Статті в журналах: "COGNITION ENHANCERS"

1

Riedel, Wim J., and Jellemer Jolles. "Cognition Enhancers in Age-Related Cognitive Decline." Drugs & Aging 8, no. 4 (April 1996): 245–74. http://dx.doi.org/10.2165/00002512-199608040-00003.

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2

Bullard, Ashley R. "Neither Licit nor Illicit." Contemporary Drug Problems 45, no. 3 (August 5, 2018): 262–82. http://dx.doi.org/10.1177/0091450918789415.

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Cognition enhancers—drugs used to enhance cognition in healthy people—have generated a substantial amount of debate in the academic literature. In these debates, cognition enhancers are considered to promise (or threaten) to drastically change society. Cognition enhancers, as a “new breed of drugs,” are significant as they disrupt the licit–illicit binary maintained in the moral logic of pharmaceutical legitimacy. Cognition enhancers, despite putatively going beyond the legitimate purpose of restoring health, are not considered illicit. Their specificity positions them differently from medical, recreational, and other enhancement or “lifestyle” drugs, such that they elicit different rationales of governance. Utilizing a discursive analysis of the debates concerning cognition enhancers, I demonstrate how cognition enhancers cannot be determined by fixed properties either internal or external to themselves, but are rendered (reasonably) coherent through the problematizations that they produce. Questions of the boundaries of treatment and enhancement, equality and fairness, authenticity and autonomy, are bound up with concerns over the nature of being human. The discourse on cognition enhancers is underpinned by the assumption that these drugs do not repair a disorder but rather enhance an already “healthy” subject to an idealized subject, a construct underpinned by conceptions of a “normal” subject that is White, heteromasculine, and nondisabled. This presumption exists in the hinterlands that constitute these drugs as “cognition enhancers.”

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3

Vitriolo, Alessandro, Michele Gabriele, and Giuseppe Testa. "From enhanceropathies to the epigenetic manifold underlying human cognition." Human Molecular Genetics 28, R2 (August 14, 2019): R226—R234. http://dx.doi.org/10.1093/hmg/ddz196.

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Abstract A vast portion of intellectual disability and autism spectrum disorders is genetically caused by mutations in chromatin modulators. These proteins play key roles in development and are also highly expressed in the adult brain. Specifically, the pivotal role of chromatin regulation in transcription has placed enhancers at the core of neurodevelopmental disorders (NDDs) studies, ushering in the coining of the term enhanceropathies. The convergence of these disorders is multilayered, spanning from molecular causes to pathophysiological traits, including extensive overlaps between enhanceropathies and neurocristopathies. The reconstruction of epigenetic circuitries wiring development and underlying cognitive functions has gone hand in hand with the development of tools that increase the sensitivity of identifying regulatory regions and linking enhancers to their target genes. The available models, including loop extrusion and phase separation, have been bringing into relief complementary aspects to interpret gene regulation datasets, reinforcing the idea that enhancers are not all the same and that regulatory regions possess shades of enhancer-ness and promoter-ness. The current limits in enhancer definition, within the emerging broader understanding of chromatin dynamics in time and space, are now on the verge of being transformed by the possibility to interrogate developmentally relevant three-dimensional cellular models at single-cell resolution. Here we discuss the contours of how these technological advances, as well as the epistemic limitations they are set to overcome, may well usher in a change of paradigm for NDDs, moving the quest for convergence from enhancers to the four-dimensional (4D) genome.

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4

Costall, Brenda, Janine Barnes, M. Hamon, W. Müller, and M. Briley. "Biochemical Models for Cognition Enhancers." Pharmacopsychiatry 23, S 2 (February 1990): 85–89. http://dx.doi.org/10.1055/s-2007-1014540.

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5

Fröstl, W., and L. Maître. "The Families of Cognition Enhancers." Pharmacopsychiatry 22, S 2 (October 1989): 54–100. http://dx.doi.org/10.1055/s-2007-1014626.

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6

Sarter, Martin. "Preclinical research into cognition enhancers." Trends in Pharmacological Sciences 27, no. 11 (November 2006): 602–8. http://dx.doi.org/10.1016/j.tips.2006.09.004.

