Main Ongoing Projects
Astrocytes in Alzheimer’s disease: Alzheimer’s disease has been consistently viewed as a “neuronal” pathology. However, recent evidences indicate that astrocytes, the most abundant subtype of glial cells, are also involved in Alzheimer’s disease pathophysiology. Our laboratory is interested in understanding the precise contribution of these cells to Alzheimer’s disease. We believe that astrocytes may play a pivotal role in Alzheimer's disease progression.
Rocha , A., In Preparation
Metabolic networks in Alzheimer’s disease: The 18F-fluorodeoxyglucose ([18F]FDG) is a radioactive glucose analogous, which has been utilized for more than 40 years to estimate cerebral glucose metabolism with positron emission tomography (PET). Currently, it is well established that cerebral [18F]FDG uptake is proportional to synaptic activity. This coupling allows the identification of brain regions that are working in synchronicity based on their energy consumption, what we call metabolic network. This assumption can be used for understading functional remodeling in brain disorders, which can potentially lead to the discovery of new mechanisms.
Zimmer ER., et al. 2017
Alzheimer’s Pattern Recognition: Alzheimer’s clinical trials have been using a multimodal and multisdisciplinary combination of technologies for undersyading Alzheimer’s disease progression. More specifically, fluid and neuroimaging biomarkers have been combined with genetic, demographics and neuropshycological data. By using innovative machine learning and deep learning algorithms, we hope to identify a disease signature that predicts Alzheimer’s disease before the onset of symptoms.
Rodrigues, YE, et al. 2017
Fontana., IC et al. In Preparation
Anti-Oligomer Drugs Platform: The most accepted hypothetical model indicates that AD begins with abnormal processing of amyloid precursor protein (APP). This dysfunction results in the deposition of aggregated forms of amyloid-beta (Aβ) plaques, progressive neurodegeneration, and cognitive decline. In this context, it is believed that a soluble conformation that precedes the formation of Aβ plaques, called Aβ oligomers (AβOs), might be responsible for the initial toxicity in AD. Whit this in mind, we hypothesize that drugs targeting AβOs can potentially prevent or even halt AD natural evolution. This project main goal is to identify potential active molecules against AβOs toxic effects using an experimental platform with high translational power.
Modifiable Risk factors in Alzheimer’s disease: Recent evidences indicate that lifestyle factors are risk factors for developing Alzheimer's disease. Modifiable risk factors include exercise, education, social engagement, cognitive stimulation, obesity and diet. In fact, observational findings indicate that changes lifestyle could reflect in a reduction in the risk of developing Alzheimer’s disease. By combining experimental studies and clinical data we expected to identify precise mechanisms that potentially links lifestyle and Alzheimer’s disease.