Caffeine is the most widely used psychostimulant in Western countries, with antioxidant, anti-inflammatory and anti-apoptotic properties. In Alzheimer’s disease (AD), caffeine is beneficial and similar effects have also been observed patients with Parkinson’s disease. Read more about the neuroprotective effects of caffeine on neurodegenerative diseases
Caffeine in neurodegenerative diseases
Caffeine (1,3,7-trimethylxanthone) is a widely used psychostimulant. It is contained in coffee, tea, energy drinks, cocoa, among others. After consumption, caffeine is rapidly absorbed by the gastrointestinal tract and the highest concentration of caffeine in the blood is reached 30-60 minutes after ingestion. Similar concentrations of caffeine are found in the brain, suggesting that caffeine can easily cross the blood brain barrier due to its hydrophobic nature. Average levels of caffeine consumption cause alertness and reduce fatigue, leading to better performance in psychomotor tasks that require rapid reactions.
Caffeine and Alzheimer’s disease
Alzheimer’s disease is a progressive and irreversible neurodegenerative disease that leads to cognitive, behavioral and memory impairments. Histopathological features include extracellular deposits of diffuse and neuritic plaques. Recently, caffeine has aroused scientific interest due to its potential as an antioxidant compound, able to protect against oxidative stress, which can aid in Alzheimer’s disease.
Caffeine and Parkinson’s disease
Parkinson’s disease (PD) is characterized by bradykinesia (slow movement), stiffness and postural instability. The etiology is not fully understood, but is believed to be the consequence of the loss of dopaminergic neurons, resulting in dopamine deficit. Neuronal insult is mainly caused by excessive oxidative stress, leading to damaged proteins, DNA and lipids. Most reactive oxygen species are initiated from microglia, which are activated by certain inflammatory or genetic factors. Data suggest that caffeine may confer neuroprotection against the degeneration of the underlying dopaminergic neuron and may influence the onset and progression of Parkinson’s disease.
Caffeine exerts its effects by different pathways, including antagonism of adenosine receptors, inhibition of phosphodiesterase and activation of rianodine receptors. However, at average levels of caffeine consumption (210-238 mg/d), the main mechanism of action is the antagonism of adenosine receptors. Caffeine consumption, at dosages of 3-5 mg/kg, is associated with a lower risk of Alzheimer’s disease and Parkinson’s disease in epidemiological and preclinical studies.
Study suggestion: Caffeine
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neurodegenerative diseases – Kolahdouzan M, Hamadeh MJ. The neuroprotective effects of caffeine in neurodegenerative diseases. CNS Neurosci Ther. 2017;23(4):272-290. doi:10.1111/cns.12684