Chronic Caffeine Ingestion Improves Motor Function and Increases Dendritic Length and Arborization in the Motor Cortex, Striatum, and Cerebellum

Olopade, Funmilayo; Femi-Akinlosotu, Omowumi; Adekanmbi, Adejoke Joan; Ighogboja, Oghenefejiro O.; Shokunbi, Temitayo

doi:10.1089/caff.2020.0017

Cited by 5 publications

(6 citation statements)

References 58 publications

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“…We suggest that the observed enhancement in motor function can be attributed to the increased dendritic lengths and arborization in pyramidal neurons, similar to the findings reported in hippocampal and cortical neurons associated with the attenuation of cognitive decline [54]. This suggests a strong relationship between dendritic morphology and motor function improvement, as discussed earlier in relation to prefrontal neurons [58].…”

Section: Dendritic Morphologysupporting

confidence: 87%

“…Understanding the structural organization of these dendritic arbors becomes particularly important in the context of diseased conditions, as it contributes to the comprehension of altered brain network dynamics [57,58]. These improvements in dendritic length and arborization in pyramidal neurons in this study demonstrate a strong association with the amelioration of motor function and the attenuation of cognitive decline in the hippocampal and prefrontal neurons affected by vanadium-induced neurotoxicity [54].…”

Section: Dendritic Morphologymentioning

confidence: 67%

“…For the Modified Golgi stain, a subset of three mouse brains per group was selected according to a protocol described in a previous study [58]. This staining method was utilized to examine the dendritic arborization of neurons in the cornus ammonis (CA) 1 region of the hippocampus, as well as the cerebral and cerebellar regions.…”

Section: Golgi Stainingmentioning

confidence: 99%

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Attenuation of Vanadium-Induced Neurotoxicity in Rat Hippocampal Slices (In Vitro) and Mice (In Vivo) by ZA-II-05, a Novel NMDA-Receptor Antagonist

Ladagu,

Olopade,

Chazot

et al. 2023

IJMS

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Exposure to heavy metals, such as vanadium, poses an ongoing environmental and health threat, heightening the risk of neurodegenerative disorders. While several compounds have shown promise in mitigating vanadium toxicity, their efficacy is limited. Effective strategies involve targeting specific subunits of the NMDA receptor, a glutamate receptor linked to neurodegenerative conditions. The potential neuroprotective effects of ZA-II-05, an NMDA receptor antagonist, against vanadium-induced neurotoxicity were explored in this study. Organotypic rat hippocampal slices, and live mice, were used as models to comprehensively evaluate the compound’s impact. Targeted in vivo fluorescence analyses of the hippocampal slices using propidium iodide as a marker for cell death was utilized. The in vivo study involved five dams, each with eight pups, which were randomly assigned to five experimental groups (n = 8 pups). After administering treatments intraperitoneally over six months, various brain regions were assessed for neuropathologies using different immunohistochemical markers. High fluorescence intensity was observed in the hippocampal slices treated with vanadium, signifying cell death. Vanadium-exposed mice exhibited demyelination, microgliosis, and neuronal cell loss. Significantly, treatment with ZA-II-05 resulted in reduced cellular death in the rat hippocampal slices and preserved cellular integrity and morphological architecture in different anatomical regions, suggesting its potential in countering vanadium-induced neurotoxicity.

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Section: Dendritic Morphologysupporting

confidence: 87%

Section: Dendritic Morphologymentioning

confidence: 67%

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Attenuation of Vanadium-Induced Neurotoxicity in Rat Hippocampal Slices (In Vitro) and Mice (In Vivo) by ZA-II-05, a Novel NMDA-Receptor Antagonist

Ladagu,

Olopade,

Chazot

et al. 2023

IJMS

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“…Caffeine can cross the blood-brain barrier and exerts its biological effects mainly via the antagonism of adenosine receptors [5] . It inhibits lipid peroxidation and the formation of reactive oxygen species [6,7] and improves mitochondrial function [8] . Caffeine is metabolized in the liver; its main metabolites are paraxanthine, theobromine, and theophylline.…”

