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Flicker Leon, Grimley Evans John (2004). «Piracetam for dementia or cognitive impairment». Cochrane Database of Systematic Reviews (1). PMID11405971. doi:10.1002/14651858.CD001011/abstract.|fechaacceso= requiere |url= (ayuda)
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Mori K, Obara Y, Hirota M, et al. (September 2008). «Nerve growth factor-inducing activity of Hericium erinaceus in 1321N1 human astrocytoma cells». Biol. Pharm. Bull.31 (9): 1727-1732. PMID18758067. doi:10.1248/bpb.31.1727.
Mori K, Inatomi S, Ouchi K, Azumi Y, Tuchida T (March 2009). «Improving effects of the mushroom Yamabushitake (Hericium erinaceus) on mild cognitive impairment: a double-blind placebo-controlled clinical trial». Phytotherapy Research23 (3): 367-372. PMID18844328. doi:10.1002/ptr.2634.
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«Rosmarinus officinalis L. leaf extract improves memory impairment and affects acetylcholinesterase and butyrylcholinesterase activities in rat brain». Fitoterapia91: 261-71. 2013. PMID24080468. doi:10.1016/j.fitote.2013.09.012.
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Spencer RC, Devilbiss DM, Berridge CW (June 2015). «The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex». Biol. Psychiatry77 (11): 940-950. PMID25499957. doi:10.1016/j.biopsych.2014.09.013. «The procognitive actions of psychostimulants are only associated with low doses. Surprisingly, despite nearly 80 years of clinical use, the neurobiology of the procognitive actions of psychostimulants has only recently been systematically investigated. Findings from this research unambiguously demonstrate that the cognition-enhancing effects of psychostimulants involve the preferential elevation of catecholamines in the PFC and the subsequent activation of norepinephrine α2 and dopamine D1 receptors. […] This differential modulation of PFC-dependent processes across dose appears to be associated with the differential involvement of noradrenergic α2 versus α1 receptors. Collectively, this evidence indicates that at low, clinically relevant doses, psychostimulants are devoid of the behavioral and neurochemical actions that define this class of drugs and instead act largely as cognitive enhancers (improving PFC-dependent function). This information has potentially important clinical implications as well as relevance for public health policy regarding the widespread clinical use of psychostimulants and for the development of novel pharmacologic treatments for attention-deficit/hyperactivity disorder and other conditions associated with PFC dysregulation.»
Ilieva IP, Hook CJ, Farah MJ (January 2015). «Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis». J. Cogn. Neurosci.: 1-21. PMID25591060. doi:10.1162/jocn_a_00776. «The present meta-analysis was conducted to estimate the magnitude of the effects of methylphenidate and amphetamine on cognitive functions central to academic and occupational functioning, including inhibitory control, working memory, short-term episodic memory, and delayed episodic memory. In addition, we examined the evidence for publication bias. Forty-eight studies (total of 1,409 participants) were included in the analyses. We found evidence for small but significant stimulant enhancement effects on inhibitory control and short-term episodic memory. Small effects on working memory reached significance, based on one of our two analytical approaches. Effects on delayed episodic memory were medium in size. However, because the effects on long-term and working memory were qualified by evidence for publication bias, we conclude that the effect of amphetamine and methylphenidate on the examined facets of healthy cognition is probably modest overall. In some situations, a small advantage may be valuable, although it is also possible that healthy users resort to stimulants to enhance their energy and motivation more than their cognition. […] Earlier research has failed to distinguish whether stimulants’ effects are small or whether they are nonexistent (Ilieva et al., 2013; Smith & Farah, 2011). The present findings supported generally small effects of amphetamine and methylphenidate on executive function and memory. Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities. […] The results of this meta-analysis cannot address the important issues of individual differences in stimulant effects or the role of motivational enhancement in helping perform academic or occupational tasks. However, they do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size.»
Wood S, Sage JR, Shuman T, Anagnostaras SG (January 2014). «Psychostimulants and cognition: a continuum of behavioral and cognitive activation». Pharmacol. Rev.66 (1): 193-221. PMID24344115. doi:10.1124/pr.112.007054.
