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Pharmacology of cognition
OAI: oai:purehost.bath.ac.uk:publications/dec563e9-038c-4770-be4b-69b2949aab16 • DOI: https://doi.org/10.1111/bph.13956
Abstract
This themed issue of the British Journal of Pharmacology arose from a British Association for Psychopharmacology (BAP) sponsored symposium at the annual meeting of the British Pharmacological Society (BPS) “Pharmacology 2015”: “Targeting cognition: a panacea for neuropsychiatric disease?”. Reflecting BAP’s founding principles and demography, the symposium addressed translational advances in understanding and treating cognition from both clinical and preclinical perspectives.
Cognition is an umbrella term that includes many complex processes such as attention, learning, consolidation, re-consolidation and retrieval. Each of these processes in turn is applicable to diverse kinds of information processing such as working memory for short-term information, episodic memory for events, procedural memory for skills. The neural basis of these processes can differ depending on many factors such as the emotional salience of the information or the context in which it is encoded. The idea that impaired cognition could potentially be treated pharmacologically came to prominence in the 1980’s; in part stimulated by the cholinergic hypothesis of geriatric memory dysfunction (Bartus, 1982) and the subsequent increased understanding of the role of both cholinergic and glutamatergic systems in learning and memory. The compelling idea that a disorder such as Alzheimer’s disease, with such profound cognitive symptoms, could be treated pharmacologically gave rise to the development of acetylcholinesterase inhibitors, such as donepezil, and more recently glutamatergic drugs such as memantine. Despite their limitations, these drugs are still among the only first-line pharmacological treatments for Alzheimer’s Disease (O’Brien et al, 2017). More recently it has become apparent that cognitive deficits are seen in a much wider range of psychiatric disorders such as anxiety, schizophrenia and depression. Research into the neuronal networks and molecular mechanisms contributing to these cognitive symptoms should give rise to novel therapeutics to meet the clinical need in these disorders.
Cognition is an umbrella term that includes many complex processes such as attention, learning, consolidation, re-consolidation and retrieval. Each of these processes in turn is applicable to diverse kinds of information processing such as working memory for short-term information, episodic memory for events, procedural memory for skills. The neural basis of these processes can differ depending on many factors such as the emotional salience of the information or the context in which it is encoded. The idea that impaired cognition could potentially be treated pharmacologically came to prominence in the 1980’s; in part stimulated by the cholinergic hypothesis of geriatric memory dysfunction (Bartus, 1982) and the subsequent increased understanding of the role of both cholinergic and glutamatergic systems in learning and memory. The compelling idea that a disorder such as Alzheimer’s disease, with such profound cognitive symptoms, could be treated pharmacologically gave rise to the development of acetylcholinesterase inhibitors, such as donepezil, and more recently glutamatergic drugs such as memantine. Despite their limitations, these drugs are still among the only first-line pharmacological treatments for Alzheimer’s Disease (O’Brien et al, 2017). More recently it has become apparent that cognitive deficits are seen in a much wider range of psychiatric disorders such as anxiety, schizophrenia and depression. Research into the neuronal networks and molecular mechanisms contributing to these cognitive symptoms should give rise to novel therapeutics to meet the clinical need in these disorders.