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7

Sarter, Martin. "Taking stock of cognition enhancers." Trends in Pharmacological Sciences 12 (January 1991): 456–61. http://dx.doi.org/10.1016/0165-6147(91)90636-7.

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8

Rudra, Pranab. "Ethical Underpinning and Implications of “Nootropic” Concept." Acta Universitatis Lodziensis. Folia Philosophica. Ethica-Aesthetica-Practica, no. 32 (December 30, 2018): 31–45. http://dx.doi.org/10.18778/0208-6107.32.03.

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The current generation paving the path for new research marks a milestone to attain the ancient goal of improving our cognition. To date, increased prevalence of cognitive enhancers by healthy people has raised the scientific community’s attention as well as media coverage. In particular, nootropics such as piracetam promise to offer modest improvements in cognitive performance. The long-lasting impetus of this “holistic enhancer” convinced scientists as well as ethicists to discuss its potential ethical implications and future directions. Moreover, there are discrepancies in the concept of a true nootropic between pharmacology and contemporary public culture. Here, I review the ethical aspects of nootropics raised by its potential use in cognition enhancement and substantiate the epistemological commentary on the concept of nootropic.

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9

Maubach, Karen. "GABAA Receptor Subtype Selective Cognition Enhancers." Current Drug Target -CNS & Neurological Disorders 2, no. 4 (August 1, 2003): 233–39. http://dx.doi.org/10.2174/1568007033482779.

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10

Flitman, Stephen S. "Tranquilizers, Stimulants, and Enhancers of Cognition." Physical Medicine and Rehabilitation Clinics of North America 10, no. 2 (May 1999): 463–72. http://dx.doi.org/10.1016/s1047-9651(18)30206-7.

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11

Dearden, John C, Mark Hewitt, Athina A Geronikaki, Taissia L Garibova, Fliur Z Macaev, and Tatiana A Voronina. "QSAR Investigation of New Cognition Enhancers." QSAR & Combinatorial Science 28, no. 10 (October 2009): 1123–29. http://dx.doi.org/10.1002/qsar.200860152.

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12

Núñez, Francisco, María J. Maraver, and Lorenza S. Colzato. "Sex Hormones as Cognitive Enhancers?" Journal of Cognitive Enhancement 4, no. 2 (December 10, 2019): 228–33. http://dx.doi.org/10.1007/s41465-019-00156-1.

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AbstractUnderstanding the differences in the way women and men think has made headway thanks to experiments showing how sex hormones influence cognitive capacities. Masculine and feminine sex hormones (androgens and estrogens, respectively) affect cognition in different ways and may account for some of the gender differences in cognitive abilities, allowing men and women to perform better in certain cognitive tests. In this opinion article, we discuss studies addressing differences in cognitive functions between males and females and the underlying neural substrates, as well as the effects of sex hormone supplementation. Even though some studies on patients receiving exogenous sex hormones showed gender differences that emerge at group levels on a few cognitive tasks, it is not yet clear whether these differences can be partially attributed to hormonal causes. Supplementation of female estrogen can enhance verbal skills, whereas masculine androgen can increase performance in mathematical and visuospatial tasks. Studies of the administration of exogenous sex hormones have allowed further insight into the use of sex hormones as possible cognitive enhancers.

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13

Hollister, L. "Problems in the Search for Cognition Enhancers." Pharmacopsychiatry 23, S 2 (February 1990): 33–36. http://dx.doi.org/10.1055/s-2007-1014529.

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14

Herrmann, Werner M., and Kurt Stephan. "Efficacy and Clinical Relevance of Cognition Enhancers." Alzheimer Disease & Associated Disorders 5 (1991): S7—S12. http://dx.doi.org/10.1097/00002093-199100051-00003.

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15

Malek, Naveed, and John Greene. "Cognition enhancers for the treatment of dementia." Scottish Medical Journal 60, no. 1 (November 27, 2014): 44–49. http://dx.doi.org/10.1177/0036933014561948.

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16

Jos, Prickaerts. "S.5.1 - TESTING COGNITION ENHANCERS IN ANIMALS." Behavioural Pharmacology 24 (October 2013): e5-e6. http://dx.doi.org/10.1097/01.fbp.0000434700.53518.5c.