Lindemann L, Hoener MC (May 2005). «A renaissance in trace amines inspired by a novel GPCR family». Trends Pharmacol. Sci.26 (5): 274-281. PMID15860375. doi:10.1016/j.tips.2005.03.007. «In addition to the main metabolic pathway, TAs can also be converted by nonspecific N-methyltransferase (NMT) [22] and phenylethanolamine N-methyltransferase (PNMT) [23] to the corresponding secondary amines (e.g. synephrine [14], N-methylphenylethylamine and N-methyltyramine [15]), which display similar activities on TAAR1 (TA1) as their primary amine precursors. […] Both dopamine and 3-methoxytyramine, which do not undergo further N-methylation, are partial agonists of TAAR1 (TA1). The dysregulation of TA levels has been linked to several diseases, which highlights the corresponding members of the TAAR family as potential targets for drug development. In this article, we focus on the relevance of TAs and their receptors to nervous system-related disorders, namely schizophrenia and depression; however, TAs have also been linked to other diseases such as migraine, attention deficit hyperactivity disorder, substance abuse and eating disorders [7,8,36]. Clinical studies report increased β-PEA plasma levels in patients suffering from acute schizophrenia [37] and elevated urinary excretion of β-PEA in paranoid schizophrenics [38], which supports a role of TAs in schizophrenia. As a result of these studies, β-PEA has been referred to as the body’s ‘endogenous amphetamine’ [39]».
«Psychostimulants and Cognition: A Continuum of Behavioral and Cognitive Activation». PHARMACOLOGICAL REVIEWS66: 193-221. 2014. doi:10.1124/pr.112.007054.
NEAL R. CUTLER et al. (septiembre de 1993). «The Use of the Computerized Neuropsychological Test Battery (CNTB) in an Efficacy and Safety Trial of BMY 21,502 in Alzheimer's Disease». Annals of the New York Academy of Sciences695: 332-336. doi:10.1111/j.1749-6632.1993.tb23079.x.La referencia utiliza el parámetro obsoleto |mes= (ayuda)
«Medications for dementia: New drugs, mechanisms are coming for Alzheimer's disease». The Journal of Family Practice1 (6). June 2002. Archivado desde el original el 6 de abril de 2012. Consultado el 8 de julio de 2015. «PTI-00703 is a beta-amyloid inhibitor derived from the cat's claw, a woody vine found in the Peruvian rain forest. It is being tested in patients with mild-to-moderate AD [Alzheimer's disease].», which cites:
Lanni C, Lenzken SC, Pascale A, et al. (March de 2008). «Cognition enhancers between treating and doping the mind». Pharmacol. Res.57 (3): 196-213. PMID18353672. doi:10.1016/j.phrs.2008.02.004.La referencia utiliza el parámetro obsoleto |mes= (ayuda)
Flicker Leon, Grimley Evans John (2004). «Piracetam for dementia or cognitive impairment». Cochrane Database of Systematic Reviews (1). PMID11405971. doi:10.1002/14651858.CD001011/abstract.|fechaacceso= requiere |url= (ayuda)
Rocchetti, M; Crescini, A; Borgwardt, S; Caverzasi, E; Politi, P; Atakan, Z; Fusar-Poli, P (November 2013). «Is cannabis neurotoxic for the healthy brain? A meta-analytical review of structural brain alterations in non-psychotic users». Psychiatry and clinical neurosciences67 (7): 483-492. PMID24118193.
Gualtieri F, Manetti D, Romanelli MN, Ghelardini C (2002). «Design and study of piracetam-like nootropics, controversial members of the problematic class of cognition-enhancing drugs». Curr. Pharm. Des.8 (2): 125-138. PMID11812254. doi:10.2174/1381612023396582.
Kolotushkina EV, Moldavan MG, Voronin KY, Skibo GG (2003). «The influence of Hericium erinaceus extract on myelination process in vitro». Fiziol Zh49 (1): 38-45. PMID12675022.
