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Pedro de la Villa

Researcher at University of Alcalá

Publications -  97
Citations -  2993

Pedro de la Villa is an academic researcher from University of Alcalá. The author has contributed to research in topics: Retina & Retinal. The author has an hindex of 30, co-authored 97 publications receiving 2390 citations. Previous affiliations of Pedro de la Villa include University of Murcia & Carlos III Health Institute.

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Cellular responses following retinal injuries and therapeutic approaches for neurodegenerative diseases

Nicolás Cuenca, +6 more
- 01 Nov 2014 - 
TL;DR: An overview of the common and distinctive features of retinal neurodegenerative diseases, including the molecular, anatomical and functional changes caused by the cellular response to damage, are provided in order to establish appropriate treatments for these pathologies.
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Balance between autophagic pathways preserves retinal homeostasis.

Natalia Rodriguez-Muela, +6 more
- 01 Jun 2013 - 
TL;DR: A marked reduction in macroautophagic activity in the retina with age is described, which coincides with an increase in chaperone‐mediated autophagy (CMA), which is also observed during retinal neurodegeneration in the Atg5flox/flox mice and nestin‐Cre mice.
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Exercise benefits on Alzheimer's disease: State-of-the-science.

Pedro L. Valenzuela, +7 more
- 16 Jun 2020 - 
TL;DR: In summary, physical exercise might provide numerous benefits through different pathways that might, in turn, help prevent risk and progression of Alzheimer's disease.
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Refractive changes induced by form deprivation in the mouse eye.

Jaime Tejedor, +1 more
- 01 Jan 2003 - 
TL;DR: Deprived eyes showed significant development of myopia compared with the contralateral fellow eye after transitory hypermetropia, regardless of whether they were deprived before or after natural eye opening, which indicates that myopia is mainly axial.
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The Protein Kinase DYRK1A Regulates Caspase-9-Mediated Apoptosis during Retina Development

Ariadna Laguna, +9 more
- 09 Dec 2008 - 
TL;DR: The data suggest a model in which dysregulation of the apoptotic response in differentiating neurons participates in the neuropathology of diseases that display DYRK1A gene-dosage imbalance effects, such as Down's syndrome.