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Biomedicines
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The Role of Adenosine A(2A) Receptor Antagonists in Neurology and...
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The Role of Adenosine A(2A) Receptor Antagonists in Neurology and Psychiatric Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 2189

Special Issue Editors

Dr. Peter Jenner

E-Mail Website
Guest Editor
Institute of Pharmaceutical Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK
Interests: neurodegenerative disease; Parkinson's disease (PD)
Dr. Akihisa Mori

E-Mail Website
Guest Editor
Kyowa Kirin Co., Ltd., Otemachi, Chiyoda-ku, Tokyo 100-0004, Japan
Interests: adenosine A2A receptor antagonist; Parkinson's disease (PD); adenosine; basal ganglia

Special Issue Information

Dear Colleagues,

The identification and cloning of the adenosine A2A receptor and the finding of its selective localisation to the brain—most notably to neurones in the basal ganglia and in limbic brain regions—and to glial cells, opened a new vista on approaches to the treatment of both neurological and psychiatric illnesses and to the potential for achieving neuroprotection and/or disease modification. In this supplement, we explore the molecular biology, biochemistry and functional roles of the adenosine A2A receptor. These are put into the context of the use of adenosine A2A receptor antagonists in the symptomatic treatment of Parkinson’s disease and the acceptable safety profile in combination with current dopaminergic therapies. In addition, we look at the functional significance of the adenosine A2A receptor in a range of other neurodegenerative diseases, including motor neurone disease, Huntington’s chorea and multiple sclerosis. We also explore the potential of adenosine A2A receptors and A2A receptor antagonists as a novel approach for the treatment of anxiety, depression, cognition and sleep disturbance. Finally, the key localisation of A2A receptors on glutamatergic neurones and their role in the control of excitotoxic mechanisms together with their involvement in the regulation of glial cell activity are used to illustrate how adenosine A2A receptor antagonists may have a future role in modifying the progression of degenerative illnesses of the central nervous system.

Dr. Peter Jenner
Dr. Akihisa Mori
Guest Editors

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Keywords

  • adenosine
  • adenosine A2A receptor
  • adenosine A2A receptor antagonist
  • basal ganglia
  • limbic system Parkinson’s disease
  • neurodegeneration
  • motor neuron disease
  • Huntington's disease
  • anxiety
  • depression
  • cognition
  • sleep disturbance. glutamatergic neurons
  • glial cells

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Published Papers (1 paper)

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Research

16 pages, 740 KiB  
Article
Divergent Effects of the Nonselective Adenosine Receptor Antagonist Caffeine in Pre-Manifest and Motor-Manifest Huntington’s Disease
by Jannis Achenbach, Andreas Matusch, David Elmenhorst, Andreas Bauer and Carsten Saft
Biomedicines 2022, 10(6), 1258; https://doi.org/10.3390/biomedicines10061258 - 27 May 2022
Cited by 2 | Viewed by 2001
Abstract
There is a controversy about potentially positive or negative effects of caffeine consumption on onset and disease progression of neurodegenerative diseases such as Huntington’s Disease (HD). On the molecular level, the psychoactive drug caffeine targets in particular adenosine receptors (AR) as a nonselective [...] Read more.
There is a controversy about potentially positive or negative effects of caffeine consumption on onset and disease progression of neurodegenerative diseases such as Huntington’s Disease (HD). On the molecular level, the psychoactive drug caffeine targets in particular adenosine receptors (AR) as a nonselective antagonist. The aim of this study was to evaluate clinical effects of caffeine consumption in patients suffering from premanifest and motor-manifest HD. Data of the global observational study ENROLL-HD were used, in order to analyze the course of HD regarding symptoms onset, motor, functional, cognitive and psychiatric parameters, using cross-sectional and longitudinal data of up to three years. We split premanifest and manifest participants into two subgroups: consumers of >3 cups of caffeine (coffee, cola or black tea) per day (>375 mL) vs. subjects without caffeine consumption. Data were analyzed using ANCOVA-analyses for cross-sectional and repeated measures analysis of variance for longitudinal parameters in IBM SPSS Statistics V.28. Within n = 21,045 participants, we identified n = 1901 premanifest and n = 4072 manifest HD patients consuming >3 cups of caffeine/day vs. n = 841 premanifest and n = 2243 manifest subjects without consumption. Manifest HD patients consuming >3 cups exhibited a significantly better performance in a series of neuropsychological tests. They also showed at the median a later onset of symptoms (all p < 0.001), and, during follow-up, less motor, functional and cognitive impairments in the majority of tests (all p < 0.050). In contrast, there were no beneficial caffeine-related effects on neuropsychological performance in premanifest HD mutation carriers. They showed even worse cognitive performances in stroop color naming (SCNT) and stroop color reading (SWRT) tests (all p < 0.050) and revealed more anxiety, depression and irritability subscores in comparison to premanifest participants without caffeine consumption. Similarly, higher self-reported anxiety and irritability were observed in genotype negative/control group high dose caffeine drinkers, associated with a slightly better performance in some cognitive tasks (all p < 0.050). The analysis of the impact of caffeine consumption in the largest real-world cohort of HD mutation carriers revealed beneficial effects on neuropsychological performance as well as manifestation and course of disease in manifest HD patients while premanifest HD mutation carrier showed no neuropsychological improvements, but worse cognitive performances in some tasks and exhibited more severe signs of psychiatric impairment. Our data point to state-related psychomotor-stimulant effects of caffeine in HD that might be related to regulatory effects at cerebral adenosine receptors. Further studies are required to validate findings, exclude potential other unknown biasing factors such as physical activity, pharmacological interventions, gender differences or chronic habitual influences and test for dosage related effects. Full article
(This article belongs to the Special Issue The Role of Adenosine A(2A) Receptor Antagonists in Neurology and Psychiatric Diseases)
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