No abstract

Caffeine is the most widely used psychotropic drug in the world. Most of the caffeine consumed comes from coffee bean (i.e., a misnomer for the seed of Coffea plants), beverages (i.e., coffee, tea, soft drinks), in products containing cocoa or chocolate and in medications (i.e., analgesics, stimulants, weight-loss products, sports nutrition). The most prominent behavioral effects of caffeine take place over low to moderate doses are amplified alertness and attention. Moderate caffeine consumption leads very rarely to health risks.

No abstract

No abstract

No abstract

: Alzheimer’s disease (AD) is the most common form of dementia in the elderly and this complex disorder is associated with environmental as well as genetic components. Early-onset AD (EOAD) and late-onset AD (LOAD, more common) are major identified types of AD. The genetics of EOAD is extensively understood with three genes variants such as APP, PSEN1, and PSEN2 leading to disease. On the other hand, some common alleles including APOE are effectively associated with LOAD identified but the genetics of LOAD is not clear to date. It has been accounted that about 5% to 10% of EOAD patients can be explained through mutations in the three familiar genes of EOAD. The APOE ε4 allele augmented the severity of EOAD risk in carriers, and APOE ε4 allele was considered as a hallmark of EOAD. A great number of EOAD patients, who are not genetically explained, indicate that it is not possible to identify disease- triggering genes yet. Although several genes have been identified through using the technology of next-generation sequencing in EOAD families including SORL1, TYROBP, and NOTCH3. A number of TYROBP variants were identified through exome sequencing in EOAD patients and these TYROBP variants may increase the pathogenesis of EOAD. The existence of ε4 allele is responsible for increasing the severity of EOAD. However, several ε4 allele carriers live into their 90s that propose the presence of other LOAD genetic as well as environmental risk factors that are not identified yet. It is urgent to find out missing genetics of EOAD and LOAD etiology to discover new potential genetics facets which will assist to understand the pathological mechanism of AD. These investigations should contribute to developing a new therapeutic candidate for alleviating, reversing and preventing AD. This article based on current knowledge represents the overview of the susceptible genes of EOAD, and LOAD. Next, we represent the probable molecular mechanism which might elucidate the genetic etiology of AD and highlight the role of massively parallel sequencing technologies for novel gene discoveries.

In recent years, the popularity of medicinal plants as a remedy has been increased manifold due to having minimal adverse effects. The current study aimed to compare the hypoglycemic, hypolipidemic and hepatoprotective effects of the ethanolic extract of Asparagus racemosus (EEAR) Linn. alone and combinedly with conventional antidiabetic agents (gliclazide and pioglitazone) in alloxan-induced diabetic rats. Diabetes was induced in male Wister albino rats by the administration of single intra-peritoneal injection of alloxan monohydrate (120 mg/kg b.w.). Effect of oral administration of two different doses of EEAR (200 and 400 mg/kg b.w.), gliclazide (10 mg/kg b.w.) and pioglitazone (10 mg/70kg/b.w.) alone for 2 weeks and a combination of EEAR (200 mg/kg b.w.) with either gliclazide (10 mg/kg b.w.) or pioglitazone (10 mg/70kg/b.w.) for 2 weeks were examined on hypoglycemic activity on 0 treatment as compared to that of disease control rats, gliclazide treated rats and pioglitazone treated rats. Proposed adjunct therapy also markedly (p < 0.001; p < 0.01, p < 0.001) improved serum TG, HDL and LDL level with insignificant change in VLDL and TC level while comparing with groups receiving gliclazide treated rats and pioglitazone treated rats. Administration of different doses of EEAR markedly (p < 0.05, p < 0.01, p < 0.001; p < 0.05, p < 0.01; p < 0.05) reduced the activity of TC, TG, LDL, VLDL and HDL cholesterol levels in a dose-dependent approach with respect to that of gliclazide treated rats and pioglitazone treated rats. The effect of combination therapy significantly (p < 0.001; p < 0.001; p < 0.01, p < 0.001) decreased the SGOT, SGPT and TP hepatic enzyme levels when compared to disease control rats, gliclazide treated rats and pioglitazone treated rats indicated improvement in liver dysfunctions. Administration of different doses of EEAR noticeably (p < 0.05, p < 0.01, p < 0.001; p < 0.05, p < 0.01; p < 0.05, p < 0.01) reduced the liver enzymes level including SGOT, SGPT and TP in a dose-dependent manner as compared to the disease control rats, gliclazide treated rats and pioglitazone treated rats. The maximum survival rate (100%) was observed in rats of combination treated rats. No significant changes in the body weight and organ weight to body weight ratio were observed except the groups that were given combined therapy showed improvement in the liver and pancreas weight. Our study suggests that the EEAR potentiates the activity of gliclazide and pioglitazone in controlling blood glucose levels, modifies the lipid profile and improves in liver dysfunction on alloxan-induced diabetic rats.

Autophagy is an intracellular catabolic system by which cells degrade and recycle cytoplasmic constituents such as organelles and proteins through the lysosome-dependent path. Belgian biochemist, Christian de Duve coined the name "autophagy" in 1963. The identification of autophagy-related genes and finally discoveries of mechanisms for autophagy led to the award of the 2016 Nobel Prize in Medicine or Physiology to Japanese cell biologist, Yoshinori Ohsumi specializing in autophagy. Autophagy shows a crucial role in removing aggregated proteins and damaged organelles in order to conserve intracellular homeostasis. In order to control cellular homeostasis and disease states autophagy illustrates a vital role. For insulin resistant patients, insulin secretion and the mass of pancreatic β-cells is increased on account of alterations in the expression and activities of numerous proteins in β-cells. Simultaneously, autophagic activity seems to also be upgraded to adjust to the dynamic changes taking place in β-cells. Actually, faulty autophagy in β-cells recaps a number of features that are perceived in pancreatic islets in the course of the formation of type 2 diabetes mellitus (T2DM). In contrast, the dyregulation of autophagic function is also appears to happen in the β-cells of T2DM patients. Furthermore, autophagy deficiency is linked with the diabetes-related organ dysfunction. Therefore the intention of this study was to provide the impacts of autophagy based on current researches in the development of T2DM and to explore new therapeutic strategies for stopping T2DM pathogenesis.