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17

Veroniki, Areti Angeliki, Huda M. Ashoor, Patricia Rios, Georgios Seitidis, Lesley Stewart, Mike Clarke, Catrin Tudur-Smith, et al. "Comparative safety and efficacy of cognitive enhancers for Alzheimer’s dementia: a systematic review with individual patient data network meta-analysis." BMJ Open 12, no. 4 (April 2022): e053012. http://dx.doi.org/10.1136/bmjopen-2021-053012.

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ObjectiveTo examine the comparative efficacy and safety of cognitive enhancers by patient characteristics for managing Alzheimer’s dementia (AD).DesignSystematic review and individual patient data (IPD) network meta-analysis (NMA) based on our previously published systematic review and aggregate data NMA.Data sourcesMEDLINE, Embase, Cochrane Methodology Register, CINAHL, AgeLine and Cochrane Central Register of Controlled Trials up to March 2016.Participants80 randomised controlled trials (RCTs) including 21 138 adults with AD, and 12 RCTs with IPD including 6906 patients.InterventionsCognitive enhancers (donepezil, rivastigmine, galantamine and memantine) alone or in any combination against other cognitive enhancers or placebo.Data extraction and synthesisWe requested IPD from authors, sponsors and data sharing platforms. When IPD were not available, we used aggregate data. We appraised study quality with the Cochrane risk-of-bias. We conducted a two-stage random-effects IPD-NMA, and assessed their findings using CINeMA (Confidence in Network Meta-Analysis).Primary and secondary outcomesWe included trials assessing cognition with the Mini-Mental State Examination (MMSE), and adverse events.ResultsOur IPD-NMA compared nine treatments (including placebo). Donepezil (mean difference (MD)=1.41, 95% CI: 0.51 to 2.32) and donepezil +memantine (MD=2.57, 95% CI: 0.07 to 5.07) improved MMSE score (56 RCTs, 11 619 participants; CINeMA score: moderate) compared with placebo. According to P-score, oral rivastigmine (OR=1.26, 95% CI: 0.82 to 1.94, P-score=16%) and donepezil (OR=1.08, 95% CI: 0.87 to 1.35, P-score=30%) had the least favourable safety profile, but none of the estimated treatment effects were sufficiently precise when compared with placebo (45 RCTs, 15 649 patients; CINeMA score: moderate to high). For moderate-to-severe impairment, donepezil, memantine and their combination performed best, but for mild-to-moderate impairment donepezil and transdermal rivastigmine ranked best. Adjusting for MMSE baseline differences, oral rivastigmine and galantamine improved MMSE score, whereas when adjusting for comorbidities only oral rivastigmine was effective.ConclusionsThe choice among the different cognitive enhancers may depend on patient’s characteristics. The MDs of all cognitive enhancer regimens except for single-agent oral rivastigmine, galantamine and memantine, against placebo were clinically important for cognition (MD larger than 1.40 MMSE points), but results were quite imprecise. However, two-thirds of the published RCTs were associated with high risk of bias for incomplete outcome data, and IPD were only available for 15% of the included RCTs.PROSPERO registration numberCRD42015023507.

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18

Sanger, D., and Danielle Joly. "Psychopharmacological Strategies in the Search for Cognition Enhancers." Pharmacopsychiatry 23, S 2 (February 1990): 70–74. http://dx.doi.org/10.1055/s-2007-1014537.

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19

Briley, M. "Biochemical Strategies in the Search for Cognition Enhancers." Pharmacopsychiatry 23, S 2 (February 1990): 75–80. http://dx.doi.org/10.1055/s-2007-1014538.

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20

Delacour, J., Marie-Héléne Bassant, M. Onofrj, V. Santucci, and H. Kleinlogel. "Electrophysiological Models for the Study of Cognition Enhancers." Pharmacopsychiatry 23, S 2 (February 1990): 90–93. http://dx.doi.org/10.1055/s-2007-1014541.

