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Comparison of Healing Effect of DMSP in Green Sea Algae and Mesenchymal Stem Cells on Various Inflammatory Disorders
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Alzheimer’s disease is the most common dementia. Many reports indicated that microglia activation and amyloid deposits appear at the early stage and then tau and Aβ fibrillary tangles were formed with aging (Wyss-Coray et al., 1997; Yan et al., 1997; Arends, 2000; Uboga & Price, 2000; Heneka et al., 2012; Boche & Nicoll, 2013). These incidences result in the disfunction of medial temporal lobe consisting of structures that are vital for declarative or long-term memory (Collie & Maruff, 2000). However, recent studies reveal that the extent of Aβ deposition and senile tangles (plaques) in the brain does not necessarily correlate with dementia because healthy elderly people can exhibit abundant plaques even in the absence of AD. Moreover, the recent findings have indicated that neurogenerative disorders are related to loss of function, aggregation, deposition and degradation of misfolding proteins in the brain (Adav & Sze, 2016). Neurofunctional studies demonstrate that age-related atrophy is incident in the hippocampal region (retrosplenial region/posterior cingulate cortex, left hippocampus, and bilateral inferior and middle frontal areas) (DE Vogelaere, 2012; Du et al., 2006). Whereas recent other reports indicated that earliest pathological diagnosis of Alzheimer’s disease is possible by the determination of the mounts of several amyloid-beta-associated peptide fragments in the blood by immunoprecipitation-coupled with mass spectrometry (Nakamura et al., 2018). For the moment, the effect of MSCs on Alzheimer’s disease are described in brief.
Fatigue, Automation, and Autonomy: Challenges for Operator Attention, Effort, and Trust
Published in Mustapha Mouloua, Peter A. Hancock, James Ferraro, Human Performance in Automated and Autonomous Systems, 2019
Gerald Matthews, Ryan Wohleber, Jinchao Lin, April Rose Panganiban
Why does sustaining attention lead to task disengagement? In fact, there are three, complementary, types of explanation (corresponding to different levels of explanation within cognitive science; Matthews, Lin, & Wohleber, 2017). First, repetitive stimuli that provide little positive reinforcement affect neural systems that influence energy and fatigue, contributing to boredom (Cummings, Gao, & Thornburg, 2016; Scerbo, 2001). Brain-imaging studies link boredom and mind-wandering to the default mode network (DMN) that includes the posterior cingulate cortex, precuneus, and areas of the prefrontal cortex, as well as parietal and temporal areas (e.g., Danckert & Merrifield, 2017). A second type of explanation is provided by the resource theory of vigilance decrement (Warm, Dember, et al., 1996, Warm, Parasuraman, et al., 2008a). Prolonged signal detection under high cognitive load leads to depletion of resources and loss of vigilance. Subjective task engagement appears to be a reliable marker for resource availability (Matthews et al., 2010, 2013). However, resource depletion may not explain performance deficits in low-workload task environments.
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Until further information is available, it is perhaps best to state that the cortical regions of the limbic system occupy intermediate associative positions between the functions of the specific areas of the cerebral cortex and functions of the subcortical limbic structures for control of behavioral patterns. Thus, in the anterior temporal cortex, one especially finds gustatory and olfactory behavioral associations. In the parahippocampal gyri, there is a tendency for complex auditory associations and complex thought associations derived from Wernicke's area of the posterior temporal lobe. In the middle and posterior cingulate cortex, there is reason to believe that sensorimotor behavioral associations occur. Short-term memory loss is often seen in the chemically sensitive and this improves by decreasing the total body pollutant load by eliminating and neutralizing specific triggering agents.
Carnosine in health and disease
Published in European Journal of Sport Science, 2019
Guilherme Giannini Artioli, Craig Sale, Rebecca Louise Jones
Carnosine synthase, an enzyme present in the human skeletal muscle, has been reported in different areas of the mammalian brain (Murakami & Furuse, 2010). As well as carnosine, this ATP-dependent enzyme can synthesise homocarnosine, although this occurs at a lower efficiency. Carnosine is likely to be taken up into brain regions following its release from glial cells, since neurons, mainly those of the olfactory bulb (where carnosine is in greater concentrations), are unable to synthesise carnosine (Hoffmann, Bakardjiev & Bauer, 1996). β-Alanine can be rapidly transported into the brain, with research in rodents demonstrating increased carnosine content in the cerebral cortex and hypothalamus following β-alanine supplementation (Murakami & Furuse, 2010). In vitro studies with isolated human retina showed that β-alanine can be transported into and can accumulate in neuronal cells (Bruun & Ehinger, 1974). It is unclear, however, whether brain carnosine can be increased with β-alanine supplementation and, if so, in what regions this would occur. An in vivo study assessing the effects of β-alanine supplementation on brain carnosine in humans has shown no increase in carnosine in the posterior cingulate cortex following four weeks of β-alanine supplementation (Solis et al., 2015). Notably, the posterior cingulate cortex is highly active and fulfils various functions, such as memory, focus of attention, processing and learning. It must be noted, however, that there are limitations in non-invasive quantification of carnosine in the human brain, such as the inability to distinguish carnosine from homocarnosine signals. It remains unknown whether other areas can benefit from β-alanine supplementation.