https://www.tandfonline.com/doi/abs/10.1080/15548627.2021.1985257
https://doi.org/10.1080/15548627.2021.198525
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4915811/
Abstract
Exercise induces beneficial responses in the brain, which is accompanied by an increase in BDNF, a trophic factor associated with cognitive improvement and the alleviation of depression and anxiety. However, the exact mechanisms whereby physical exercise produces an induction in brain Bdnf gene expression are not well understood. While pharmacological doses of HDAC inhibitors exert positive effects on Bdnf gene transcription, the inhibitors represent small molecules that do not occur in vivo. Here, we report that an endogenous molecule released after exercise is capable of inducing key promoters of the Mus musculus Bdnf gene. The metabolite Ξ²-hydroxybutyrate, which increases after prolonged exercise, induces the activities of Bdnf promoters, particularly promoter I, which is activity-dependent. We have discovered that the action of Ξ²-hydroxybutyrate is specifically upon HDAC2 and HDAC3, which act upon selective Bdnf promoters. Moreover, the effects upon hippocampal Bdnf expression were observed after direct ventricular application of Ξ²-hydroxybutyrate. Electrophysiological measurements indicate that Ξ²-hydroxybutyrate causes an increase in neurotransmitter release, which is dependent upon the TrkB receptor. These results reveal an endogenous mechanism to explain how physical exercise leads to the induction of BDNF.
Hi Reddit!
I am an Assistant Professor in the Department of Psychiatry and the Director of the Experimental Psychopathology Lab at the New York State Psychiatric Institute, and I am the lead author of a new study that showed that an aerobic exercise training program improved cognitive functioning in people with schizophrenia.
This proof of concept study showed that patients who received the exercise training improved their aerobic fitness by 18% (vs. -0.5% in patients who received treatment as usual) and cognitive function by 15.1% (vs. -2% in patients who received treatment as usual). Improvement in cognitive functioning was associated with improvement in aerobic fitness and increase in brain-derived neurotrophic factor (BDNF), a protein involved in brain plasticity. If replicated, this finding may lead to integration of aerobic exercise in standard psychiatric treatment.
My work centers on two primary areas: 1) The use of translational approaches to elucidate the mechanisms of development and recovery from psychopathology in individuals with schizophrenia and related disorders; and 2) The development and dissemination of cognitive and behavioral interventions to improve affective, social and cognitive functioning. I will be answering questions at 1:30 p.m. EST. Ask Me Anything!
I'd feel different about the pharmaceutical industry if they release a treatment like this. Memory improvements are definite. Depending on the antidepressant, there could be a plethora of benefits from BDNF increasing.
I'm excited for the future.
https://www.ncbi.nlm.nih.gov/pubmed/31700717 ; https://assets.cureus.com/uploads/original_article/pdf/22650/1568057289-20190909-1481-1k9rmla.pdf
Gyorkos A1, Baker MH2, Miutz LN3, Lown DA4, Jones MA5, Houghton-Rahrig LD6.
Abstract
Introduction
Metabolic syndrome (MetS) has been recognized as one of the most important clinical challenges and global health issues of today. Growing evidence suggests that mechanisms of energy metabolism may also play a key role in mediating aspects of cognitive function. Brain-derived neurotrophic factor (BDNF) is one such factor well known for its critical role in neuronal plasticity, including memory and learning, and more recently metabolic processes. BDNF levels have been shown separately to be dependent on diet and exercise programming.
Purpose
The purpose of this study was to investigate the effect of diet and exercise on BDNF levels and cognitive functioning with any metabolic association in individuals characterized with MetS.
Methods
Twelve subjects with MetS followed a randomized crossover design with two four-week interventions, including a carbohydrate (CHO)-restricted Paleolithic-based diet (CRPD; <50gCHO) with sedentary activity (CRPD-Sed) and CRPD with high intensity interval training (HIIT; CRPD-Sed), separated by a four-week washout period. The HIIT exercise consisted of 10 x 60 s cycling intervals interspersed with 60 s of active recovery 3 day/week for four-week. Serum BDNF was detected and quantified viaΒ enzyme-linked immunosorbent assay (ELISA). Cognitive executive function (Stroop Test) and self-perceived cognitive symptoms and function (MOS-CFS) were quantified.Β A two-way analy
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