Blanca Rodríguez defends her PhD thesis on biological aging and its role in Alzheimer’s disease

Blanca Rodríguez, a researcher in the Genomics Group at the Barcelonaβeta Brain Research Center (BBRC), has defended her PhD thesis titled “The role of biological aging on Alzheimer's disease risk.” Her work focused on understanding how telomere length—a key marker of biological aging—influences brain vulnerability and the development of Alzheimer’s disease (AD).

Blanca joined the BBRC in 2020 after earning a degree in Basic and Experimental Biomedicine from the University of Seville and a master’s degree in Omics Data Analysis from the University of Vic. Since then, she has focused her research on studying how systemic aging processes contribute to the risk of developing AD.

Throughout her thesis, she adopted a multidisciplinary approach to analyze the relationship between telomere length in blood leukocytes and various clinical, molecular, and neuroimaging indicators associated with the preclinical stages of AD. Telomeres, made up of repetitive DNA sequences at the ends of chromosomes, protect our genetic material during cell division. Their gradual shortening with age limits the ability of cells to divide, promoting cellular senescence and contributing to tissue and organ aging.

Her study combined data from cerebrospinal fluid biomarkers, cognitive testing, and advanced brain imaging techniques to explore the potential causal role of biological aging in AD.

Through this innovative approach, Blanca Rodríguez demonstrated that shorter telomere length is associated with greater brain vulnerability, poorer episodic memory performance, and higher levels of neurodegeneration-related biomarkers. Overall, her work contributes to a broader understanding of AD by highlighting the need to consider systemic aging factors as part of the pathological process and opens new avenues for early-life research and prevention.

What are the main conclusions of your thesis?
My thesis focuses on understanding how biological aging—that is, the functional and molecular changes that occur in our bodies over time, regardless of chronological age—influences brain vulnerability and the risk of developing dementia.

Specifically, we focused on telomere length in blood leukocytes as a key marker of biological aging. Our findings show that shorter telomeres are associated with an increased risk of developing dementia, suggesting that promoting healthy aging could be a key strategy in preventing the disease.

This increased risk manifests at multiple levels: on the one hand, it is linked to lower cognitive reserve, and on the other, at a molecular level, it is associated with higher levels of biomarkers related to neuronal death, synaptic dysfunction, and especially glial reactivity and neuroinflammation.

Taken together, these findings reinforce the idea that AD does not originate solely in the brain but is also connected to the aging of the body as a whole.

What opportunities do these findings open in Alzheimer’s research?
We know that age is the main risk factor for developing AD, but we also know that people don’t age at the same pace or with the same consequences. Our findings underscore the need to approach Alzheimer’s from a systemic perspective, where biological aging is not just a backdrop, but an active player in the disease’s development.

Adopting this approach could broaden the search for new therapeutic targets—not only to slow the progression of Alzheimer’s but also to promote healthy aging and prevent other aging-related diseases.

Additionally, integrating different markers of biological aging could help us identify earlier intervention windows, before clinical symptoms appear, allowing us to design more specific and personalized prevention strategies tailored to each individual’s life history and vulnerability. This would be key to improving brain health in later life and reducing the global burden of the disease.

How are you approaching your new stage as a postdoctoral researcher? What areas of research would you like to explore further?
I’m approaching this new stage with great enthusiasm and a strong commitment to continue contributing to Alzheimer’s prevention research. I’m particularly interested in deepening our understanding of biological aging by incorporating new molecular and systemic biomarkers that allow us to better understand how the body ages and how that process affects brain health.

I want to focus especially on immune system aging and chronic inflammatory processes, which may play a key role in the earliest phases of Alzheimer’s and complement current approaches that are primarily brain-focused.

Moreover, I’d like to integrate into this research certain social and potentially modifiable factors—such as economic insecurity or chronic stress—which we know can accelerate biological aging and increase vulnerability to the disease.