Abstract
This paper reviews the results of studies conducted on the role of caffeine in the management of different neurological disorders, such as Parkinson’s disease (PD) and Alzheimer’s disease (AD). To highlight the potential role of caffeine in managing different neurodegenerative diseases, we identified studies by searching PubMed, Web of Science, and Google Scholar by scrutinizing the lists of pertinent publications. According to the collected overall findings, caffeine may reduce the elevated oxidative stress; inhibit the activation of adenosine A2A, thereby regulating the accumulation of Aβ; reduce the hyperphosphorylation of tau; and reduce the accumulation of misfolded proteins, such as α-synuclein, in Alzheimer’s and Parkinson’s diseases. The studies have suggested that caffeine has promising protective effects against different neurodegenerative diseases and that these effects may be used to tackle the neurological diseases and/or their consequences. Here, we review the ongoing research on the role of caffeine in the management of different neurodegenerative disorders, focusing on AD and PD. The current findings suggest that caffeine produces potent antioxidant, inflammatory, and anti-apoptotic effects against different models of neurodegenerative disease, including AD, PD, and other neurodegenerative disorders. Caffeine has shown strong antagonistic effects against the adenosine A2A receptor, which is a microglial receptor, and strong agonistic effects against nuclear-related factor-2 (Nrf-2), thereby regulating the cellular homeostasis at the brain by reducing oxidative stress, neuroinflammation, regulating the accumulation of α-synuclein in PD and tau hyperphosphorylation, amyloidogenesis, and synaptic deficits in AD, which are the cardinal features of these neurodegenerative diseases.
Highlights
Neurodegenerative diseases are characterized by their sudden onset and progression and are pathologically characterized by chronic loss of function and death of specific neuronal cells [1].Morphologically, neuronal cell loss is associated with gliosis, and misfolding and accumulation of proteins, leading to abnormal extracellular and intracellular filamentous deposits in specific cell types, showing the main characteristics of neurodegenerative diseases [2]
Similar results were obtained when D-galactose-treated mice were mice, as well as in CNS cell type-specific treated with caffeine; the findings showed that caffeine markedly reduced phospho-c-Jun n-terminal kinase (p-JNK)-induced inflammation, heterozygous A2AR KO mice, caffeine synaptic, and memory e striatum in the MPTP-treated mice. dysfunction in mice [19]
Our results suggested that caffeine may reduce cadmium-induced oxidative stress, as revealed from the reactive oxygen species (ROS) and lipid peroxidation (LPO) assays and by regulating the level of nuclear-related factor-2 (Nrf-2) and heme oxygenase-1 (HO-1), which act as endogenous antioxidant regulators
Summary
Neurodegenerative diseases are characterized by their sudden onset and progression and are pathologically characterized by chronic loss of function and death of specific neuronal cells [1]. One of the features responsible for neuronal cell loss is elevated oxidative stress, which is defined as an unevenness between the amounts of reactive oxygen species (ROS) produced and the extracellular and intracellular antioxidant defense systems, which are responsible for scavenging the ROS [3]. Neuroinflammation plays a critical role in the execution of neuronal cell loss and neurodegenerative disorders [9]. PD is called a movement disorder characterized by dopaminergic neurodegeneration, accumulation of α-synuclein, and levy bodies [13]. Another life-threatening neurodegenerative disease is traumatic brain injury, which triggers neurodegeneration and AD-like pathological conditions [14]. We have shed light on the effects of caffeine in the management of other toxins, such as cadmium-, aluminum-, and lipopolysaccharides (LPS)-induced neurodegenerative conditions
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