Efficacy of Rivastigmine Augmentation on Positive and Negative Symptoms, General Psychopathology, and Quality of Life in Patients with Chronic Schizophrenia: A Randomized Controlled Trial.

The study aimed to assess Rivastigmine augmentation on positive and negative symptoms (PNSs), general psychopathology, and quality of life in patients with chronic Schizophrenia. A double-blind, parallel-design, randomized, placebo-controlled trial of 60 schizophrenia patients was conducted. Intervention group received rivastigmine 3 mg/day + Treatment as Usual (TAU) and the control group: TAU + placebo. Negative and positive symptoms, general psychopathology; and quality of life were measured using Positive and Negative Symptom Scale (PANSS) and Manchester Short Assessment of Quality of Life (MANSA). T-test, ANOVA, and the general univariate linear model tests were used for the analyses. Out of 60 participants, 52 (86.6%) were male. At baseline, no significant relationship was found for demographic and clinical characteristics between intervention and control groups. Between-group analysis indicated that all outcome measures PNSs, general psychopathology symptoms, and QoL score in rivastigmine group was significantly improved (p = 0.001). According to within-group analysis, a significant association was found between Rivastigmine and placebo groups in PNSs (p < 0.05). Rivastigmine augmentation improved PNSs and psychopathology in schizophrenia patients. However, no significant association found for improving the life quality after 8 weeks treatment.

Quality of Life in Patients with Phenylketonuria: A Systematic Review.

The impact of phenylketonuria (PKU) on Quality of life (QoL) has been a topic of interest in recent research. This article reviews current researches on the impact of PKU on QoL. The review examines factors that may influence QoL, such as age, metabolic control, and treatment adherence. In this systematic review study, relevant articles were identified using a search strategy built with the keywords phenylketonuria, PKU, or hyperphenylalaninemia (or their synonyms) and QoL in Web of Science, Scopus, and PubMed databases. After identifying the articles, duplicates, reviews, scientific abstracts, articles published in languages other than English, and non relevant studies were excluded. The search strategy identified 951 records from databases, and after excluding duplicates, irrelevant studies, and those published in non English languages, 26 records were left that contained data on 1816 patients with PKU/hyperphenylalaninemia. The studies included both children/adolescents and adults. Overall, the studies found that the QoL of PKU patients was comparable to normative data, but some aspects such as emotional health and school functioning were lower. Metabolic control was found to significantly correlate with QoL. Younger patients and men had better QoL in several studies, while late treated patients and those with lower education had worse outcomes. It is concluded that QOL in patients with PKU is similar to the general population. However, given the chronic nature of the condition, it is important to pay special attention to their QoL. Poor QOL is associated with female gender, lower education, older age, and poor metabolic control.

Exercise and Dementia.

Several experimental and human studies documented the preventive and therapeutic effects of exercise on various diseases as well as the normal physiological function of different systems during aging. The findings of several basic animal studies and clinical investigations identified the advantageous effects of exercise as non-pharmaceutical intervention on dementia and Alzheimer's disease (AD). The main positive effects suggested for exercise are less cognitive and behavioral impairment or decline, development of health-associated conditions (stress, sleep), reduction of dementia risk factors including chronic non-communicable disease (diabetes, cardiovascular disease), increase in neurotrophins, enhancement of brain blood flow, angiogenesis, neurogenesis, synaptogenesis and synaptic plasticity in the brain memory-related region (e.g., hippocampus), and reduction of neuroinflammation and apoptosis. However, regarding the controversial evidence in literature, designing standard clinical and experimental studies to reveal the correlation between physical activity and dementia sign and symptom including biomarker alternation, brain supramolecular and molecular changes, and neuropsychological manifestation is necessary for preparation of effective guidelines and recommendations.

The effects of moderate exercise and overtraining on learning and memory, hippocampal inflammatory cytokine levels, and brain oxidative stress markers in rats.

