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Neurological disorders are diseases of the central and peripheral nervous system. In other words, the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction and muscles. We divide these disorders into two categories according to the primary type of dysfunction:
Disorders of cerebral circulation (hypoxia, cerebral ischemia, stroke, dementia). Disorders of the GABA system (parkinsonism, epilepsy, anxiety disorders, schizophrenia)
In chronic brain diseases – Alzheimer’s and Parkinson’s disease, epilepsy, depressive disorders, schizophrenia – oxidative stress prevails and harmful degenerative processes are continuous and progressing at an alarming rate.
The GABA system refers to the system for regulating the neurotransmitter gamma-aminobutyric acid (GABA) in the central nervous system (CNS). GABA is the main inhibitory neurotransmitter in the brain, which means that its main function is to reduce neuronal excitability in the CNS. This system has a key role in maintaining the balance between excitation and inhibition of neurons, which is essential for normal brain functioning.
Evolution has ensured that healthy and young nerve cells in the brain contain sufficient amounts of carnosine to protect these very important cells from damage and degenerative changes. The protective properties are mainly associated with the antioxidant effect of carnosine and the prevention of glycation and carbonyl processes. carnosine also protects the proteasome, which has a central role in removing harmful carbonylated proteins. carnosine stops the deformation of proteins and opens the way to prevent and delay the progression of Alzheimer’s disease and other types of dementia and mild cognitive impairment.
Oxidative stress increases the activity of the enzyme phospholipase A2 (PLA2), which breaks down the fatty acids of cell membranes, thereby causing disruption of membrane integrity and thus severe damage to cell function and even their death. carnosine not only reduces oxidative stress and the level of phospholipase A2 (PLA2), but also reduces the damage of other processes (glycation, carbonyl, AGEs).
Carnosine also acts as a neurotransmitter, anticonvulsant and chelating agent (binds heavy metals). Thanks to these abilities, it is a universal substance that protects against various neurological and mental disorders and diseases.
The use of common anesthetics often leads to an increase in serotonin melanoid (SDM). Carnosine protects against the neurotoxic effects of SDM. Therefore, carnosine may be an important tool to limit postoperative cognitive dysfunction.
In mice, carnosine prevents swelling, cell death, and free radical stress that occurs when the brain is deprived of blood (cerebral ischemia). Also, carnosine treatment significantly improved neurological function after a stroke-like event. It is not surprising that carnosine can affect neurological function, since carnosine is produced by the brain and that carnosine-specific transporters are found in parts of the blood-brain barrier.
Because carnosine binds zinc, it probably plays some role in controlling the availability of zinc ions in neuronal tissue, particularly in the olfactory lobe, where both carnosine and zinc are found in high amounts. This is important because the olfactory lobe controls the sense of smell – loss of smell is the first sign of neurodegeneration.
For various reasons, peroxidation of membrane lipids is the most significant damaging factor caused by free radicals on brain tissue. First, radical products accumulate and are then replaced by molecular products of lipid modification. Imine relationships and cross-links between the molecular components of neuronal membranes appear in the system (Kagan, 1988). This modification disrupts the plasticity of the membrane response to external signals and imposes limitations on the functions of the membrane as an excitation generator. At first, it seemed that the main processes of free radical damage to neurons consisted only in lipid modification. A remarkable similarity between the damage caused to excitable tissues by cerebral ischemia, some neurodegenerative diseases and aging has attracted considerable attention of researchers (Olanow, 1993; Smith, Collinge, 1995). carnosine inhibits lipid peroxidation and thus protects the cell membrane.
The anticonvulsant effect of carnosine has been observed in a preclinical model of epilepsy. The researchers applied pentylenetetrazol, which induces clonic seizures and myoclonic twitches in animals. Carnosine treatment resulted in a reduction in seizure stage and also prolonged the latency to myoclonic twitches in a dose-dependent manner.
Another study was conducted on animals that were artificially induced to have a stroke. Carnosine has shown a significant neuroprotective effect (protecting nerve cells from damage) in ischemic brains (brains that are insufficiently supplied with oxygen). The carnosine-supplemented rats had normal EKGs, less accumulated lactic acid (a general indicator of the severity of damage), and better parameters of blood circulation in the brain.
Carnosine has also been shown to moderate the toxic effect of zinc in vascular dementia. One of the key triggers in the pathogenesis of vascular dementia is zinc-induced neuronal death. A group of Japanese scientists investigated the effect of carnosine on immortalized hypothalamic neurons (GT-17), which are more sensitive to the toxic effect of zinc compared to some other neuronal cells. The results suggest that carnosine prevents neuronal cell death in a dose-dependent manner.
Fedorova, T.N., Devyatov, A.A., Berezhnoi, D.S., Stvolinskii, S.L., Morozova, M.P., Gavrilova, S.A. and Tutelyan, V.A., 2018. Oxidative status in different areas of the cerebral cortex of Wistar rats during focal ischemia and its modulation with carnosine. Bulletin of experimental biology and medicine, 165(6), pp.746-750.
Devyatov, A.A., Fedorova, T.N., Stvolinsky, S.L., Ryzhkov, I.N., Riger, N.A. and Tutelyan, V.A., 2018. Study of the neuroprotective effects of carnosine in an experimental model of focal cerebral ischemia/reperfusion. Biomedit sinskaya khimiya, 64(4), pp.344-348.
Davis, C.K., Laud, P.J., Bahor, Z., Rajanikant, G.K. and Majid, A., 2016. Systematic review and stratified meta-analysis of the efficacy of carnosine in animal models of ischemic stroke. Journal of Cerebral Blood Flow & Metabolism, 36(10), pp.1686-1694.
Ouyang, L., Tian, Y., Bao, Y., Xu, H., Cheng, J., Wang, B., Shen, Y., Chen, Z. and Lyu, J., 2016. Carnosine decreased neuronal cell death through targeting glutamate system and astrocyte mitochondrial bioenergetics in cultured neuron/astrocyte exposed to OGD/recovery. Brain research bulletin, 124, pp.76-84.
Mizuno, D. and Kawahara, M., 2014. Carnosine: A possible drug for vascular dementia. Journal of Vascular Medicine & Surgery.
Wu, X.H., Ding, M.P., Zhu-Ge, Z.B., Zhu, Y.Y., Jin, C.L. and Chen, Z., 2006. Carnosine, a precursor of histidine, ameliorates pentylenetetrazole-induced kindled seizures in rat. Neuroscience letters, 400(1-2), pp.146-149.
