Brain-derived neurotrophic factor (BDNF) is one of the most studied neurotrophins in the healthy and diseased brain. As a result, there is a large body of evidence that associates BDNF with neuronal maintenance, neuronal survival, plasticity, and neurotransmitter regulation. Patients with psychiatric and neurodegenerative disorders often have reduced BDNF concentrations in their blood and brain. A current hypothesis suggests that these abnormal BDNF levels might be due to the chronic inflammatory state of the brain in certain disorders, as neuroinflammation is known to affect several BDNF-related signaling pathways. Activation of glia cells can induce an increase in the levels of pro- and antiinflammatory cytokines and reactive oxygen species, which can lead to the modulation of neuronal function and neurotoxicity observed in several brain pathologies. Understanding how neuroinflammation is involved in disorders of the brain, especially in the disease onset and progression, can be crucial for the development of new strategies of treatment. Despite the increasing evidence for the involvement of BDNF and neuroinflammation in brain disorders, there is scarce evidence that addresses the interaction between the neurotrophin and neuroinflammation in psychiatric and neurodegenerative diseases. This review focuses on the effect of acute and chronic inflammation on BDNF levels in the most common psychiatric and neurodegenerative disorders and aims to shed some light on the possible biological mechanisms that may influence this effect. In addition, this review will address the effect of behavior and pharmacological interventions on BDNF levels in these disorders.

/pdf/brain-derived-neurotrophic-factor-in-brain-disorders-focus-5311blpues.pdf

Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation

https://www.nature.com/articles/s41591-022-02001-z.pdf

Long-term neurologic outcomes of COVID-19

Neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) enforce an overwhelming social and economic burden on society. They are primarily characterized through the accumulation of modified proteins, which further trigger biological responses such as inflammation, oxidative stress, excitotoxicity and modulation of signalling pathways. In a hope for cure, these diseases have been studied extensively over the last decade to successfully develop symptom-oriented therapies. However, so far no definite cure has been found. Therefore, there is a need to identify a class of drug capable of reversing neural damage and preventing further neural death. This review therefore assesses the reliability of the neuroprotective benefits of epigallocatechin-gallate (EGCG) by shedding light on their biological, pharmacological, antioxidant and metal chelation properties, with emphasis on their ability to invoke a range of cellular mechanisms in the brain. It also discusses the possible use of nanotechnology to enhance the neuroprotective benefits of EGCG.

/pdf/potential-neuroprotective-properties-of-epigallocatechin-3-458avnb4rg.pdf

Potential neuroprotective properties of epigallocatechin-3-gallate (EGCG).