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21

Lanni, Cristina, Silvia C. Lenzken, Alessia Pascale, Igor Del Vecchio, Marco Racchi, Francesca Pistoia, and Stefano Govoni. "Cognition enhancers between treating and doping the mind." Pharmacological Research 57, no. 3 (March 2008): 196–213. http://dx.doi.org/10.1016/j.phrs.2008.02.004.

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22

SENNEF, C., H. NIELSEN, A. LOLK, C. HAGELUKEN, and P. KRAGH-SORENSON. "CLINICAL PARADIGMS FOR THE STUDY OF COGNITION ENHANCERS." Behavioural Pharmacology 3, Supplement (April 1992): 89. http://dx.doi.org/10.1097/00008877-199204001-00274.

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23

Pitsikas, Nikolaos. "The Effect ofCrocus sativusL. and Its Constituents on Memory: Basic Studies and Clinical Applications." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/926284.

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Memory-related disorders are a common public health issue. Memory impairment is frequent in degenerative diseases (such as Alzheimer’s disease and Parkinson disease), cerebral injuries, and schizophrenia. The dried stigma of the plantCrocus sativusL. (C. sativus), commonly known as saffron, is used in folk medicine for various purposes. Several lines of evidence suggest thatC. sativusand its constituents are implicated in cognition. Here we critically review advances in research of these emerging molecular targets for the treatment of memory disorders, and discuss their advantages over currently used cognitive enhancers as well remaining challenges. Current analysis has shown thatC. sativusand its components might be a promising target for cognition impairments.

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24

Abdi, Zeinab, and Tonmoy Sharma. "Social Cognition and Its Neural Correlates in Schizophrenia and Autism." CNS Spectrums 9, no. 5 (May 2004): 335–43. http://dx.doi.org/10.1017/s1092852900009317.

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AbstractThe study of social cognition in psychiatric disorders has become increasingly popular in recent years. This is due to the its proposed link to social functioning and the inability of general neurocognitive skills to explain the spectrum of impairments observed in patients. This article reviews research into two of the processes thought to underlie social cognition (emotion perception and theory of mind) in schizophrenia and autism. This is followed by a look at neuroimaging studies and their efforts to localize the neural correlates of emotion perception and theory of mind in the two disorders. We concluded that while a specific impairment in emotion perception and theory of mind skills cannot be generalized to all individuals with autism and schizophrenia, there are subpopulations that have lingering deficits of social cognition tasks. Neuroimaging work consistently points to the involvement of the fusiform gyrus and amygdala in emotion processing, while the medial prefrontal and frontal cortex are implicated in tasks invoking theory of mind. We propose that deficits of social cognition may benefit from cognitive remediation therapy and pharmacological cognitive enhancers.

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25

Allain, H., P. Boyer, L. Kossmann, J. Lépine, and S. Kanowski. "Therapeutic Target for Cognition Enhancers: Diagnosis and Clinical Phenomenology." Pharmacopsychiatry 23, S 2 (February 1990): 49–52. http://dx.doi.org/10.1055/s-2007-1014532.

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26

Schwartz, Gerri, J. Bisserbe, Dianne Bradford, C. Sennef, and L. Hollister. "Late Clinical Testing of Cognition Enhancers: Demonstration of Efficacy." Pharmacopsychiatry 23, S 2 (February 1990): 60–64. http://dx.doi.org/10.1055/s-2007-1014535.

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27

Franceschi, M., M. Alberoni, S. Bressi, L. Preda, C. Cattaneo, and J. Parini. "SCOPOLAMINE MODEL IN PHASE I STUDIES OF COGNITION ENHANCERS." Clinical Neuropharmacology 15 (1992): 571B. http://dx.doi.org/10.1097/00002826-199202001-01114.

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Stoppe, G., H. Sandholzer, J. Staedt, S. Winter, J. Kiefer, and E. Rüther. "What are the factors influencing prescribing of cognition enhancers." European Psychiatry 11 (January 1996): 278s. http://dx.doi.org/10.1016/0924-9338(96)88842-0.

