Summary: A new study has revealed critical metabolic impairments in Parkinson’s disease ( PD), focusing on purine metabolism and ATP recycling. Scientists discovered that PD patients have significantly lower levels of lactic acid and other purine compounds in their blood and spinal substance, which have an impact on brain power generation.
This finding challenges previously held beliefs about purine digestion and suggests that ATP disposal could be used to create novel PD solutions. The analyze emphasizes the need for treatments that aim to enhance energy metabolism more than just raising uric acid levels.
Important Facts:
- Parkinson’s people have lower levels of lactic acid, linked to ATP disturbance.
- Purine molecules ‘ lower levels indicate a weaker power recycling system.
- Using ATP production as a therapeutic option for PD may be discovered.
Origin: Fujita Health University
With its progressive nature and crippling effects on motor function, Parkinson’s disease ( PD), the second-most prevalent neurodegenerative disorder worldwide, has long puzzled scientists.
A recent study from Fujita Health University’s School of Medicine revealed fresh insight into the physiological alterations that PD patients experience. Researchers have discovered significant changes in purine metabolism and the recycling of adenosine triphosphate ( ATP), the molecule responsible for energy production in cells, by studying the blood and cerebrospinal fluid ( CSF ) of the patients.
Researchers have been monitoring the uric acid levels in people with PD for centuries. Initial theories suggested that a strong position would be played by a substance known for its antioxidant properties: ric acid, which reduces oxidative stress in the mind.
However, this investigation, published in , NPJ Parkinson’s Disease , on 09 September 2024 reveals that the condition is more difficult.
” Our observations suggest that decreased uric acid levels in people with PD are influenced by factors beyond purine digestion, including outside factors such as gender, mass, and age”, said Dr. Watanabe, the lead author of the study.
This implies that the connection between uric acid and Police is more complex than previously believed, and that it involves far more than just oxidative stress.
By assessing the rates of purine compounds, including inosine, hypoxanthine, xanthine, and lactic acid, using a technique called intended metabolomics, they found that people with PD have significantly lower levels of lactic acid in both blood and CSF compared to good controls. Furthermore, the rates of hypoxanthine, another purine molecule, were reduced.
The study found that body fat and sex were factors in the reductions in blood and CSF lactic acid, but not the inland metabolite xanthine, which challenges previous hypotheses about purine metabolism.
As Dr. Watanabe explains,  ,” Our studies indicate that plasma and CSF uric acid levels are not directly related to inland xanthine amounts, suggesting forces beyond traditional purine digestion pathways”.
This finding is significant because it demonstrates a malfunction in the ATP disposal method. Cellular electricity use requires ATP, and its breakdown and reuse are necessary to maintain healthy body function. In PD, this method seems to be malfunctioning, leading to an power imbalance that could further compound the disease’s symptoms.
Inosine, a prelude to lactic acid, was another crucial component of the investigation. The group observed no significant decline in plasma inosine but a significant decrease in CSF inosine in patients with PD.
Our research found that the decrease in CSF inosine may indicate a decrease in genetic manufacturing within the central nervous system, which could have significant effects on energy generation in the brain, according to Dr. Watanabe.
The study somewhat discovered that people with PD had significantly lower serum and CSF hypoxanthine levels than good settings. In the salvage pathway, which is crucial for maintaining energy production, over 90 % of hypoxanthine is recycled as inosine monophosphate ( IMP ) in the crucial role of.
New treatment options are available as a result of the discovery that energy metabolism is disrupted in PD. Current therapies largely focus on managing symptoms, but this research suggests that targeting the body’s energy recycling system could slow the disease’s progression.
This study demonstrates that medications that aim to raise serum uric acid levels may have a limited impact on the treatment of Parkinsonism. Instead, focusing on the purine recycling system, particularly enhancing ATP production, could hold more promise.
As the study progresses, the team wants to look into possible ways to improve energy metabolism and ATP recycling through exercise and nutritional interventions.
In conclusion, this amazing study brings us one step closer to comprehending the intricate metabolic processes that drive PD. Scientists could create new treatments that both lower the rate of disease progression and improve the patient’s quality of life by focusing on energy metabolism and the purine recycling system.
About this Parkinson’s disease research news
Author: Hisatsugu Koshimizu
Source: Fujita Health University
Contact: Hisatsugu Koshimizu – Fujita Health University
Image: The image is credited to Neuroscience News
Original Research: Open access.
” Uric acid and alterations of purine recycling disorders in Parkinson’s disease: a cross-sectional study” by Hirohisa Watanabe et al. npj Parkinson’s Disease
Abstract
Uric acid and alterations of purine recycling disorders in Parkinson’s disease: a cross-sectional study
The relationship between reduced serum uric acid ( UA) levels and Parkinson’s disease ( PD), particularly purine metabolic pathways, is not fully understood.
Our study compared serum and cerebrospinal fluid ( CSF ) levels of inosine, hypoxanthine, xanthine, and UA in PD patients and healthy controls. We analyzed 132 samples ( serum, 45 PD, and 29 age- and sex-matched healthy controls, CSF, 39 PD, and 19 age- and sex-matched healthy controls ) using liquid chromatography-tandem mass spectrometry.
Results showed significantly lower serum and CSF UA levels in PD patients than in controls ( p <, 0.0001, effect size , r = 0.5007 in serum,  , p = 0.0046,  , r = 0.3720 in CSF).
Decreased serum hypoxanthine levels were observed ( p = 0.0002,  , r = 0.4338 ) in PD patients compared to controls with decreased CSF inosine and hypoxanthine levels ( p <, 0.0001,  , r = 0.5396:  , p = 0.0276,  , r = 0.2893 ).
A general linear model analysis revealed that external factors, such as sex and weight in serum and age and weight in CSF, were primarily responsible for the lower UA levels, which were not related to the purine metabolic pathway.
Our findings highlight the need for further investigation into the underlying mechanisms and potential therapeutic approaches. They also highlight that decreased UA levels in PD are affected by factors beyond purine metabolism, including external factors such as sex, weight, and age.