The recognition of the human microbiome (HM) as a substantial contributor to nutrition, health and disease is a relatively recent one, and currently, peerreviewed studies linking alterations in microbiota to the etiopathology of human disease are few. Emerging studies indicate that the HM may contribute to the regulation of multiple neuro-chemical and neuro-metabolic pathways through a complex series of highly interactive and symbiotic host-microbiome signaling systems that mechanistically interconnect the gastrointestinal (GI) tract, skin, liver, and other organs with the central nervous system (CNS). For example, the human GI tract, containing 95% of the HM, harbors a genetically diverse microbial population that plays major roles in nutrition, digestion, neurotrophism, inflammation, growth, immunity and protection against foreign pathogens (Forsythe et al., 2012; Collins et al., 2013; Douglas-Escobar et al., 2013; see below). It has been estimated that about 100 trillion bacteria from up to 1000 distinct bacterial species co-inhabit the human GI tract, albeit in different stoichiometries amongst individuals, and the varying combinations and strains of bacterial species amongst human populations might contribute, in part, to “humanbiochemical” or “genetic-individuality” and resistance to disease (Aziz et al., 2013; Lukiw, 2013). Interestingly, HM participation in human physiology may also help explain the genome-complexity conundrum—for example why the 26,600 protein-encoding transcripts in Homo sapiens are far fewer in number, than for example, the rice genome (Oryza sativa; which has about 46,000 functional genes). One thousand different strains of bacteria might be expected to contribute up to 4 × 106 potential mRNAs to the human transcriptome, thus making the human host-plus-microbiome genetic complexity closer to 4,026,600 mRNA transcripts, and a clear “winner” of human genetic complexity over that of rice and other species (Venter et al., 2001; Foster and McVey Neufeld, 2013; Lukiw, 2013). The very recent observation of microbiomederived small non-coding RNA (sncRNA) and micro RNA (miRNA) translocation and signaling across endothelial barriers, between cells and tissues, and even perhaps between individual species indicates that human neurobiology may be significantly impacted by the actions of HMmediated sncRNA or miRNA trafficking, and the integration of a cell, tissue or an entire organism into its local environment (Zhao et al., 2006; Alexandrov et al., 2012; Sarkies and Miska, 2013; Reijerkerk et al., 2013; unpublished). This opinion paper encompasses what we know concerning the contribution of the HM to neurological disease, with specific emphasis on Alzheimer’s disease (AD) wherever possible. Firstly, the microbiome of the human GI tract is the largest reservoir of microbes in the body, containing about 1014 microorganisms; over 99% of microbiota in the gut are anaerobic bacteria, with fungi, protozoa, archaebacteria and other microorganismsmaking up the remainder. There is currently an expanding interest in the ability of intestinal bacteria to influence neuro-immune functions well beyond the GI tract. Since mitochondria are believed to originate from bacteria via endosymbiotic relationships that formed very early in the evolutionary history of eukaryotes, cross-reactivity of mitochondria and immunological responses to intestinal bacterial constituents could have deleterious effects on mitochondrial function through some form of molecular mimicry; this is partially evidenced by the inflammatory basal ganglia disorder Sydenham’s chorea, rheumatic fever and the link to the facultative anaerobe Streptococcus (Carrasco-Pozo et al., 2012; Douglas-Escobar et al., 2013; Hayashi, 2013; Hornig, 2013 see below). Established pathways of GI-CNS communication currently include the autonomic nervous system (ANS), the enteric nervous system (ENS), the neuroendocrine system, and the immune system (Camfield et al., 2011; Heijtz et al., 2011; Forsythe et al., 2012; Aziz et al., 2013; Collins et al., 2013; Foster and McVey Neufeld, 2013; Schwartz and Boles, 2013). Stress further influences the composition of the HM, and reciprocal communication between the CNS and the HM also influences stress reactivity (Forsythe et al., 2012; Foster and McVey Neufeld, 2013). Surprisingly, neuronal signaling pathways along the bidirectional GI-CNS axis remain poorly understood despite their important roles: (i) in coordinating metabolicand nutritivefunctions, and (ii) in their functional disruption in chronic diseases such as metabolic syndrome, diabetes, obesity, anxiety, autoimmune-disease and stressinduced neuropsychiatric disease (Lukiw and Bazan, 2006; Bravo et al., 2012; Foster and McVey Neufeld, 2013; Hornig, 2013; Udit and Gautron, 2013). Studies of the ENS in “germ-free” mice, i.e., those

/pdf/alzheimer-s-disease-and-the-microbiome-4nj7h6b5g1.pdf

Alzheimer's disease and the microbiome

Cognitive Reserve (CR) designates the brain's capacity to actively cope with insults through a more efficient use of its resources/networks. It was proposed in order to explain the discrepancies between the observed cognitive ability and the expected capacity for an individual. Typical proxies of CR include education and Intelligence Quotient but none totally account for the variability of CR and no study has shown if the brain's greater efficiency associated with CR can be measured. We used a validated model to estimate CR from the residual variance in memory and general executive functioning, accounting for both brain anatomical (i.e., gray matter and white matter signal abnormalities volume) and demographic variables (i.e., years of formal education and sex). Functional connectivity (FC) networks and topological properties were explored for associations with CR. Demographic characteristics, mainly accounted by years of formal education, were associated with higher FC, clustering, local efficiency and strength in parietal and occipital regions and greater network transitivity. Higher CR was associated with a greater FC, local efficiency and clustering of occipital regions, strength and centrality of the inferior temporal gyrus and higher global efficiency. Altogether, these findings suggest that education may facilitate the brain's ability to form segregated functional groups, reinforcing the view that higher education level triggers more specialized use of neural processing. Additionally, this study demonstrated for the first time that CR is associated with more efficient processing of information in the human brain and reinforces the existence of a fine balance between segregation and integration. Hum Brain Mapp 37:3310-3322, 2016.. © 2016 The Authors Human Brain Mapping Published by Wiley Periodicals, Inc.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1002/hbm.23242

The functional connectome of cognitive reserve.

: The Brazilian scenario has shown a significant increase in the cases of non-communicable chronic diseases, such as obesity, hypertension, osteoporosis, diabetes mellitus, cancer, and conditions affecting memory loss, such as Alzheimer's disease. This study aims to analyze and discuss the relevance of functional foods and their nutritional components in individual health and their relationship with Alzheimer's disease. The methodology adopted included a qualitative and descriptive literature review based on sources such as books, websites

非 Alzheimer 型認知症

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非 Alzheimer 型認知症

衛 橋本

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