Impaired verbal self-monitoring was evident in both hallucinators and non-hallucinators. As both groups had delusions, the results suggest an association between delusions and impaired judgements about ambiguous sensory stimuli. The specific tendency of hallucinators to misattribute their distorted voice to someone else may reflect impaired awareness of internally generated verbal material.

The Semliki Forest Virus (SFV) is an RNA virus with a positive-strand that belongs to the Togaviridae family’s Alphavirus genus. An epidemic was observed among French troops stationed in the Central African Republic, most likely caused by the SFV virus. The two transmembrane proteins El and E2 and the peripheral protein E3 make up the viral spike protein. The virus binds to the host cell and is internalized via endocytosis; endosome acidification causes the E1/E2 heterodimer to dissociate and the E1 subunits to trimerize. Lupenone was evaluated against the E1 spike protein of SFV in this study based on state-of-the-art cheminformatics approaches, including molecular docking, molecular dynamics simulation, and binding free energy calculation. The molecular docking study envisaged major interactions of Lupenone with binding cavity residues involved non-bonded van der Waal’s and Pi-alkyl interactions. Molecular dynamic simulation of a time scale 200 ns corroborated interaction pattern with molecular docking studies between Lupenone and E1 spike protein. Nevertheless, Lupenone intearcation with the E1 spike protein conforming into a stable complex substantiated by free energy landscape (FEL), PCA analysis. Free energy decomposition of the binding cavity resdiues of E1 spike protein also ensured the efficient non-bonded van der Waal’s interaction contributing most energy to interact with the Lupenone. Therefore, Lupenone interacted strongly at the active site conforming into higher structural stability throughout the dynamic evolution of the complex. Thus, this study perhaps comprehend the efficiency of Lupenone as lead molecule against SFV E1 spike protein for future therapeutic purpose.

It is widely recognized that Alzheimer's disease (AD) is a common type of progressive neurodegenerative disorder that results in cognitive impairment over time. Approximately 152 million cases of AD are predicted to be reported by 2050. Amyloid plaques and tau proteins are two major hallmarks of AD which can be seen under electron microscope. Mitochondria plays a vital role in the pathogenesis of AD and mitochondria disruption leads to mitochondrial DNA (mtDNA) dysfunction, alteration of mitochondria dependent Ca2+ homeostasis, copper dysfunction, immune cell dysfunction, etc. In this review, we try to cover all the mechanisms related with mitochondrial dysfunction and mitochondrial pathogenesis that may help us to better understand AD as well as open a new era for therapeutic target of AD and treat this progressive disease.

Alzheimer's disease (AD) is considered to be the most typical form of dementia that provokes irreversible cognitive impairment. Along with cognitive impairment, circadian rhythm dysfunction is a fundamental factor in aggravating AD. A link among circadian rhythms, sleep, and AD has been well‐documented. The etiopathogenesis of circadian system disruptions and AD serves some general characteristics that also open up the possibility of viewing them as a mutually reliant path. In this review, we have focused on different factors that are related to circadian rhythm dysfunction. The various pathogenic factors, such as amyloid‐beta, neurofibrillary tangles, oxidative stress, neuroinflammation, and circadian rhythm dysfunction may all contribute to AD. In this review, we also tried to focus on melatonin which is produced from the pineal gland and can be used to treat circadian dysfunction in AD. Aside from amyloid beta, tau pathology may have a notable influence on sleep. Conclusively, the center of this review is primarily based on the principal mechanistic complexities associated with circadian rhythm disruption, sleep deprivation, and AD, and it also emphasizes the potential therapeutic strategies to treat and prevent the progression of AD.

Background The aim of this study was to evaluate the relationship between vitamin D and postpartum depression in reproductive-aged Iranian women. Methods and Results This study was conducted on 120 women (60 with postpartum depression and 60 without) in Izeh, Iran. A socio-demographic questionnaire and Beck Depression Scale were used for data collection. The ELISA method was used for measuring 25-OH vitamin D (ng). The participants were classified according to their vitamin D level as follows: 25-OH-D < 10ng/ml considered as severe deficiency, 10–20n g/ml as moderate insufficiency, 20–30 ng/ml as mild insufficiency and >30ng/ml as normal. Data were analyzed using the independent t-test or Mann-Whitney test, chi-square and logistic regression test. The mean level of vitamin D of women with postpartum depression was lower than that in normal women (16.89±7.05 vs. 21.28±7.13, p=0.001). More than 53% of women with postpartum depression had vitamin D <20 ng/ml compared to 31.7% of women with no depression (p=0.005). Moreover, 16.7% of women with postpartum depression had vitamin D < 10ng/ml compared to only 6.7% in the normal group (p = 0.005). Women with vitamin D less than 20ng/ml compared to vitamin D > 20ng/ml were 3.30 times more likely to have postpartum depression (OR: 3.3, CI: 1.32–8.24, p= 0.01). Discussion There is a significant relationship between a low level of vitamin D and postpartum depression among reproductive-aged Iranian women. Health policy makers should pay attention to the measuring vitamin D level as one of the primary tests of pregnant women.

Memory loss, emotional fluctuations, and functioning impairments are frequent signs of Alzheimer's disease (AD). Dementia, which includes AD, affects 50 million people worldwide, the majority of whom are elderly. AD is the world's fifth biggest cause of mortality, according to the World Health Organization (WHO), with the number of fatalities expected to quadruple by 2050 if present trend continue. 1,2 Brain imaging, physical and cognitive examinations, laboratory testing, and medical history are used to diagnose AD. 3 Risk factors of the AD include apolipoprotein E4 (APOE4) genotype and traumatic brain injury, family history and age, obesity, diabetes, hypercholesterolemia, hypertension, and illiteracy. The most prevalent causes of AD are mutations in the genes producing the amyloid precursor protein (APP), presenilin 2 (PSEN2), and presenilin 1 (PSEN1). 4 As a result, both pharmaceutical and nonpharmacological therapies, such as physical, social, and cognitive activities, should be included in the treatment plan. Lithium and sodium valproate are two medicines used to treat mild to severe cognitive impairment. 5,6 Nonsteroidal anti-inflammatory medications (NSAIDs) like naproxen and ibuprofen are also used to treat neuroinflammation and prevent neurodegeneration. 7,8 Ganstigmine, metrifonate, lecithin, ibuprofen, rofecoxib, latrepiridine, omega-3 polyunsaturated fatty acids, vitamin B, and vitamin E are among the medications that have failed clinical studies. These drugs have been linked to headaches, nausea, vomiting, neuromuscular dysfunction, and respiratory problems. 5,9 Only five FDA-approved medications are now available to treat the symptoms of Alzheimer's disease. Aducanumab was just authorized for use in the year 2021. Memantine (N-methyl-D-aspartate receptor) has been on the market for 10 years (NMDAR antagonist). The remaining five medications are rivastigmine, donepezil (both cholinesterase inhibitors [ChEls]), memantine (an NMDAR antagonist), and galantamine (an NMDAR antagonist). 3,10 In recent years, stem cell therapy has exhibited significant progress in treating AD, as seen by multiple improvements in clinical studies. Self-generation, multiplication, division, and reprogramming for multi-lineage activities are among their many astonishing abilities. Consequently, they can be integrated into existing neural network topologies in this fashion.

Objective: Alzheimer's disease (AD) is one of the most prevalent neurological ailments, affecting around 50 million individuals globally. The condition is characterized by nerve cell damage due to the formation of amyloid-beta plaques and neurofibrillary tangles. Only a few US Food and Drug Administration (FDA)-approved medications are available in the market which are devoid of side effects, thus, making it imperative to investigate new alternatives for countering this disease. According to a recent study, microtubule affinity regulation kinase 4 (MARK4) is attributed as one of the most promising drug targets for AD, thus, being selected for this study. Compounds from Ganoderma lucidum (Reishi mushroom) extracts were selected to be used as ligands for this study. Methods:In this study, the five most potent compounds from Ganoderma lucidum were selected and their absorption, distribution, metabolism, excretion, and toxicity (ADMET) analysis was performed, followed by molecular docking, and molecular dynamics simulation of each compound with MARK4 and supported by molecular mechanics generalized born surface area (MMGBSA) binding free energy calculations. Results:The promising compounds were selected based on their ADMET profile and interactions with the active site residues of MARK4. Based on docking scores of −9.1 and −10.3 kcal/ mol, respectively, stability assessment by molecular dynamics simulation, and MMGBSA calculations, ganoderic acid A and ganoderenic acid B were found to be the most promising compounds against MARK4 which will require further in vitro and in vivo validations. Conclusion:Through this study, it is suggested that ganoderic acid A and ganoderenic acid B might be a class of promising compounds against AD, based on computational research, and can be further studied for preclinical and clinical studies.

BackgroundParkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease (AD). The exact mechanism behind PD disease is still unknown and PD is marked by symptoms like bradikynesia, tremors, walking or gait difficulties, etc. The current medication used for PD is levodopa, and researchers are trying to develop a promising drug for PD. In our study, we took Ganodema lucidium mushroom, known as “Reishi mushroom,” which has antioxidant, antiinflammatory, antihepatic properties, etc. In our study we took the most five potent Ganodema lucidium extracts, which target Leucine‐rich repeat kinase 2 (LRRK2) that is involved in onset of PD.ObjectiveThis study aims to find the most promising Ganodema lucidium targeting LRRK2 involved in PD.MethodsFirst ADMET analysis was performed for five compounds followed by molecular docking of each compound. Then, we perform molecular dynamics simulation of all five compounds and finally MMGBSA of all five compounds.ResultsBased on molecular dynamics and MMGBSA result we reach the conclusion that Ganoderic Acid A (GAA) is the most promising compound targeting LRRK2. Therefore, GAA needs further validation through in vitro and in vivo studies.