In a long-term longitudinal study of aging in rhesus monkeys, a primary objective has been to determine the effects of aging and caloric restriction (CR) on behavioral and neural parameters. Through the use of automated devices, locomotor activity can be monitored in the home cages of the monkeys. Studies completed thus far indicate a clear age-related decline in activity consistent with such observations in many other species, including humans. However, no consistent effects of CR on activity have been observed.
By applying calorie restriction (CR) at 30-50% below ad libitum levels, studies in numerous species have reported increased life span, reduced incidence and delayed onset of age-related diseases, improved stress resistance, and decelerated functional decline. Whether this nutritional intervention is relevant to human aging remains to be determined; however, evidence emerging from CR studies in nonhuman primates suggests that response to CR in primates parallels that observed in rodents. To evaluate CR effects in humans, clinical trials have been initiated.
Across phyla, aging is associated with reduced sleep duration and efficiency. Both aging and sleep involve complex genetic architecture and diverse cell types and are heavily influenced by diet and environment. Therefore, understanding the molecular mechanisms of age-dependent changes in sleep will require integrative approaches that go beyond examining these two processes independently. The fruit fly, Drosophila melanogaster, provides a genetically amenable system for dissecting the molecular basis of these processes.
Developments in molecular biology over the past three decades have led to an increasing awareness of the importance of epigenetic phenomena in a variety of genome functions. Epigenetic aspects of complex multifactorial diseases including schizophrenia, however, have not been investigated sufficiently. Various facets of epigenetics are reevaluated through their putative relevance to four theories of schizophrenia: neurodevelopmental, dopamine dysfunction, viral, and genetic anticipation with unstable DNA.
American Journal of Pharmacogenomics: Genomics-Related Research in Drug Development and Clinical Practice
No specific gene has been identified for any major psychiatric disorder, including schizophrenia, in spite of strong evidence supporting a genetic basis for these complex and devastating disorders. There are several likely reasons for this failure, ranging from poor study design with low statistical power to genetic mechanisms such as polygenic inheritance, epigenetic interactions, and pleiotropy. Most study designs currently in use are inadequate to uncover these mechanisms.
Addiction research focusing on homocysteine metabolism and its association with aspects of alcohol dependence has revealed important findings. Recent literature on this topic has been taken into account for the review provided. Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme in the homocysteine metabolism. Plasma homocysteine levels are influenced by the single-nucleotide polymorphism (SNP) MTHFR C677T. Besides genetic factors, environmental factors have an impact on homocysteine plasma levels too.
Although there is evidence to link schizophrenia (SCZ) and bipolar disorder (BD) to genetic and environmental factors, specific individual or groups of genes/factors causative of the disease have been elusive to the research community. An understanding of the molecular aberrations that cause these mental illnesses requires comprehensive approaches that examine both genetic and epigenetic factors.
Impairment of oligodendroglia (OL)-dependent myelination in the central nervous system (CNS) is a remarkable parallel recently identified in major psychiatric disorders and chronic drug abuse. Neuroimaging and neuropathological studies revealed myelin defects and microarray-profiling analysis demonstrated aberrant expression of myelin-related genes in schizophrenia (SZ), bipolar disorder (BD), major depressive disorder (MDD) and cocaine addiction. However, the etiology underlying myelin impairment in these clinically distinct subjects remains elusive.
OBJECTIVE: The pathophysiology of eating disorders such as anorexia nervosa (AN) and bulimia nervosa (BN) has been linked to an impaired dopaminergic neurotransmission, still the origin of this disturbance remains unknown. The aim of the present study was, therefore, to evaluate whether the expression of dopaminergic genes is altered in the blood of patients suffering from eating disorders and if these alterations can be explained by changes in the promoter specific DNA methylation of the genes.