Observational studies are carried out to attempt to determine whether a particular substance, e.g., a food type, has a positive or negative impact on a medical condition, e.g., Alzheimer’s disease, Parkinson’s disease, colon cancer, and others. Yet, because of three factors (1) complex pathogenesis,,(2) lack of hypotheses, and (3) lack of methodologies of hypothesis testing in these areas of scientific research, the impact of the substance and the disease is not fully explained.
What are the proposed mechanisms of action of coffee consumption decreasing risk of Alzheimer’s disease and Parkinson’s disease?
Dennis
Dennis Mazur
Hi dear. It is possible that it could be by reducing the activity of adenylate cyclase
Thank you for your replay.. Are you/Is anyone aware of any researchers writing in peer-reviewed medical or scientific journals who have speculated on possible mechanisms of action of coffee, caffeine, or other components of the coffee bean?
Dennis
Dennis Maue
Hi. Your welcome..As far as I know I have not seen anything about the mechanism, but you must search more
Caffeine is antagonist of A2aReceptor...finally reduced the activity of adenyl cycle.
J Alzheimers Dis. 2010;20 Suppl 1:S205-20. doi: 10.3233/JAD-2010-091459.
Effects of caffeine in Parkinson's disease: from neuroprotection to the management of motor and non-motor symptoms.
Abstract
Parkinson's disease (PD) is the second most common neurodegenerative disorder affecting approximately 1% of the population older than 60 years. Classically, PD is considered to be a motor system disease and its diagnosis is based on the presence of a set of cardinal motor signs (rigidity, bradykinesia, rest tremor) that are consequence of a pronounced death of dopaminergic neurons in the substantia nigra pars compacta. Nowadays there is considerable evidence showing that non-dopaminergic degeneration also occurs in other brain areas which seems to be responsible for the deficits in olfactory, emotional and memory functions that precede the classical motor symptoms in PD. The present review attempts to examine results reported in epidemiological, clinical and animal studies to provide a comprehensive picture of the antiparkinsonian potential of caffeine. Convergent epidemiological and pre-clinical data suggest that caffeine may confer neuroprotection against the underlying dopaminergic neuron degeneration, and influence the onset and progression of PD. The available data also suggest that caffeine can improve the motor deficits of PD and that adenosine A2A receptor antagonists such as istradefylline reduces OFF time and dyskinesia associated with standard 'dopamine replacement' treatments. Finally, recent experimental findings have indicated the potential of caffeine in the management of non-motor symptoms of PD, which do not improve with the current dopaminergic drugs. Altogether, the studies reviewed provide strong evidence that caffeine may represent a promising therapeutic tool in PD, thus being the first compound to restore both motor and non-motor early symptoms of PD together with its neuroprotective potential.
Hi,
You could check our article: Eskelinen MH, Kivipelto M. Caffeine as a protective factor in dementia and Alzheimer's disease. J Alzheimers Dis. 2010;20 Suppl 1:S167-74. doi: 10.3233/JAD-2010-1404. In the discussion we are speculating some possible mechanisms of coffee consumption and the risk of Alzheimer's disease. There are also quite many newer articles about coffee drinking and AD/PD, but at least here you could start...
Dennis:
Wonderful discussion, and great contributions! Here I play the gadfly in the hope of stimulating further and more critical appraisal on this important issue.
A CONTRARIAN PERSPECTIVE
There are many significant methodological issues that compromise any foundation for unequivocal conclusions, which I sketch briefly and highly selectively (in turn abbreviated from an as yet unpublished internal review commissioned by a European regulatory authority):
1. Absence of accurate data on the coffe intake duration in the diverse populations studied, which renders indeterminate precisely at what onset of coffee consumption age is associated with clinically relevant positive effect.
2. Indeterminate quantification: in the many studies, consumption levels of coffee are variously described as ‘low’, ‘moderate’, or ‘high’, with further confounding as to the amount of caffeine delivered in a cup, with variance between
It is my pleasure.You are welcome.If you need more informations ,please feel free to contact me directly.Sincerely,
Constantine
Please see the attached file as an additional information
Article Evaluation of the relationship between habitual consumption ...
An in vitro screen was conducted for natural products that support PP2A activity toward phospho-tau, and a suitable activity was identified in coffee extracts. The active agent was purified to homogeneity and identified as eicosanoyl-5-hydroxytryptamide (EHT). Synthetic EHT exhibited the same ability to support PP2A activity as EHT isolated from coffee. Dietary supplementation with synthetic EHT exhibited neuroprotective efficacies in mouse models for Parkinson's disease
Hello.The probable mechanism is the effect of caffeine on adenosine receptors
Or interacting with xanthine...
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