Dietary Caffeine and Brain Dopaminergic Function in Parkinson Disease

 Whatever this means I'm still going to be doing a 12 cup pot of coffee daily to prevent Parkinsons!

Parkinson’s Disease May Have Link to Stroke March 2017

How coffee protects against Parkinson’s Aug. 2014  

The latest here:

Dietary Caffeine and Brain Dopaminergic Function in Parkinson Disease

Emmi K Saarinen BM, Tomi Kuusimäki MD, PhD, Kari Lindholm RN, Kalle Niemi MD, Emma A Honkanen MD, PhD, Tommi Noponen PhD, Marko Seppänen MD, PhD … See all authors

First published: 20 May 2024

https://doi.org/10.1002/ana.26957

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Abstract

Objective

This study was undertaken to investigate the effects of dietary caffeine intake on striatal dopamine function and clinical symptoms in Parkinson disease in a cross-sectional and longitudinal setting.

Methods

One hundred sixty-three early Parkinson disease patients and 40 healthy controls were investigated with [¹²³I]FP-CIT single photon emission computed tomography, and striatal dopamine transporter binding was evaluated in association with the level of daily coffee consumption and clinical measures. After a median interval of 6.1 years, 44 patients with various caffeine consumption levels underwent clinical and imaging reexamination including blood caffeine metabolite profiling.

Results

Unmedicated early Parkinson disease patients with high coffee consumption had 8.3 to 15.4% lower dopamine transporter binding in all studied striatal regions than low consumers, after accounting for age, sex, and motor symptom severity. Higher caffeine consumption was further associated with a progressive decline in striatal binding over time. No significant effects of caffeine on motor function were observed. Blood analyses demonstrated a positive correlation between caffeine metabolites after recent caffeine intake and dopamine transporter binding in the ipsilateral putamen.(So tell us in understandable words; is caffeine good for Parkinson's patients? Or are you that incompetent you can't figure that out?)

Interpretation

Chronic caffeine intake prompts compensatory and cumulative dopamine transporter downregulation, consistent with caffeine's reported risk reduction in Parkinson disease. However, this decline does not manifest in symptom changes. Transiently increased dopamine transporter binding after recent caffeine intake has implications for dopaminergic imaging guidelines. ANN NEUROL 2024

Caffeine (1,3,7-trimethylxanthine) is the most extensively consumed psychostimulant worldwide.¹ Together with its various acute effects on wakefulness, motor coordination, and blood pressure,² regular consumption has been hypothesized to reduce the risk of Parkinson disease (PD).³ This caffeine-induced risk reduction seems dose-dependent and has been observed in both case–control^{4, 5} and epidemiological studies, including prospectively followed cohorts.^6-10 Experiments with animal models, such as the 1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine (MPTP) neurotoxin and alpha-synuclein models, have additionally provided evidence of the neuroprotective effects of caffeine in PD-type neurodegeneration.^{11, 12} Notably, decaffeinated coffee fails to provide the same protective benefits, highlighting the specific mechanistic role of caffeine itself rather than other chemical compounds present in coffee and caffeine-containing products.¹³

Although the positive effects of caffeine on PD prevention are well documented, the impact of caffeine on symptomatic individuals already diagnosed with PD is unclear despite several studies on this topic. In one controlled randomized trial of PD patients undergoing 6–18 months of treatment with caffeine, there was no clinical improvement, but there was increased dyskinesia, leading to the conclusion that caffeine cannot be recommended as symptomatic therapy for parkinsonism.¹⁴ However, this trial focused on symptomatic therapy and did not address the potential of caffeine for disease modification. On the other hand, a meta-analysis of 4 studies with follow-up periods ranging from 4 to 10 years suggested that caffeine consumption in patients with early PD may slow disease progression.¹⁵ Nevertheless, only 4 studies were included in the meta-analysis, and there was substantial heterogeneity in the parameters used to assess both caffeine consumption and PD progression in these studies, which limits the generalizability of their findings.

Caffeine-induced modification of the nigrostriatal dopamine system could be one of the underlying factors in the possible protection against PD. Caffeine modulates dopaminergic function in the central nervous system by interacting with adenosine receptors, which are colocalized and functionally interact with dopamine receptors.^{16, 17} This adenosine–dopamine interaction has been proposed to play a role in the pathogenesis and treatment of PD,^{11, 18, 19} leading to the testing of multiple adenosine A_2A receptor antagonists as potential PD treatments.²⁰ Human dopaminergic functional imaging studies focusing on caffeine have indicated that typical dietary doses of caffeine can increase postsynaptic dopamine D2/D3 receptor availability.^{21, 22} However, the results of presynaptic dopamine transporter (DAT) imaging studies in PD patients have yielded mixed results, with one study reporting no significant changes in striatal DAT binding after chronic coffee consumption,²³ whereas another has observed lower caudate nucleus DAT binding in coffee-drinking PD patients than in nonconsumers.²⁴ The long-term effects of caffeine consumption on brain presynaptic dopamine function or PD progression have not yet been examined.

Our study was designed to test the hypothesis that caffeine improves dopaminergic function in PD patients and enhances motor function in the long term. To elucidate this matter, we conducted a study to investigate the dopaminergic effects of caffeine in PD patients in a cross-sectional and longitudinal setting using conventionally available brain DAT imaging.

 

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