Redox Biology and Neurodegeneration

Neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS), are characterized by a progressive loss of synapses and neurons in the central nervous system. Although their origin is complex and multifactorial, the disruption of redox homeostasis plays a central role in these processes. Aging is the main risk factor, and the disease often progresses silently for decades before the appearance of the first clinical symptoms.

Currently, there are no curative therapies for these conditions, highlighting the urgent need to identify new therapeutic targets and early biomarkers that enable early diagnosis and the development of personalized treatments. Research in redox biology and the study of molecular mechanisms involved in synaptic loss are essential to advance the fight against neurodegenerative diseases.

 Main research lines:

Redox imbalance and stress granule dynamics in ALS, exploring the interaction between oxidative stress, mitochondrial dysfunction, and stress granule behavior as a reflection of RNA metabolic pathway functionality.

Study of the synaptic lipid profile, integrated evaluation of data obtained through transcriptomic and lipidomic analyses of synaptic dysfunction in Alzheimer's disease.

Peripheral redox and inflammatory signatures in Parkinson's disease, aiming to identify gene and protein biomarkers in blood.

Development of NRF2-based neuroprotective therapies for tauopathies, integrating molecular and translational approaches to validate NRF2 as a pharmacological target.

 

To understand how redox dysregulation and oxidative damage, especially in brain lipids, contribute to synaptic and neuronal vulnerability, we use cellular and animal models, as well as human samples, along with advanced molecular and bioinformatic analysis tools.

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