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Bio-Inspired NoC Fault-Tolerant Algorithms
Published in Muhammad Athar Javed Sethi, Bio-Inspired Fault-Tolerant Algorithms for Network-on-Chip, 2020
Synaptogenesis is a self-adapting mechanism in the human brain where two neurons attempt to connect and communicate with each other. In this phenomenon, the growth cone (having lamellipodium and filopodia) at the top of the axon and dendrites terminals, finds a path to a target neuron. The filopodia actually finds the path for a connection with the target neuron. A chemical attractant is released by the target neuron to attract the growth cone. A synapse is formed between the source and target neuron using this method (Breedlove, Watson, and Rosenzweig 2007). The synaptogenesis process is shown in Figure 4.3.
Puberty Blockers for Children: Can They Consent?
Published in The New Bioethics, 2022
Brain maturation continues in young people until at least the mid 20’s (Whiteford 2007) and sex hormones testosterone and oestrogen contribute to this development significantly (Goddings et al. 2013). Both androgens and oestrogens induce synaptogenesis and synaptic pruning in rat and non-human primates and it is likely that this process also occurs in humans, modulating brain growth across puberty. Sex hormone receptors for both oestrogens and androgens are found throughout the brain in varying concentrations, with high levels in subcortical regions, particularly the hippocampus and amygdala. (Goddings et al. 2013, p. 246)The effect of blocking the sex hormones during a critical age for brain development is unknown but must be of major concern. The effect of normal puberty on the brain may be dependent on the age at which puberty begins. Delaying this effect may have irreversible consequences. We simply do not know as yet.
Response of brain-derived neurotrophic factor to combining cognitive and physical exercise
Published in European Journal of Sport Science, 2018
Toshiaki Miyamoto, Saya Hashimoto, Hideya Yanamoto, Mai Ikawa, Yoshiki Nakano, Takashi Sekiyama, Keihou Kou, Shin-Ichiro Kashiwamura, Chisako Takeda, Hiroyuki Fujioka
BDNF is well known as one of the potential mediators responsible for the beneficial effects of PE on cognitive function (Coelho et al., 2013). BDNF, a protein and member of the neurotrophin family of growth factors, promotes angiogenesis, neurogenesis, and brain synaptogenesis (Deslandes et al., 2009; Eggermont, Swaab, Luiten, & Scherder, 2006; Lista & Sorrentino, 2010). Regardless of acute or chronic PE, moderate- to high-intensity PE has been shown to significantly increase peripheral BDNF levels and improve cognitive function (Erickson et al., 2011; Ferris, Williams, & Shen, 2007; Schmidt-Kassow et al., 2012). Through peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), moderate- to high-intensity PE induces the production of fibronectin type III domain-containing protein 5 (FNDC5) in the skeletal muscles. The FNDC5 is cleaved into irisin, which has the ability to cross the blood–brain barrier and induce BDNF expression in the hippocampus (Phillips, Baktir, Srivatsan, & Salehi, 2014). Therefore, it has been considered that the BDNF expression is regulated by PGC-1α in the skeletal muscles (Farshbaf et al., 2016).
Acute exercise increases BDNF serum levels in patients with Parkinson’s disease regardless of depression or fatigue
Published in European Journal of Sport Science, 2022
Lílian Viana dos Santos Azevedo, Jéssica Ramos Pereira, Renata Maria Silva Santos, Natalia Pessoa Rocha, Antônio Lúcio Teixeira, Paulo Pereira Christo, Victor Rodrigues Santos, Paula Luciana Scalzo
The brain-derived neurotrophic factor (BDNF), a member of the neurotrophins family, is critically important for specific processes, including neuron survival, the growth and differentiation of dendrites and axons, the regulation of synaptogenesis, and synaptic plasticity (Adachi, Numakawa, Richards, Nakajima, & Kunugi, 2014; He, Zhang, Yung, Zhu, & Wang, 2013). In central motor structures, BDNF may also improve dopaminergic neurotransmission and activate anti-apoptotic signaling cascades that enhance the survival of dopaminergic neurons (Adachi et al., 2014; He et al., 2013).