Carnosine and Neurological Disorders

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 will classify these disorders into 2 categories to the primary type of dysfunction involved:

  1. Cerebral Circulation Disorders (hypoxia, cerebral ischemia, stroke, dementia)
  2. GABA System Disorders (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 progress at an alarming pace.

GABA is the major inhibitory neurotransmitter in the brain. Participates in the regulation of neuronal stimulus and is directly responsible for the regulation of muscle tone (less GABA – stronger hyper-tonus) Carnosine is a reserve form of GABA in CNS, which is used to maintain the level of GABA at a necessary level.

Karnozin Extra is a universal neuro-protector.

Evolution has ensured that healthy and young nerve cells of the brain contain a sufficient amount of carnosine to protect these very important cells from damage and degenerative changes. The protective qualities are mainly related to the antioxidant effect of carnosine and prevention of glycation and carbonylation. Also, carnosine protects the proteasome, which have a central role in the removal of 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 fatty acids of cell membranes, thus causes distortion of membrane integrity and therefore difficult damage of cells’ function and even their death. Carnosine not only reduces oxidative stress and level of the phospholipase A2 (PLA2) but also reduces the damage of other processes (glycation, carbonylation, AGEs).

Carnosine also acts as a neurotransmitter, anticonvulsant agent and chelating substance (bind heavy metals). Because of these capabilities, it is a universal substance that protects against a variety of neurological and mental disorders and diseases.

Taking common anaesthetics often results in an increase in serotonin-derived melanoid (SDM). Carnosine protects against the neurotoxic effects of SDM. Therefore, Carnosine may be an important tool for limiting postoperative cognitive dysfunction.

In mice, Carnosine prevents the swelling, cell death, and free radical stress that occurs when the brain is starved of blood (cerebral ischemia). Also, treatment with Carnosine significantly improved neurological function after a stroke-like event. That Carnosine can affect neurological function is no surprise seeing as Carnosine is produced by the brain and that Carnosine-specific transporters are found in parts of the blood-brain barrier.

Because Carnosine binds to zinc, it likely plays some role in controlling the availability of zinc ions in neuronal tissue, especially the olfactory lobe where both Carnosine and zinc are found in high amounts. This is important because the olfactory lobe controls smell – a loss of which is the first sign of neurodegeneration.

Carnosine increases mental capability in schizophrenics.

For a variety of reasons, peroxidation of membrane lipids is the most significant damaging factor inflicted by free radicals on brain tissue. Radical products are accumulated first, and then they are replaced by the molecular products of lipid modification. Imine relations and cross-links between molecular components of neuronal membranes appear in the system (Kagan, 1988). This modification disturbs the plasticity of the membrane response to external signals and imposes restrictions on the membrane functions as generators of excitation. It appeared at first sight that the main processes of free radical damage to neurons consist only in lipid modification. Considerable attention of researches was attracted to the remarkable similarity between the damages induced to excitable tissues by brain ischemia, some neurodegenerative diseases, and ageing (Olanow, 1993; Smith, Collinge, 1995). Carnosine inhibits lipids peroxidation and therefore protects cell membrane.

Anticonvulsant effect of carnosine was observed in a preclinical epilepsy model. The researchers applied pentylenetetrazol which induces clonic seizures and myoclonic twitches in animals. Treatment with carnosine resulted in a reduction of seizure stage and also prolonged the latency to myoclonic twitches in a dose-dependent manner.

Another study was conducted on animals to which was artificially induced brain attack. Carnosine has demonstrated significant neuroprotective effect (protection of nerve cells from damages) in ischemic brains (brain which is insufficiently supplied with oxygen). Rats supplemented with carnosine had a normal EKG, a smaller amount of accumulated lactic acid (a general indicator of the severity of damage) and showed better parameters of blood circulation in the brain.

Carnosine was also shown to have implications in ameliorating 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 examined the effect of carnosine on immortalized hypothalamic neurons (GT-17), which are more sensitive to toxic zinc effect in comparison to some other neuronal cells. The results indicate that carnosine prevents neuronal cell death in a dose-dependent mannner.


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 medicine165(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. Biomeditsinskaya khimiya64(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 & Metabolism36(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 bulletin124, 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 letters400(1-2), pp.146-149.