Parkinson’s disease (PD) is associated with a selective loss of the neurons in the midbrain area called the substantia nigra pars compacta and the loss of projecting nerve fibers in the striatum. Predominant pathological hallmarks of PD are the degeneration of discrete neuronal populations and progressive accumulation of α-synuclein-containing intracytoplasmic inclusions called Lewy bodies and dystrophic Lewy neuritis. There is currently no therapy to terminate or delay the neurodegenerative process as the exact mechanisms underlying the pathogenesis of PD require further investigation. The identification and validation of novel biomarkers for the diagnosis of PD is a great challenge using contemporary approaches and optimizing sampling handling as well as interpretation using bioinformatics analysis. In this review, recent evidences associated with multi-omic data-sets and molecular mechanisms underlying PD are examined. A combined mapping of several transcriptional evidences could establish a patient-specific signature for early diagnose of PD though eligible systems biology tools, which can also help develop effective drug-based therapeutic approaches. © 2019 the Author(s), licensee AIMS Press.Subarachnoid hemorrhage (SAH) frequently arises after an aneurysm in a cerebral artery ruptures, resulting into bleeding as well as clot formation. High-mobility group box 1 (HMGB1) is an extremely preserved, universal protein secreted in the nuclei of all cell varieties. This review explores the biomarker as well as therapeutic potentials of HMBG1 in SAH especially during the occurrence of cerebral vasospasms. Plasma HMGB1 levels have proven to be very useful prognosticators of effective outcome as well as death after SAH. Correspondingly, higher HMGB1 levels in the cerebrospinal fluid (CSF) of SAH patients correlated well with poor outcome; signifying that, CSF level of HMGB1 is a novel predictor of outcome following SAH. Nonetheless, the degree of angiographic vasospasm does not always correlate with the degree of neurological deficits in SAH patients. HMGB1 stimulated cerebral vasospasm, augmented gene as well as protein secretory levels of receptor for advance glycation end product (RAGE) in neurons following SAH; which means that, silencing HMGB1 during SAH could be of therapeutic value. Compounds like resveratrol, glycyrrhizin, rhinacanthin, purpurogallin, 4′-O-β-D-Glucosyl-5-O-Methylvisamminol (4OGOMV) as well as receptor-interacting serine/threonine-protein kinase 3 (RIPK3) gene are capable of interacting with HMGB1 resulting in therapeutic benefits following SAH. © 2019 the Author(s), licensee AIMS Press.Alzheimer’s disease (AD) impairs memory and learning related behavioural performances of the affected person. Compared with the controls, memory and learning related behavioural performances of the AD model rats followed by hippocampal proteomics had been observed in the present study. In the eight armed radial maze, altered performance of the AD rats had been observed. Using liquid chromatography coupled tandem mass spectrometry (LC-MS/MS), 822 proteins had been identified with protein threshold at 95.0%, minimum peptide of 2 and peptide threshold at 0.1% FDR. Among them, 329 proteins were differentially expressed with statistical significance (P less then 0.05). Among the significantly regulated (P less then 0.05) 329 proteins, 289 met the criteria of fold change (LogFC of 1.5) cut off value. Number of proteins linked with AD, oxidative stress (OS) and hypercholesterolemia was 59, 20 and 12, respectively. Number of commonly expressed proteins was 361. The highest amount of proteins differentially expressed in the AD rats were those involved in metabolic processes followed by those linked with OS. Most notable was the perturbed state of the cholesterol metabolizing proteins in the AD group. Current findings suggest that proteins associated with oxidative stress, glucose and cholesterol metabolism and cellular stress response are among the mostly affected proteins in AD subjects. Thus, novel therapeutic approaches targeting these proteins could be strategized to withstand the ever increasing global AD burden. © 2019 the Author(s), licensee AIMS Press.Grundy, Bialystok, and colleagues have reported that at short response-stimulus intervals bilinguals have smaller sequential congruency effects in flanker tasks compared to monolinguals. They interpret these differences to mean that bilinguals are more efficient at disengaging attentional control. ONO-AE3-208 research buy Ten empirical studies are presented that show no differences between bilinguals and monolinguals under conditions that produced robust sequential congruency effects. These null results are discussed with respect to the rate at which sequential congruency effects dissipate and the fact these effects are not adaptive in the sense of improving overall performance. Arguments made by Goldsmith and Morton [1] that smaller sequential congruency effects should not be interpreted as “advantages” are extended. Evidence is also presented that neither simple congruency effects, nor sequential congruency effects, correlate across tasks. This lack of convergent validity is inconsistent with the hypothesis that either provides a measure of domain-general control that could underlie an advantage accrued through experience in switching languages. Results from other tasks purporting to show bilingual advantages in the disengagement of attention are also reviewed. We conclude that sequential congruency effects in nonverbal interference tasks and differences in the rate of disengaging attention are unlikely to contribute to our understanding of bilingual language control and that future research might productively examine differences in proactive rather than reactive control. © 2019 the Author(s), licensee AIMS Press.Several pathophysiological functions of the human β-amyloid precursor protein (APP) have been recently proposed in different human diseases such as neurodevelopmental and neurodegenerative disorders including rare diseases such as autism, fragile X syndrome, amyotrophic lateral sclerosis, multiple sclerosis, Lesch-Nyhan disease; common and complex disorders such as Alzheimer’s disease; metabolic disorders such as diabetes; and also cancer. APP as well as all of its proteolytic fragments including the amyloid-β (Aβ) peptide, are part of normal physiology. The targeting of the components of APP proteolytic processing as a pharmacologic strategy will not be without consequences. Recent research results highlight the impact of alternative splicing (AS) process on human disease, and may provide new directions for the research on the impact of the human APP on human diseases. The identification of molecules capable of correcting and/or inhibiting pathological splicing events is therefore an important issue for future therapeutic approaches.