. On the other hand, diabetes mellitus (DM) is a risk factor for the cognitive dysfunction. The pathogenesis of the neuronal impairment caused by diabetic hyperglycemia is intricate, which contains neuro-inflammation and/or neurodegeneration and dementia. Glucagon-like peptide-1 (GLP1) is interesting as a possible link between metabolism and brain impairment. Modulation of GLP1 activity can influence amyloid-beta peptide aggregation via the phosphoinositide-3 kinase/AKT/mTOR signaling pathway in AD. The GLP1 receptor agonists have been shown to have favorable actions on the brain such as the improvement of neurological deficit. They might also exert a beneficial effect with refining learning and memory on the cognitive impairment induced by diabetes. Recent experimental and clinical evidence indicates that dipeptidyl-peptidase-4 (DPP4) inhibitors, being currently used for DM therapy, may also be effective for AD treatment. The DPP-4 inhibitors have demonstrated neuroprotection and cognitive improvements in animal models. Although further studies for mTOR, GLP1, and DPP4 signaling pathways in humans would be intensively required, they seem to be a promising approach for innovative AD-treatments. We would like to review the characteristics of AD pathogenesis, the key roles of mTOR in AD and the preventive and/ or therapeutic suggestions of directing the mTOR signaling pathway.

<abstract> <p>Psychiatric disorders may extremely impair the quality of life with patients and are important reasons of social disability. Several data have shown that psychiatric disorders are associated with an altered composition of gut microbiota. Dietary intake could determine the microbiota, which contribute to produce various metabolites of fermentation such as short chain fatty acids. Some of the metabolites could result in epigenetic alterations leading to the disease susceptibility. Epigenetic dysfunction is in fact implicated in various psychiatric and neurologic disorders. For example, it has been shown that neuroepigenetic dysregulation occurs in psychiatric disorders including schizophrenia. Several studies have demonstrated that the intestinal microbiome may influence the function of central nervous system. Furthermore, it has been proved that the alterations in the gut microbiota-composition might affect in the bidirectional communication between gut and brain. Similarly, evidences demonstrating the association between psychiatric disorders and the gut microbiota have come from preclinical studies. It is clear that an intricate symbiotic relationship might exist between host and microbe, although the practical significance of the gut microbiota has not yet to be determined. In this review, we have summarized the function of gut microbiota in main psychiatric disorders with respect to the mental health. In addition, we would like to discuss the potential mechanisms of the disorders for the practical diagnosis and future treatment by using bioengineering of microbiota and their metabolites.</p> </abstract>