Laura Estela Castro Aldrete
Currently, I am a postdoctoral researcher at the Karolinska Institute and an invited lecturer at the Monterrey Institute of Technology and Higher Education. I am currently studying the rescue of mitochondrial functions using pharmacological compounds in Alzheimer’s disease.
I got my PhD in Neuroscience under the supervision of Dr. Nigel Hooper and Dr. Andrew Doig at the University of Manchester. My thesis was focused on mitochondrial dysfunction in iPSC-derived neurons of Alzheimer’s disease patients.
I believe that to develop new medical interventions, we need to start incorporating sex and gender differences in preclinical and clinical research. Therefore, in my free time, I support and advocate for the mission of the Women’s Brain Project.
Neuroinflammation. New methods to halt chronic inflammation in Alzheimer’s disease
Age-related diseases are one of the most considerable challenges to our society and health care system. Neurodegenerative diseases most often affect older adults’ growing populations and are especially difficult to tackle since no disease-modifying drugs are available. To develop such urgently needed treatments, we need to understand the cellular and molecular mechanisms of the disease processes. The focus of my research is to study mitochondrial dysfunction and chronic inflammation, both central pathological hallmarks of Alzheimer’s disease (AD). Interestingly, the cellular pathways regulating mitochondrial function and onset of inflammation converge at mitochondria-endoplasmic reticulum (ER) contacts (MERCS). My aim is to investigate if modulation of MERCS structure and function regulate the inflammatory response in AD and related models.
Drug target identification to rescue mitochondrial functions in Alzheimer's disease.
Several strategies have been attempted to improve mitochondrial ATP production, including gene therapy, mitochondrial transplantation, metabolic manipulation and the use of small molecules to target mitochondrial dysfunction. However, most of the drugs tested do not directly target mitochondria but instead affect their function through indirect unknown mechanisms. In preclinical studies, polyphenols showed encouraging therapeutic performance in increasing mtDNA copy number and consequently mitochondrial biogenesis. These compounds function as free radical scavengers. However, results from clinical trials indicate limited beneficial outcomes due to rapid metabolism or low bioavailability in the brain. The novel mitotherapeutic term is used to designate small molecules that enhanced/boost the capacity of the mitochondrial to produce ATP and therefore restore mitochondrial function. Up today, mitochondria-targeting clinical trials using small-molecules that are positively charged and/or high affinity to mitochondrial membrane lipids showed the most encouraging results. In this project, I investigate the potential MoA of potential mitotherapeutics and MERCS modulators to rescue mitochondrial functions in AD.
Invited lecturer. Monterrey Institute of Technology and Higher Education (Mexico)
Teaching assistant. The University of Manchester (UK)
PhD in Neuroscience. The University of Manchester (UK)
MSc in Biotechnology and Enterprise. The University of Manchester (UK).
BSc in Biotechnology Engineering. Monterrey Institute of Technology and Higher Education (Mexico)