Mori K, Obara Y, Hirota M, et al. (September 2008). «Nerve growth factor-inducing activity of Hericium erinaceus in 1321N1 human astrocytoma cells». Biol. Pharm. Bull.31 (9): 1727-1732. PMID18758067. doi:10.1248/bpb.31.1727.
Mori K, Inatomi S, Ouchi K, Azumi Y, Tuchida T (March 2009). «Improving effects of the mushroom Yamabushitake (Hericium erinaceus) on mild cognitive impairment: a double-blind placebo-controlled clinical trial». Phytotherapy Research23 (3): 367-372. PMID18844328. doi:10.1002/ptr.2634.
«Rosmarinus officinalis L. leaf extract improves memory impairment and affects acetylcholinesterase and butyrylcholinesterase activities in rat brain». Fitoterapia91: 261-71. 2013. PMID24080468. doi:10.1016/j.fitote.2013.09.012.
Spencer RC, Devilbiss DM, Berridge CW (June 2015). «The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex». Biol. Psychiatry77 (11): 940-950. PMID25499957. doi:10.1016/j.biopsych.2014.09.013. «The procognitive actions of psychostimulants are only associated with low doses. Surprisingly, despite nearly 80 years of clinical use, the neurobiology of the procognitive actions of psychostimulants has only recently been systematically investigated. Findings from this research unambiguously demonstrate that the cognition-enhancing effects of psychostimulants involve the preferential elevation of catecholamines in the PFC and the subsequent activation of norepinephrine α2 and dopamine D1 receptors. […] This differential modulation of PFC-dependent processes across dose appears to be associated with the differential involvement of noradrenergic α2 versus α1 receptors. Collectively, this evidence indicates that at low, clinically relevant doses, psychostimulants are devoid of the behavioral and neurochemical actions that define this class of drugs and instead act largely as cognitive enhancers (improving PFC-dependent function). This information has potentially important clinical implications as well as relevance for public health policy regarding the widespread clinical use of psychostimulants and for the development of novel pharmacologic treatments for attention-deficit/hyperactivity disorder and other conditions associated with PFC dysregulation.»
Ilieva IP, Hook CJ, Farah MJ (January 2015). «Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis». J. Cogn. Neurosci.: 1-21. PMID25591060. doi:10.1162/jocn_a_00776. «The present meta-analysis was conducted to estimate the magnitude of the effects of methylphenidate and amphetamine on cognitive functions central to academic and occupational functioning, including inhibitory control, working memory, short-term episodic memory, and delayed episodic memory. In addition, we examined the evidence for publication bias. Forty-eight studies (total of 1,409 participants) were included in the analyses. We found evidence for small but significant stimulant enhancement effects on inhibitory control and short-term episodic memory. Small effects on working memory reached significance, based on one of our two analytical approaches. Effects on delayed episodic memory were medium in size. However, because the effects on long-term and working memory were qualified by evidence for publication bias, we conclude that the effect of amphetamine and methylphenidate on the examined facets of healthy cognition is probably modest overall. In some situations, a small advantage may be valuable, although it is also possible that healthy users resort to stimulants to enhance their energy and motivation more than their cognition. […] Earlier research has failed to distinguish whether stimulants’ effects are small or whether they are nonexistent (Ilieva et al., 2013; Smith & Farah, 2011). The present findings supported generally small effects of amphetamine and methylphenidate on executive function and memory. Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities. […] The results of this meta-analysis cannot address the important issues of individual differences in stimulant effects or the role of motivational enhancement in helping perform academic or occupational tasks. However, they do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size.»
Bagot KS, Kaminer Y (April 2014). «Efficacy of stimulants for cognitive enhancement in non-attention deficit hyperactivity disorder youth: a systematic review». Addiction109 (4): 547-557. PMID24749160.
Wood S, Sage JR, Shuman T, Anagnostaras SG (January 2014). «Psychostimulants and cognition: a continuum of behavioral and cognitive activation». Pharmacol. Rev.66 (1): 193-221. PMID24344115. doi:10.1124/pr.112.007054.
