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Wileidy Gomez, PhD, MD

Wileidy Gomez, PhD, MD

Postdoctoral Research Fellow

Biography

Dr. Wileidy Gomez is from Venezuela. She received her B.S in Biology in 2007 and a Master's degree in Cellular Biology in 2010 at Universidad de Los Andes (Venezuela). In 2017, she moved to Chile to pursue a doctoral degree in Integrative Genomics at Universidad Mayor. In 2021 she received her PhD in Genomic Integrative. Subsequently, she joined Dr. Rodrigo Morales' lab at the University of Texas Health Science Center at Houston as a Postdoctoral Research Fellow. Here, She plans to continue expanding her knowledge regarding Alzheimer's disease by identifying misfolded Aβ conformational variants or “strains,” similarly as it has been described for prion diseases.

linkedin.com/in/wileidy-gomez-18b1b765

Publications

PubMed

Education

PhD in Integrative Genomic (Chile), 2021.

Master in Cell Biology, University of the Andes (Venezuela), 2010.

Bachelor in Biology, University of the Andes (Venezuela), 2007.

Advisor

Dr. Rodrigo Morales

Research Description

The amyloid cascade hypothesis proposes that amyloid beta (Aβ) misfolding is the initial pathological event in Alzheimer’s disease (AD). Specifically, this hypothesis propose that misfolded Aβ peptides lead the misfolding of tau proteins and the formation of neurofibrillary tangles (NFTs). In turn, tau tangles are a leading pathological driver in AD. However, the precise mechanisms of how pathological Aβ and tau interact are unclear. Recent studies have reported the existence of structurally heterogeneous misfolded Aβ aggregates (Aβ strains) which can self-aggregate through seeding mechanisms. These events are similar to those found for infectious prions which are responsible to induce different pathology and clinical manifestations in susceptible animal models. We hypothesize that Aβ strains variability could explain the heterogeneity of amyloid deposits observed in the patients' brains and the diversity of pathological and clinical manifestations in AD. Unfortunately, the potential differential role of these Aβ strains in initiating tau pathology has not been explored. Here, we propose to evaluate in vitro and in vivo the “cross-seeding” events linking Aβ strains and tau tangles.

https://orcid.org/0000-0002-3980-6365 https://orcid.org/0000-0002-3980-6365