URIC ACID AND NEURODEGENERATIVE DISEASES: FINDING A PREDICTOR OF COGNITIVE DECLINE

LETTER TO THE EDITOR

REVISTA DE LA FACULTAD DE MEDICINA HUMANA 2024 - Universidad Ricardo Palma
10.25176/RFMH.v24i3.6639

URIC ACID AND NEURODEGENERATIVE DISEASES: FINDING A PREDICTOR OF COGNITIVE DECLINE

ÁCIDO ÚRICO Y ENFERMEDADES NEURODEGENERATIVAS: ENCONTRANDO UN PREDICTOR DEL DETERIORO COGNITIVO

Patricia Pernia-Gavedia ORCID 1,a

1 Instituto de Investigaciones en Ciencias Biomédicas, Universidad Ricardo Palma, Lima, Perú.

a Medical student

Dear Editor:

I am writing to highlight the growing concern about the prevalence of neurodegenerative diseases globally and the urgent need to find predictors of early cognitive development.

Neurodegenerative diseases represent a significant burden for affected individuals, their families, and society at large(1-3). Alzheimer's disease (AD) and Parkinson's disease (PD) are estimated to affect around 50 and 6.1 million people worldwide, respectively(1,2). Meanwhile, amyotrophic lateral sclerosis (ALS), although less common than AD or PD, remains a devastating disease, affecting 2 per 100,000 people each year, and the average life expectancy after diagnosis is around 2 to 5 years(3). Finding early predictors of cognitive development could have a substantial impact on the management and treatment of these diseases(4,5). Uric acid (UA) has emerged among the factors that can modify cognitive function both in the general population and in people with neurodegenerative diseases(4).

The role of UA as a predictor of cognitive function has been little studied. However, in the last four years, various investigations have left a promising panorama, with Europe and Asia being the continents that have done the most research in this regard(5-9). In 2020, a cohort study conducted in Italy whose objective was to evaluate whether serum UA levels differ between older people with AD compared to those with mild cognitive impairment and healthy controls, found that people with late AD presented significantly lower serum UA levels compared to controls(5). In 2021, in China, a longitudinal study aimed to evaluate the progression of mild cognitive impairment and AD in early stages by combining blood biomarkers, clinical and neuropsychological assessments; showing that higher levels of serum UA have a detrimental effect on normal cognition but a protective tendency in individuals with cognitive impairment(6). In 2022, in the same country, two cohort studies were carried out that sought to find a relationship between the level of UA and cognitive impairment in patients with neurodegenerative diseases. In the first, it was shown that serum UA levels were inversely proportional to cognitive dysfunction in patients with PD(7), and in the other study, it was found that serum UA was significantly lower in AD and PD compared to controls(8). And in the present year, 2024, a cohort study carried out in Italy, whose objective was to explore the correlation between UA levels and cognitive impairment, concluded that patients suffering from ALS with frontotemporal dementia presented lower levels of uric acid compared to patients who had ALS with intermediate cognition or normal cognition(9). Therefore, these studies may lead us to think that UA could prevent or delay the deterioration of cognitive function in patients with AD, PD, and ALS.

Nevertheless, according to the author, research on neurodegenerative diseases has not yet been carried out in Latin America, including Peru. This lack of research can be attributed to limited resources, poor access to specialized medical care, research priorities in other areas of public health, lack of international collaboration, and need for government support. In Peru, there may also be limitations in research infrastructure, training of specialized personnel, and public awareness of the importance of these diseases.

In summary, the findings support the likely potential utility of serum UA as an early predictor of cognitive decline in patients with neurodegenerative diseases. The inverse correlation between UA levels and the degree of cognitive impairment suggests that monitoring UA levels could be a valuable tool in the early identification and monitoring of the progression of these diseases. These results open the door to future research that further explores the role of UA in the pathogenesis and progression of neurodegenerative diseases, as well as the development of potential therapeutic strategies based on the modulation of UA levels.

It is recommended that more resources be allocated to research in this field, both nationally and internationally, to advance the identification of UA as a predictor of cognitive impairment in neurodegenerative diseases and improve our understanding of these pathologies. Furthermore, it is crucial to foster collaboration between researchers, institutions, and governments to address this challenge comprehensively.


Author Contributions: The authors participated in the generation, data collection, drafting, and final version of the original article.

Funding: Self-funded.

Conflict of Interest: The authors declare no conflict of interest in the publication of this article.

Received: May 28, 2024

Approved: July 3, 2024


Correspondence: Patricia Pernia-Gavedia

Address: Av. Benavides block 5440, Santiago de Surco, Lima-Peru

Phone: +51 941286501

Email: pperniag2410@gmail.com


Article published by the Journal of the faculty of Human Medicine of the Ricardo Palma University. It is an open access article, distributed under the terms of the Creatvie Commons license: Creative Commons Attribution 4.0 International, CC BY 4.0(https://creativecommons.org/licenses/by/4.0/), that allows non-commercial use, distribution and reproduction in any medium, provided that the original work is duly cited. For commercial use, please contact revista.medicina@urp.edu.pe.


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