Amphetamine-related drugs neurotoxicity in humans and in
experimental animals: Main mechanisms

J 2017

Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms

MORATALLA, Rosario; Amit Suresh KHAIRNAR; Nicola SIMOLA; Noelia GRANADO; Jose Ruben GARCIA-MONTES et al.

Základní údaje

Originální název

Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms

Autoři

MORATALLA, Rosario; Amit Suresh KHAIRNAR; Nicola SIMOLA; Noelia GRANADO; Jose Ruben GARCIA-MONTES; Pier Francesca PORCEDDU; Yousef TIZABI; Giulia COSTA a Micaela MORELLI

Vydání

PROGRESS IN NEUROBIOLOGY, OXFORD, PERGAMON-ELSEVIER SCIENCE LTD, 2017, 0301-0082

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30103 Neurosciences

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 14.163

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:14740/17:00097313

Organizační jednotka

Středoevropský technologický institut

Klíčová slova anglicky

Dopamine; Ecstasy; Methamphetamine; METH; MDMA; Mouse; Neurodegeneration; Neuroinflammation neurotoxicity; Non-human primate; Rat

Štítky

rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 16. 5. 2018 10:50, Mgr. Pavla Foltynová, Ph.D.

Anotace

V originále

Amphetamine-related drugs, such as 3,4-methylenedioxymethamphetamine (MDMA) and methamphetamine (METH), are popular recreational psychostimulants. Several preclinical studies have demonstrated that, besides having the potential for abuse, amphetamine-related drugs may also elicit neurotoxic and neuroinflammatory effects. The neurotoxic potentials of MDMA and METH to dopaminergic and serotonergic neurons have been clearly demonstrated in both rodents and nonhuman primates. This review summarizes the species-specific cellular and molecular mechanisms involved in MDMA and METH-mediated neurotoxic and neuroinflammatory effects, along with the most important behavioral changes elicited by these substances in experimental animals and humans. Emphasis is placed on the neuropsychological and neurological consequences associated with the neuronal damage. Moreover, we point out the gap in our knowledge and the need for developing appropriate therapeutic strategies to manage the neurological problems associated with amphetamine-related drug abuse. (C) 2015 Elsevier Ltd. All rights reserved.

Citovat

MORATALLA, Rosario; Amit Suresh KHAIRNAR; Nicola SIMOLA; Noelia GRANADO; Jose Ruben GARCIA-MONTES; Pier Francesca PORCEDDU; Yousef TIZABI; Giulia COSTA a Micaela MORELLI. Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms. PROGRESS IN NEUROBIOLOGY. OXFORD: PERGAMON-ELSEVIER SCIENCE LTD, 2017, roč. 155, August, s. 149-170. ISSN 0301-0082. Dostupné z: https://doi.org/10.1016/j.pneurobio.2015.09.011.

@article{1386743,
   author = {Moratalla, Rosario and Khairnar, Amit Suresh and Simola, Nicola and Granado, Noelia and GarciaandMontes, Jose Ruben and Porceddu, Pier Francesca and Tizabi, Yousef and Costa, Giulia and Morelli, Micaela},
   article_location = {OXFORD},
   article_number = {August},
   doi = {https://doi.org/10.1016/j.pneurobio.2015.09.011},
   keywords = {Dopamine; Ecstasy; Methamphetamine; METH; MDMA; Mouse; Neurodegeneration; Neuroinflammation neurotoxicity; Non-human primate; Rat},
   language = {eng},
   issn = {0301-0082},
   journal = {PROGRESS IN NEUROBIOLOGY},
   title = {Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms},
   url = {http://www.sciencedirect.com/science/article/pii/S0301008215001008?via%3Dihub},
   volume = {155},
   year = {2017}
}

TY  - JOUR
ID  - 1386743
AU  - Moratalla, Rosario - Khairnar, Amit Suresh - Simola, Nicola - Granado, Noelia - Garcia-Montes, Jose Ruben - Porceddu, Pier Francesca - Tizabi, Yousef - Costa, Giulia - Morelli, Micaela
PY  - 2017
TI  - Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms
JF  - PROGRESS IN NEUROBIOLOGY
VL  - 155
IS  - August
SP  - 149-170
EP  - 149-170
PB  - PERGAMON-ELSEVIER SCIENCE LTD
SN  - 03010082
KW  - Dopamine
KW  - Ecstasy
KW  - Methamphetamine
KW  - METH
KW  - MDMA
KW  - Mouse
KW  - Neurodegeneration
KW  - Neuroinflammation neurotoxicity
KW  - Non-human primate
KW  - Rat
UR  - http://www.sciencedirect.com/science/article/pii/S0301008215001008?via%3Dihub
L2  - http://www.sciencedirect.com/science/article/pii/S0301008215001008?via%3Dihub
N2  - Amphetamine-related drugs, such as 3,4-methylenedioxymethamphetamine (MDMA) and methamphetamine (METH), are popular recreational psychostimulants. Several preclinical studies have demonstrated that, besides having the potential for abuse, amphetamine-related drugs may also elicit neurotoxic and neuroinflammatory effects. The neurotoxic potentials of MDMA and METH to dopaminergic and serotonergic neurons have been clearly demonstrated in both rodents and nonhuman primates. This review summarizes the species-specific cellular and molecular mechanisms involved in MDMA and METH-mediated neurotoxic and neuroinflammatory effects, along with the most important behavioral changes elicited by these substances in experimental animals and humans. Emphasis is placed on the neuropsychological and neurological consequences associated with the neuronal damage. Moreover, we point out the gap in our knowledge and the need for developing appropriate therapeutic strategies to manage the neurological problems associated with amphetamine-related drug abuse. (C) 2015 Elsevier Ltd. All rights reserved.
ER  -

MORATALLA, Rosario; Amit Suresh KHAIRNAR; Nicola SIMOLA; Noelia GRANADO; Jose Ruben GARCIA-MONTES; Pier Francesca PORCEDDU; Yousef TIZABI; Giulia COSTA a Micaela MORELLI. Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms. \textit{PROGRESS IN NEUROBIOLOGY}. OXFORD: PERGAMON-ELSEVIER SCIENCE LTD, 2017, roč.~155, August, s.~149-170. ISSN~0301-0082. Dostupné z: https://doi.org/10.1016/j.pneurobio.2015.09.011.

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