Section: Function Of Caffeine In the Brainmentioning

confidence: 99%

Caffeine, chocolate, and adenosine antagonism in Parkinson’s disease

Reichmann¹

2022

Ageing Neur Dis

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Parkinson’s disease (PD) is the second most common neurodegenerative disorder. It is generally accepted that dopamine replacement therapy substantially improves motor symptoms; however, there is a worldwide tendency to include nutrients in treatment strategies. In the present review, caffeine and chocolate are discussed. Caffeine use seems to postpone the occurrence of PD in men, and perhaps also in women who do not take postmenopausal hormone replacement therapy. There are contradictory data concerning possible caffeine-induced improvements in PD symptoms. Given that the basic action of caffeine is the antagonism of adenosine receptors, adenosine antagonists may be a new option for treating PD patients. Furthermore, PD patients tend to have increased chocolate consumption; this may be causally related to ingredients such as phenylethylamine. Thus, nutrients such as caffeine and chocolate may play an important role in postponing and/or improving symptoms in PD.

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“…Adenosin A 2A Rezeptoren sind ein vielversprechendes nicht-dopaminerges Angriffsziel, da sie selektiv in den Basalganglien lokalisiert sind und die striato-thalamo-kortikalen Schleifen modulieren, die nicht nur für die Entwicklung motorischer Symptome bei Parkinson relevant sind [1]. Die Blockade der Adenosin-Rezeptoren A 1 , A 2A , A 3 und A 2B der Gliazellen, Astrozyten, Oligodentrozyten und Neurone moduliert die Freisetzung von Dopamin, Serotonin, Acetylcholin, GABA, Adrenalin und Noradrenalin im Nucleus accumbens (NAc), Hippocampus und anderen Gehirnregionen [7][8][9]. Zudem spielt sie eine Rolle bei synaptischer Plastizität und Neuroprotektion [9].…”

Section: Rationale: Rolle Des Adenosin a 2a Rezeptors Auf Motorische ...unclassified

Adenosin A2A Rezeptorantagonisten als Therapieoption beim idiopathischen Parkinson-Syndrom?

Jost

Tönges

2022

Fortschr Neurol Psychiatr

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ZusammenfassungBeim Parkinson-Syndrom wurde sich lange Zeit auf die motorischen Symptome und die Therapie mit dopaminergen Substanzen fokussiert. In den letzten Jahren gewannen die nicht-motorischen Symptome immer mehr Bedeutung, da sie früh im Krankheitsverlauf auftreten und die Lebensqualität erheblich einschränken. Dadurch wurde aber auch die Notwendigkeit einer Behandlung nicht nur des dopaminergen Defizits offensichtlich. Als weitere therapeutische Option wurden die Adenosin A2A Rezeptorantagonisten entwickelt, da Adenosin A2A Rezeptorantagonisten nicht-dopaminerg und selektiv in den Basalganglien lokalisiert sind. Somit besteht die Möglichkeit striato-thalamo-kortikalen Schleifen zusätzlich zu modulieren. Bereits 2013 wurde ein Adenosin A2A Rezeptorantagonist in Japan und in 2019 in den USA als Add-on zu L-DOPA zugelassen. Mit einer Zulassung in Europa wird in naher Zukunft gerechnet. In dieser Übersicht möchten wir die theoretischen Grundlagen dieses Therapieansatzes darstellen und die aktuellen Daten zur Wirksamkeit und dem therapeutischen Einsatz referieren.

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Chronic Caffeine Ingestion Improves Motor Function and Increases Dendritic Length and Arborization in the Motor Cortex, Striatum, and Cerebellum

Cited by 5 publications

References 58 publications

Attenuation of Vanadium-Induced Neurotoxicity in Rat Hippocampal Slices (In Vitro) and Mice (In Vivo) by ZA-II-05, a Novel NMDA-Receptor Antagonist

Attenuation of Vanadium-Induced Neurotoxicity in Rat Hippocampal Slices (In Vitro) and Mice (In Vivo) by ZA-II-05, a Novel NMDA-Receptor Antagonist

Caffeine, chocolate, and adenosine antagonism in Parkinson’s disease

Adenosin A2A Rezeptorantagonisten als Therapieoption beim idiopathischen Parkinson-Syndrom?

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