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29

Sahakian, Barbara J., Annette B. Bruhl, Jennifer Cook, Clare Killikelly, George Savulich, Thomas Piercy, Sepehr Hafizi, et al. "The impact of neuroscience on society: cognitive enhancement in neuropsychiatric disorders and in healthy people." Philosophical Transactions of the Royal Society B: Biological Sciences 370, no. 1677 (September 19, 2015): 20140214. http://dx.doi.org/10.1098/rstb.2014.0214.

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In addition to causing distress and disability to the individual, neuropsychiatric disorders are also extremely expensive to society and governments. These disorders are both common and debilitating and impact on cognition, functionality and wellbeing. Cognitive enhancing drugs, such as cholinesterase inhibitors and methylphenidate, are used to treat cognitive dysfunction in Alzheimer's disease and attention deficit hyperactivity disorder, respectively. Other cognitive enhancers include specific computerized cognitive training and devices. An example of a novel form of cognitive enhancement using the technological advancement of a game on an iPad that also acts to increase motivation is presented. Cognitive enhancing drugs, such as methylphenidate and modafinil, which were developed as treatments, are increasingly being used by healthy people. Modafinil not only affects ‘cold’ cognition, but also improves ‘hot’ cognition, such as emotion recognition and task-related motivation. The lifestyle use of ‘smart drugs' raises both safety concerns as well as ethical issues, including coercion and increasing disparity in society. As a society, we need to consider which forms of cognitive enhancement (e.g. pharmacological, exercise, lifelong learning) are acceptable and for which groups (e.g. military, doctors) under what conditions (e.g. war, shift work) and by what methods we would wish to improve and flourish.

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30

Hills, Thomas, and Ralph Hertwig. "Why Aren’t We Smarter Already." Current Directions in Psychological Science 20, no. 6 (December 2011): 373–77. http://dx.doi.org/10.1177/0963721411418300.

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Pharmacological enhancers of cognition promise a bright new future for humankind: more focus, more willpower, and better memory, with applications ranging from education to military combat. Underlying such promises is a linear, more-is-better vision of cognition that makes intuitive sense. This vision is at odds, however, with our understanding of cognition’s evolutionary origins. The mind has evolved under various constraints and consequently represents a delicate balance among these constraints. Evidence of the trade-offs that have shaped cognition include (a) inverted U-shaped performance curves commonly found in response to pharmacological interventions and (b) unintended side effects of enhancement on other traits. Taking an evolutionary perspective, we frame the above two sets of findings in terms of within-task (exemplified by optimal-control problems) and between-task (associated with a gain/loss asymmetry) trade-offs, respectively. With this framework, psychological science can provide much-needed guidance to enhancement development, a field that still lacks a theoretical foundation.

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Giovannini, M. G., F. Casamenti, L. Bartolini, and G. Pepeu. "The brain cholinergic system as a target of cognition enhancers." Behavioural Brain Research 83, no. 1-2 (February 1997): 1–5. http://dx.doi.org/10.1016/s0166-4328(97)86038-x.

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Malabadi, Ravindra B., Kiran P. Kolkar, Neelambika T. Meti, and Raju K. Chalannavar. "Recent updates on the role of herbal medicine for Alzheimer's disease (Dementia)." International Journal of Current Research in Biosciences and Plant Biology 8, no. 1 (January 6, 2021): 14–45. http://dx.doi.org/10.20546/ijcrbp.2021.801.002.

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This review paper highlights the use of medicinal plants in the management of Alzheimer's disease and memory deficit. Alzheimer’s disease is the most common form of dementia, a serious brain disorder that impacts daily living through memory loss and cognitive changes. Alzheimer's disease is also age-related neurodegenerative disorders caused by progressive loss of structure or function of neurons, resulting in neuronal cell death. Alzheimer's patients have an acetylcholine deficiency. Stressful conditions, free radicle scavanging and oxidation are often associated with loss of memory and cognitive functions, which may lead to threats of schizophrenia and Alzheimer's disease. However, the use of allopathic drugs has resulted in the adverse side effects on the human body and thus limits the use of such drugs. Herbal cognitive enhancer drugs have shown their potent effect in Alzheimer’s disease due to their antioxidant and neuropharmacological actions. The use of natural cognitive enhancers evidenced to improve mental functions such as cognition, memory, intelligence, motivation, attention and concentration. Traditional Ayurvedic herbal system of medicine is fundamentally preventive, protective, nutritive, curative and less expensive. Therefore, the use of herbal medicine for the treatment of Alzheimer's disease is a novel approach without any side effects.