Lindemann L, Hoener MC (May 2005). «A renaissance in trace amines inspired by a novel GPCR family». Trends Pharmacol. Sci.26 (5): 274-281. PMID15860375. doi:10.1016/j.tips.2005.03.007. «In addition to the main metabolic pathway, TAs can also be converted by nonspecific N-methyltransferase (NMT) [22] and phenylethanolamine N-methyltransferase (PNMT) [23] to the corresponding secondary amines (e.g. synephrine [14], N-methylphenylethylamine and N-methyltyramine [15]), which display similar activities on TAAR1 (TA1) as their primary amine precursors. […] Both dopamine and 3-methoxytyramine, which do not undergo further N-methylation, are partial agonists of TAAR1 (TA1). The dysregulation of TA levels has been linked to several diseases, which highlights the corresponding members of the TAAR family as potential targets for drug development. In this article, we focus on the relevance of TAs and their receptors to nervous system-related disorders, namely schizophrenia and depression; however, TAs have also been linked to other diseases such as migraine, attention deficit hyperactivity disorder, substance abuse and eating disorders [7,8,36]. Clinical studies report increased β-PEA plasma levels in patients suffering from acute schizophrenia [37] and elevated urinary excretion of β-PEA in paranoid schizophrenics [38], which supports a role of TAs in schizophrenia. As a result of these studies, β-PEA has been referred to as the body’s ‘endogenous amphetamine’ [39]».
Fuller, SJ; Tan, RS; Martins, RN (September 2007). «Androgens in the etiology of Alzheimer's disease in aging men and possible therapeutic interventions». Journal of Alzheimer's disease : JAD12 (2): 129-142. PMID17917157.
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«Medications for dementia: New drugs, mechanisms are coming for Alzheimer's disease». The Journal of Family Practice1 (6). June 2002. Archivado desde el original el 6 de abril de 2012. Consultado el 8 de julio de 2015. «PTI-00703 is a beta-amyloid inhibitor derived from the cat's claw, a woody vine found in the Peruvian rain forest. It is being tested in patients with mild-to-moderate AD [Alzheimer's disease].», which cites:
Óscar Taboada Díaz (Segundo trimestre de 2006). «Farmacoterapia en la enfermedad de Alzheimer. Diez años después». Informaciones Psiquiátricas (Hospital de Día-Programa Sociosanitario. Hospital Juan Canalejo. A Coruña.) (184). Archivado desde el original el 3 de agosto de 2015. Consultado el 18 de julio de 2015.La referencia utiliza el parámetro obsoleto |mes= (ayuda)
Óscar Taboada Díaz (Segundo trimestre de 2006). «Farmacoterapia en la enfermedad de Alzheimer. Diez años después». Informaciones Psiquiátricas (Hospital de Día-Programa Sociosanitario. Hospital Juan Canalejo. A Coruña.) (184). Archivado desde el original el 3 de agosto de 2015. Consultado el 18 de julio de 2015.La referencia utiliza el parámetro obsoleto |mes= (ayuda)
Frampton M, Harvey RJ, Kirchner V. (2008). «Propentofilina para la demencia». La Biblioteca Cochrane Plus (4). Archivado desde el original el 7 de julio de 2015. Consultado el 5 de julio de 2015.
HIDERGINA PARA LA DEMENCIA Olin J, Schneider L, Novit A, Luczak S. La Biblioteca Cochrane Plus, 2008 Número 4. Oxford.
«Medications for dementia: New drugs, mechanisms are coming for Alzheimer's disease». The Journal of Family Practice1 (6). June 2002. Archivado desde el original el 6 de abril de 2012. Consultado el 8 de julio de 2015. «PTI-00703 is a beta-amyloid inhibitor derived from the cat's claw, a woody vine found in the Peruvian rain forest. It is being tested in patients with mild-to-moderate AD [Alzheimer's disease].», which cites:
