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Diseases of the Nervous System
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
In addition to the various direct neurological alterations brought about by the lesion of the function and structural system, specific symptoms may be associated with the involvement of focal regions of the cerebral hemispheres (Figure 1). Damage to the frontal lobe causes changes in mood and careless behaviour; parietal lobe damage produces inability to formulate ideas or to carry out actions through the transmission of the motor pathways. This may be associated with sensory inattention. These defects may be due to a hemisphere damage or to localized impairment of biochemical processes. Temporal lobe involvement is often linked with seizures; extensive bilateral changes lead to pronounced memory disturbances. Lesions of the occipital lobe cause vision defects and bring about hallucinations. Diffuse degenerative conditions involving central regions can be associated with generalized hyperreflexia and dysarthria. Lesions of the hypothalamus and pituitary may produce endocrine diseases. Besides these important interrelationships and generalized effects, only some specialized aspects of brain metabolism, which are peculiar to the nervous system, will be discussed in this chapter. Particularly, the role of neurotransmitters, certain amino acids, and neuropeptides will be emphasized.256,334,340,346,450,451,520,598,602,616 This information is essential for the basic understanding of the interplay of biochemical and associated pathological alterations that underlie the clinical manifestations of neurological disease processes.
Images from Radioactivity: Radionuclide Scans, SPECT, and PET
Published in Suzanne Amador Kane, Boris A. Gelman, Introduction to Physics in Modern Medicine, 2020
Suzanne Amador Kane, Boris A. Gelman
These nuclear medicine imaging techniques can play a role in diagnosing brain cancer, differentiating between different kinds of dementia, assessing stroke, and diagnosing and planning treatments for some forms of epilepsy. They are also being used to explore the causes of conditions such as speech disorders, depression, learning disorders, and drug dependency. Using PET, functional MRI (Chapter 8), and electrical imaging techniques, brain metabolism in living patients afflicted with psychiatric disorders such as schizophrenia and depression can be studied. In addition, PET and functional MRI have opened new frontiers in basic research into mental processes. It is important to be clear about what can be measured in this research. PET cannot allow researchers to literally see thoughts, emotions, or memories, although such analogies often are used in the popular media. The brain works as a network, and most mental processes cannot be neatly localized into a specific part of the brain that “lights up” during a scan. Scientists can use PET to measure quantities that reflect the brain's metabolic activity – its use of energy and biochemicals – in broadly defined regions. PET also has important limitations. Each scan takes much longer than the time required for nerve cells to send a signal. Since PET has such a poor spatial resolution, typically several mm at best, it may miss essential, small-scale details in the brain's activity. However, when researchers bear in mind problems such as these, PET brain scans can yield important clues to outstanding problems in neuroscience.
Cerebral Metabolic Impairments
Published in Zaven S. Khachaturian, Teresa S. Radebaugh, Alzheimer’s Disease, 2019
In humans, the brain typically accounts for about 2% of body weight and 20% of the oxygen utilized, making the nervous system the “most oxidative” tissue in the body. (See Reference 5 for a detailed discussion of brain metabolism). The major and quantitatively only significant pathways for cerebral oxidative metabolism are glycolysis (glucose to pyruvate/lactate), pyruvate dehydrogenase (pyruvate to acetyl-coenzyme A), the Krebs tricarboxylic acid cycle (formation of CO2 and reducing equivalents), and electron transport (oxidation of reducing equivalents to H2O). Glycolysisoccurs in the cytosol, and the tricarboxylic acid cycle and electron transport in the inner mitochondrial compartment (Figure 1).
Brain Health: A Concept Analysis
Published in Issues in Mental Health Nursing, 2021
Boniface Harerimana, Cheryl Forchuk, Julie Walsh, Jennifer Fogarty, Michael Borrie
Evidence regarding the beneficial effect of mitochondrial metabolic functions on brain health is scarce. An available scholarly work by Castro et al. (2018) indicated that chaperones’ roles in mitochondrial protein homeostasis (mitostasis) processes, (re)folding and degradation can prevent the accumulation of different types of damaging particles, such as ROS and mitochondrial DNA mutations or misfolded/aggregated proteins. Chaperone plays a role in alleviating mitochondrial dysfunction. Mitochondrial dysfunctions lead to oxidative stress which can affect brain metabolism and lead to the resistance of insulin, not only initially in the brain but also peripheral tissues later on (Castro et al., 2018). As a result, the insulin resistance may hamper the whole-body metabolic homeostasis, a metabolic shift that precedes aging, neurodegenerative and metabolic disease onset and progression (Castro et al., 2018).
Akkermansia muciniphila and environmental enrichment reverse cognitive impairment associated with high-fat high-cholesterol consumption in rats
Published in Gut Microbes, 2021
Sara G. Higarza, Silvia Arboleya, Jorge L. Arias, Miguel Gueimonde, Natalia Arias
One additional finding is the decrease in brain metabolic levels when introducing EE, which was clearly observed not only in the HFHC+EE group but also in the NC+EE group. Decreased brain CCO activity after EE has been previously reported by several authors in rats and mice, and may be related to higher metabolic efficiency requiring less energy demands by brain cells to perform an improved behavioral response39,40 by comparison to the HFHC condition. These results are in line with previous data by Tong et al.41 showing that exercise decreased the hippocampal expression of genes involved in mitochondrial metabolic processes, including cytochrome c-oxidase. In fact, physical activity and EE have been found to regulate metabolic and redox activity, resulting in beneficial modulation of brain function.42 Similarly, our results support the overall effect of EE on brain metabolism through the reduction in metabolic levels in both healthy and HFHC conditions. However, a better understanding of the EE-induced brain network modifications could be a key factor to understand mechanisms of memory processes and thus would help to develop new therapeutic strategies to alleviate memory deficits such as those related to HFHC brain dysfunction.
Hypothermia prevents hippocampal oxidative stress and apoptosis via the GSK-3β/Nrf2/HO-1 signaling pathway in a rat model of cardiac arrest-induced brain damage
Published in Neurological Research, 2020
Meng-Yuan Diao, Jinhao Zheng, Yi Shan, Shaosong Xi, Ying Zhu, Wei Hu, Zhaofen Lin
CA interrupts cardiac function, which leads to cessation of organ blood flow and damage to multiple organs, including the brain. Global brain I/R injury after CA results in heterogeneous injury to the brain, and the hippocampus is among the most vulnerable areas. Hypothermia therapy has been demonstrated to be effective in a large number of clinical studies and has been strongly recommended by many professional associations [7,8]. The effect of hypothermia on preserving neurological function occurs throughout the brain after CA. Hypothermia may play a neuroprotective role through a variety of molecular mechanisms during the above single or collaborative phases, including decreasing brain metabolism, reducing ROS production, attenuating excitatory amino-acid release, decreasing immune responses during reperfusion, and inhibiting apoptosis [23].