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Wagner, F. F., Y. L. Zhang, D. M. Fass, N. Joseph, J. P. Gale, M. Weïwer, P. McCarren, et al. "Kinetically selective inhibitors of histone deacetylase 2 (HDAC2) as cognition enhancers." Chemical Science 6, no. 1 (2015): 804–15. http://dx.doi.org/10.1039/c4sc02130d.

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Young, Jared W., J. David Jentsch, Timothy J. Bussey, Tanya L. Wallace, and Daniel M. Hutcheson. "Consideration of species differences in developing novel molecules as cognition enhancers." Neuroscience & Biobehavioral Reviews 37, no. 9 (November 2013): 2181–93. http://dx.doi.org/10.1016/j.neubiorev.2012.10.002.

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35

Pittaluga, Anna, Roberto Pattarini, and Maurizio Raiteri. "Putative cognition enhancers reverse kynurenic acid antagonism at hippocampal NMDA receptors." European Journal of Pharmacology 272, no. 2-3 (January 1995): 203–9. http://dx.doi.org/10.1016/0014-2999(94)00641-j.

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Ballesteros, Virginia. "Smart drugs: de la terapia al transhumanismo / Smart Drugs: from therapy to transhumanism." Revista Internacional de Tecnología, Ciencia y Sociedad 7, no. 2 (November 21, 2018): 37–42. http://dx.doi.org/10.37467/gka-revtechno.v7.1659.

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ABSTRACT Enhancing human cognitive capacities is one of the central axes of transhumanist proposals. In recent decades, halfway between the actual and the possible, another way of approaching human mind enhancement has appeared: smart drugs —also known as cognitive enhancers or nootropics— psychopharmaceuticals that promise an improvement in cognition, memory, intelligence, attention, concentration... These drugs are currently used in the therapeutic field, but many think that the barriers between therapy and human enhancement are fading away. This paper presents three smart drugs —methylphenidate, modafinil and pyracetam— and reflects on the limits between therapy and enhancement, placing special emphasis on the axiological problems entailed.RESUMENLa superación de las capacidades cognitivas humanas conforma uno de los ejes centrales de las propuestas transhumanistas. A mitad de camino entre lo actual y lo posible, aparece en las últimas décadas otra forma de aproximarse a la superación de la mente humana: las smart drugs —también conocidas como cognitive enhancers o nootrópicos—, psicofármacos que prometen una mejora de la cognición, la memoria, la inteligencia, la atención, la concentración... Estos fármacos son actualmente empleados en el ámbito terapéutico, pero son muchos quienes consideran que las barreras entre terapia y mejora humana comienzan a desdibujarse. Este trabajo presenta tres smart drugs —metilfenidato, modafinilo y piracetam— y reflexiona sobre los límites entre terapia y mejora, poniendo especial énfasis en los problemas axiológicos que comportan.

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Toma, I. De, L. Manubens Gil, S. Ossowski, and M. Dierssen. "Where Environment Meets Cognition: A Focus on Two Developmental Intellectual Disability Disorders." Neural Plasticity 2016 (2016): 1–20. http://dx.doi.org/10.1155/2016/4235898.

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One of the most challenging questions in neuroscience is to dissect how learning and memory, the foundational pillars of cognition, are grounded in stable, yet plastic, gene expression states. All known epigenetic mechanisms such as DNA methylation and hydroxymethylation, histone modifications, chromatin remodelling, and noncoding RNAs regulate brain gene expression, both during neurodevelopment and in the adult brain in processes related to cognition. On the other hand, alterations in the various components of the epigenetic machinery have been linked to well-known causes of intellectual disability disorders (IDDs). Two examples are Down Syndrome (DS) and Fragile X Syndrome (FXS), where global and local epigenetic alterations lead to impairments in synaptic plasticity, memory, and learning. Since epigenetic modifications are reversible, it is theoretically possible to use epigenetic drugs as cognitive enhancers for the treatment of IDDs. Epigenetic treatments act in a context specific manner, targeting different regions based on cell and state specific chromatin accessibility, facilitating the establishment of the lost balance. Here, we discuss epigenetic studies of IDDs, focusing on DS and FXS, and the use of epidrugs in combinatorial therapies for IDDs.

