More women than men have Alzheimer’s disease (AD) or other dementias. There are a number of potential biological and social reasons for the sex difference in the risk of AD, such as women live longer than men on average, and estrogen depletion after menopause in women, biological or genetic variations, and education, occupation or rates of heart disease. Recent studies showed a link between reproductive history and dementia risk in women. Women with fertility history showed lower risk of dementia compared to women with no child. Other studies also suggested that women’s pregnancy history may influence AD’s risk. In this review, we will focus on the relationship between women fertility and cognition and discuss the potential role of sex hormones in the brain and cognition, especially on AD pathogenesis.

Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme for the critical process of one-carbon circulation, which convert 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate and participate in folate and homocysteine conversion correlated to methyl group supply. The enzyme activity decline depends on the gene polymorphism. MTHFR impacts on the methylation process which is related to psychiatric diseases. Studies have shown association between MTHFR gene polymorphisms and mental disorders, some of which stratified by folate and cobalamin levels. In this review, we will summarize the testimony on the relationship between methylation and MTHFR polymorphism as well as the implication on psychiatric diseases by MTHFR mutation.

The presidential research program Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative was established 5 years ago in the United States; it has been a driving force of the United States government and private factors to promote technology development in basic and translational neuroscience research. We here summarize the research plan and recent progress in cellular neuroscience, electrical and optical engineering, chemical and systems neurobiology, and brain mapping technologies. The research plan recognizes the importance of identifying different cell populations and unknown cell types in the human brain and diseased models. Technological advances in multielectrode arrays and chemical flow measurement probes not only demonstrate the capacity of detecting neural activities in large areas, but also enable a new era of studying the neural coding information. Large-scale coordination of neuronal activity and brain mapping information will allow for the identification of therapeutic targets in neurological disorders, which is benefited by big data acquisition and analysis. Specifically, increased brain databases will expedite the dissection of thoughts, emotions, cognition, and will thereby help the development of better understanding and treatments of brain disorders. Since cell therapy demonstrates potential for regenerative medicine, the utilization of the newly advanced technologies may further improve the translational potentials and precision controls of transplanted grafts. The development of new diagnostic and therapeutic tools also requires international collaborations on science, technology, advocating, healthcare and medical ethics to advance the innovation and clinical practices.

Objective: Published studies have found prepulse inhibition (PPI) in schizophrenia is impaired, suggesting PPI may be a biomarker of schizophrenia. We aim to examine whether PPI deficits exist in antipsychotic-naïve, first-episode schizophrenia, and evaluate the effect size of PPI deficits between patients and healthy controls. Methods: The effect size of PPI deficits was evaluated for PPI% by calculating standard mean differences (SMDs) between patients with antipsychotic-naïve, first-episode schizophrenia and healthy controls. Results: Twelve studies met the inclusion criteria, consisting 390 antipsychotic-naïve, first-episode schizophrenia and 406 healthy controls. The effect sizes of 76 dB PPI in 60 ms and 120 ms interstimulus interval (ISI) were -0.19 and -0.41 respectively, and the 76 dB PPI overall effect size was -0.30. The effect sizes of 85/86 dB PPI in 30 ms, 60 ms and 120 ms ISI were -0.25, -0.42 and -0.59 respectively, and the 85/86 dB PPI overall effect size was -0.46. One study were excluded due to heterogeneity in the 85/86 dB, 120 ms ISI group, the pooled effect size of the PPI differences between patient group and health control dropped to -0.42, and the overall effect size changed to -0.39. There were no statistical differences in startle magnitude (overall effect size = -0.18) and habituation% (overall effect size = -0.17) between patients and healthy controls. Conclusions: Antipsychotic-naïve, first-episode schizophrenia patients exhibit robust and reliable deficits in PPI, 85/86 dB PPI deficit was more severe than 76 dB PPI, and 85/86 dB, 60-ms ISI PPI was more likely to be a biomarker for schizophrenia, it suggested that the parameters of PPI are particularly significant to affect the effect size so that should be interpreted with cautions in the future studies.