To investigate the exercise intensity effects on rats' memory and learning, animals were divided into control, moderate training (MT), and overtraining (OT) groups. At training last week, learning and memory was assessed using Morris water maze (MWM) and passive avoidance (PA) tests. Finally, the rat's brains were removed for evaluating oxidative stress and inflammatory cytokines. Overtraining impaired animal's performance in MWM and PA tests. In MT group, hippocampal levels of interleukin 1 beta (IL-1ß) and malondialdehyde (MDA) increased, and thiol contents in hippocampal and cortical tissues decreased compared to control. In OT group, tumor necrosis factor α, IL-1ß, and C-reactive protein hippocampal levels increased, MDA and nitric oxide metabolite in hippocampal and cortical tissues increased, thiol contents, catalase and superoxide dismutase activity in hippocampal and cortical tissues decreased compared to control and MT groups. Overtraining might lead to learning and memory impairment by increasing the inflammatory cytokine and oxidative stress markers.

The effects of exercise on hippocampal inflammatory cytokine levels, brain oxidative stress markers and memory impairments induced by lipopolysaccharide in rats.

The exercise effects on behavioral tests, hippocampal and cortical oxidative stress, and hippocampal inflammatory cytokines of lipopolysaccharide (LPS) administered rats were investigated. The rats were divided into four groups (N = 8): (1) control; (2) moderate training (MT, 15 m/min, 30 min/day, 9 weeks); (3) LPS (1 mg/kg LPS) and (4) LPS + MT (1 mg/kg LPS; 15 m/min, 30 min/day, 9 weeks). LPS was injected 2 h before the behavioral experiments during the last week of training. Finally, the rats' brain were removed for biochemical assessments. LPS increased escape latency and traveled distance to reach the platform in Morris water maze (MWM) test (P < 0.05-P < 0.001). In the passive avoidance (PA) test, LPS decreased the latency to enter the dark compartment and the time spent in the light compartment and increased the time spent in the dark compartment (P < 0.01-P < 0.001), while MT improved the rats performances in MWM and PA tests (P < 0.01-P < 0.001). Additionally, LPS increased tumor necrosis factor α (TNF-α), interleukin 1 beta (IL-1ß) and C-reactive protein levels in the hippocampal tissues, malondialdehyde (MDA) and nitric oxide metabolite in hippocampal and cortical tissues, and decreased thiol contents and catalase (CAT) and superoxide dismutase (SOD) activity in hippocampal and cortical tissues compared to the control group (P < 0.01-P < 0.001); while moderate training decreased the levels of TNF-α, IL-1ß and MDA; increased thiol contents, and SOD and CAT activity in the LPS + MT compared to the LPS group (P < 0.001). These results indicated that moderate training improved LPS-induced learning and memory impairments by attenuating the hippocampal cytokine levels and brain oxidative damage.

Neuroprotective effects of exercise in rodent models of memory deficit and Alzheimer's.

Alzheimer's disease (AD) is a fastest growing neurodegenerative condition with no standard treatment. There are growing evidence about the beneficial effects of exercise in brain health promotion and slowing the cognitive decline. The aim of this study was to review the protective mechanisms of treadmill exercise in different models of rodent memory deficits. Online literature database, including PubMed-Medline, Scopus, Google scholar were searched from 2003 till 2017. Original article with English language were chosen according to following key words in the title: (exercise OR physical activity) AND (memory OR learning). Ninety studies were finally included in the qualitative synthesis. The results of these studies showed the protective effects of exercise on AD induced neurodegerative and neuroinflammatory process. Neuroperotective effects of exercise on the hippocampus seem to be increasing in immediate-early gene c-Fos expression in dentate gyrus; enhancing the Wnt3 expression and inhibiting glycogen synthase kinase-3ß expression; increasing the 5-bro-mo-2'-deoxyridine-positive and doublecortin-positive cells (dentate gyrus); increasing the level of astrocytes glial fibrillary acidic protein and decrease in S100B protein, increasing in blood brain barrier integrity; prevention of oxidative stress injury, inducing morphological changes in astrocytes in the stratum radiatum of cornu ammonis 1(CA1) area; increase in cell proliferation and suppress apoptosis in dentate gyrus; increase in brain-derived neurotrophic factor and tropomyosin receptor kinase B expressions; enhancing the glycogen levels and normalizing the monocarboxylate transporter 2 expression.