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Piplani, Poonam, Anita Rani, Ruchika Saihgal, and Meenakshi Sharma. "Synthesis and pharmacological evaluation of some quinoline derivatives as potential cognition enhancers." Arzneimittelforschung 61, no. 07 (November 27, 2011): 373–78. http://dx.doi.org/10.1055/s-0031-1296213.

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Hall, Sue, A. Puech, K. Schaffler, K. Wesnes, and E. Gamzu. "Group Report 3: Early Clinical Testing of Cognition Enhancers: Prediction of Efficacy." Pharmacopsychiatry 23, S 2 (February 1990): 57–59. http://dx.doi.org/10.1055/s-2007-1014534.

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40

Romanelli, M. N., N. Galeotti, C. Ghelardini, D. Manetti, E. Martini, and F. Gualtieri. "Pharmacological Characterization of DM232 (Unifiram) and DM235 (Sunifiram), New Potent Cognition Enhancers." CNS Drug Reviews 12, no. 1 (March 2006): 39–52. http://dx.doi.org/10.1111/j.1527-3458.2006.00039.x.

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41

Yamamoto, Kozo, Hideyuki Kishida, Toshiaki Miwa, Yoshihide Fuse, and Takayoshi Hidaka. "Effect of KST compounds, novel cognition enhancers, on animal models of amnesia." Japanese Journal of Pharmacology 61 (1993): 188. http://dx.doi.org/10.1016/s0021-5198(19)51629-8.

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42

Sternfeld, Francine, Robert W. Carling, Richard A. Jelley, Tamara Ladduwahetty, Kevin J. Merchant, Kevin W. Moore, Austin J. Reeve та ін. "Selective, Orally Active γ-Aminobutyric AcidAα5 Receptor Inverse Agonists as Cognition Enhancers". Journal of Medicinal Chemistry 47, № 9 (квітень 2004): 2176–79. http://dx.doi.org/10.1021/jm031076j.

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43

Sarter, Martin, Jim Hagan, and Paul Dudchenko. "Behavioral screening for cognition enhancers: from indiscriminate to valid testing: Part I." Psychopharmacology 107, no. 2-3 (June 1992): 144–59. http://dx.doi.org/10.1007/bf02245132.

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44

Sarter, Martin, Jim Hagan, and Paul Dudchenko. "Behavioral screening for cognition enhancers: from indiscriminate to valid testing: Part II." Psychopharmacology 107, no. 4 (June 1992): 461–73. http://dx.doi.org/10.1007/bf02245257.

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45

Andersson, Hanna, and Mathias Hallberg. "Discovery of Inhibitors of Insulin-Regulated Aminopeptidase as Cognitive Enhancers." International Journal of Hypertension 2012 (2012): 1–18. http://dx.doi.org/10.1155/2012/789671.

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Анотація:

The hexapeptide angiotensin IV (Ang IV) is a metabolite of angiotensin II (Ang II) and plays a central role in the brain. It was reported more than two decades ago that intracerebroventricular injection of Ang IV improved memory and learning in the rat. Several hypotheses have been put forward to explain the positive effects of Ang IV and related analogues on cognition. It has been proposed that the insulin-regulated aminopeptidase (IRAP) is the main target of Ang IV. This paper discusses progress in the discovery of inhibitors of IRAP as potential enhancers of cognitive functions. Very potent inhibitors of the protease have been synthesised, but pharmacokinetic issues (including problems associated with crossing the blood-brain barrier) remain to be solved. The paper also briefly presents an overview of the status in the discovery of inhibitors of ACE and renin, and of AT1R antagonists and AT2R agonists, in order to enable other discovery processes within the RAS system to be compared. The paper focuses on the relationship between binding affinities/inhibition capacity and the structures of the ligands that interact with the target proteins.

