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AMYLOID SPECIES, NEUROCHEMISTRY AND AUTOIMMUNITY LINKED TO PARKINSONIAN-LIKE SYMPTOMS

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Артикул: 622944.01.99
Sewell, R. AMYLOID SPECIES, NEUROCHEMISTRY AND AUTOIMMUNITY LINKED TO PARKINSONIAN-LIKE SYMPTOMS / R. Sewell, M. A. Gruden. - Текст : электронный // Znanium.com. - 2017. - №1-12. - URL: https://znanium.com/catalog/product/529092 (дата обращения: 25.04.2024)
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for each cannabinoid receptor or for the proteins involved in endocannabinoids inactivation. The generation of genetically modified mice with selective mutations in these endocannabinoid system components has now provided important advances in establishing their specific contribution to drug addiction. These genetic tools have identified the particular interest of CB1 cannabinoid receptor and endogenous anandamide as potential targets for drug addiction treatment. Novel genetic tools will allow determining if the modulation of CB2 cannabinoid receptor activity and 2-arachidonoylglycerol tone can also have an important therapeutic relevance for drug addiction.
     References
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2. Flores A, Maldonado R, Berrendero F. Cannabinoid-hypocretin crosstalk in the central nervous system: what we know so far. Front Neurosci. 2013 Dec 20;7:256. doi: 10.3389/fnins.2013.00256.
3. Maldonado R1, Robledo P, Berrendero F. Endocannabinoid system and drug addiction: new insights from mutant mice approaches. Curr Opin Neurobiol. 2013     Aug;23(4):480-6. doi:    10.1016/j.conb.2013.02.004.
   Epub 2013 Mar 13.
4. Maldonado R, Berrendero F, Ozaita A,  Robledo P.  Neurochemical basis
   of cannabis addiction. Neuroscience. 2011 May 5;181:1-17.
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   and their role in nicotine addiction. Curr Drug Targets. 2010 Apr;11(4):440-9. Review.
DOI:10.12737/12271





                AMYLOID SPECIES, NEUROCHEMISTRY AND AUTOIMMUNITY LINKED TO PARKINSONIAN-LIKE SYMPTOMS




R. D. E. Sewell¹, M. A. Gruden²

¹Cardiff School of Pharmacy & Pharmaceutical Sciences, Cardiff University, Cardiff, CF10 3NU., UK,
²P. K. Anokhin Research Institute of Normal Physiology, Moscow, 125009, Russia

     Parkinson’s disease (PD) is a neurodegenerative disorder in which a-synuclein (a-syn) toxic aggregates specifically from the synuclein protein family and neurotransmitters such as dopamine (DA) play a critical role. a-Syn itself is known to be natively unstructured but it is in equilibrium with subpopulations of more compact structures and it is these aggregates that are thought to be linked to amyloid formation. In this respect, there are elevated autoantibody serum titers to a-synuclein monomers, oligomers and fibrils which appear to reach a zenith in Parkinsonian patients at the 5-year disease stage (Gruden et al., 2011). We have also demonstrated that in vitro, a-syn can form

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