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Our Lab

Our research interests are focused on the understanding of the molecular mechanisms which lead to neurodegeneration in diseases such as Parkinson’s, Huntington’s, or Alzheimer’s disease. These diseases are intimately associated with protein misfolding and aggregation in specific regions of the brain.
Because the molecular pathways involved in protein homeostasis are highly conserved, we employ a wide variety of model organisms, from the simple but powerful budding yeast to mammalian cell culture and mice, to study the origin of the problems.
Our ultimate goals are to develop novel therapeutic approaches for these and other related disorders. We are working closely together with clinicians in order to accelerate drug discovery efforts, translating basic research into clinical applications that will improve the lives of patients.

Research Areas

  • Protein misfolding, oligomerization and aggregation

  • Yeast models for Parkinson’s and Huntington’s disease

  • Modulators of protein aggregation and toxicity

  • Microscopy-based methods for investigating the molecular nature of the toxic proteinaceous species in Parkinson’s disease

  • In vivo imaging using multi-photon microscopy

  • Development of novel therapeutic approaches for neurodegenerative disease

Head of the Department
Head of the DepartmentProf. Dr. Tiago Outeiro
ORCIDResearchgatePubMed

Highlights

Selected Publications

Systematic Comparison of the Effects of Alpha-synuclein Mutations on Its Oligomerization and Aggregation

December 7th, 2018|Categories: AG-Outeiro, Selected Publications|

Aggregation of alpha-synuclein (ASYN) in Lewy bodies and Lewy neurites is the typical pathological hallmark of Parkinson's disease (PD) and other synucleinopathies. Furthermore, mutations in the gene encoding [...]

Environmental and genetic factors support the dissociation between α-synuclein aggregation and toxicity

December 6th, 2018|Categories: AG-Outeiro, Selected Publications|

Synucleinopathies are a group of progressive disorders characterized by the abnormal aggregation and accumulation of α-synuclein (aSyn), an abundant neuronal protein that can adopt different conformations and biological [...]

Glycation potentiates α-synuclein-associated neurodegeneration in synucleinopathies

December 6th, 2018|Categories: AG-Outeiro, Selected Publications|

α-Synuclein misfolding and aggregation is a hallmark in Parkinson’s disease and in several other neurodegenerative diseases known as synucleinopathies. The toxic properties of α-synuclein are conserved from yeast [...]

α-synuclein interacts with PrPC to induce cognitive impairment through mGluR5 and NMDAR2B

December 6th, 2018|Categories: AG-Outeiro, Selected Publications|

Synucleinopathies, such as Parkinson's disease and dementia with Lewy bodies, are neurodegenerative disorders that are characterized by the accumulation of α-synuclein (aSyn) in intracellular inclusions known as Lewy [...]

Nuclear localization and phosphorylation modulate pathological effects of Alpha-Synuclein

December 6th, 2018|Categories: AG-Outeiro, Selected Publications|

Alpha-synuclein (aSyn) is a central player in Parkinson’s disease (PD) but the precise molecular mechanisms underlying its pathogenicity remain unclear. It has recently been suggested that nuclear aSyn may [...]

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