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46

Balanzá-Martínez, Vicent, Flavio M. Shansis, Amparo Tatay-Manteiga, and Pilar López-García. "Diet and Neurocognition in Mood Disorders - An Overview of the Overlooked." Current Pharmaceutical Design 26, no. 20 (June 21, 2020): 2353–62. http://dx.doi.org/10.2174/1381612826666200318152530.

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Bipolar disorder and major depression are associated with significant disability, morbidity, and reduced life expectancy. People with mood disorders have shown higher ratios of unhealthy lifestyle choices, including poor diet quality and suboptimal nutrition. Diet and nutrition impact on brain /mental health, but cognitive outcomes have been less researched in psychiatric disorders. Neurocognitive dysfunction is a major driver of social dysfunction and a therapeutic target in mood disorders, although effective cognitive-enhancers are currently lacking. This narrative review aimed to assess the potential cognitive benefits of dietary and nutritional interventions in subjects diagnosed with mood disorders. Eight clinical trials with nutrients were identified, whereas none involved dietary interventions. Efficacy to improve select cognitive deficits has been reported, but results are either preliminary or inconsistent. Methodological recommendations for future cognition trials in the field are advanced. Current evidence and future views are discussed from the perspectives of precision medicine, clinical staging, nutritional psychiatry, and the brain-gut-microbiota axis.

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47

Geronikaki, Athina A., John C. Dearden, Dmitrii Filimonov, Irina Galaeva, Taissia L. Garibova, Tatiana Gloriozova, Valentina Krajneva, et al. "Design of New Cognition Enhancers: From Computer Prediction to Synthesis and Biological Evaluation." Journal of Medicinal Chemistry 47, no. 11 (May 2004): 2870–76. http://dx.doi.org/10.1021/jm031086k.

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48

Hamelin, Servane M., and John C. Lehmann. "Effects of putative cognition enhancers on the NMDA receptor by [3H]MK801 binding." European Journal of Pharmacology 281, no. 3 (August 1995): R11—R13. http://dx.doi.org/10.1016/0014-2999(95)00432-k.

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Young, JW, and MA Geyer. "Developing treatments for cognitive deficits in schizophrenia: The challenge of translation." Journal of Psychopharmacology 29, no. 2 (December 16, 2014): 178–96. http://dx.doi.org/10.1177/0269881114555252.

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Schizophrenia is a life-long debilitating mental disorder affecting tens of millions of people worldwide. The serendipitous discovery of antipsychotics focused pharmaceutical research on developing a better antipsychotic. Our understanding of the disorder has advanced however, with the knowledge that cognitive enhancers are required for patients in order to improve their everyday lives. While antipsychotics treat psychosis, they do not enhance cognition and hence are not antischizophrenics. Developing pro-cognitive therapeutics has been extremely difficult, however, especially when no approved treatment exists. In lieu of stumbling on an efficacious treatment, developing targeted compounds can be facilitated by understanding the neural mechanisms underlying altered cognitive functioning in patients. Equally importantly, these cognitive domains will need to be measured similarly in animals and humans so that novel targets can be tested prior to conducting expensive clinical trials. To date, the limited similarity of testing across species has resulted in a translational bottleneck. In this review, we emphasize that schizophrenia is a disorder characterized by abnormal cognitive behavior. Quantifying these abnormalities using tasks having cross-species validity would enable the quantification of comparable processes in rodents. This approach would increase the likelihood that the neural substrates underlying relevant behaviors will be conserved across species. Hence, we detail cross-species tasks which can be used to test the effects of manipulations relevant to schizophrenia and putative therapeutics. Such tasks offer the hope of providing a bridge between non-clinical and clinical testing that will eventually lead to treatments developed specifically for patients with deficient cognition.

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Perlovich, German L., Alexey N. Proshin, Tatyana V. Volkova, Sergey V. Kurkov, Vlaimir V. Grigoriev, Ludmila N. Petrova, and Sergey O. Bachurin. "Novel Isothiourea Derivatives as Potent Neuroprotectors and Cognition Enhancers: Synthesis, Biological and Physicochemical Properties." Journal of Medicinal Chemistry 52, no. 7 (April 9, 2009): 1845–52. http://dx.doi.org/10.1021/jm8012882.

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