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Blood-borne tau aggregates. A window into peripheral pathogenesis and therapeutic intervention

The progression of tau pathology in the brain of Alzheimer’s patients correlates with the neurodegenerative process and cognitive decline. Under experimental conditions, tau aggregates can spread and accelerate the progression of tauopathies. Moreover, it is possible to modify the levels of beta-amyloid in the brain by changing its balance in the periphery. Our aim is to explore the role of vascular tau aggregates in the development or treatment of the disease.


Funded by Ministerio de Ciencia e Innovación

Diabetes and Alzheimer. Molecular mechanisms of protein cross-seeding.

Extensive epidemiological studies have reported an association between type 2 diabetes (T2D) and Alzheimer’s disease (AD). Nearly 80% of all AD patients exhibit glucose tolerance impairment or have been diagnosed with diabetes. Our goal is to determine whether the presence of aggregated amylin, commonly found in T2D patients, could be a risk factor to develop AD, explaining the cause of increased comorbidity between both diseases through a cross-seeding mechanism.

Funded by Ministerio de Ciencia, Innovación y Universidades.

Depression as risk factor for converting mild cognitive impairment into Alzheimer’s disease

Clinical studies suggest that depressive symptoms could be considered an important risk factor for the future development of cognitive decline and even Alzheimer’s disease (AD). In fact, there is a strong association between depression during late-life depression and AD. This project focuses on understanding the impact of depression during adult life on protein aggregation to further analyze the possible mechanisms involved in the onset and development of AD

Funded by Brain and Behavior Research Foundation, FEDER Funds and University of Malaga.

Stem cell-derived anti-inflammatory treatment for Alzheimer's disease

Current treatments for AD only ameliorate the symptoms, but none of them delays or halts disease progression. In recent years, stem cells have received growing attention as a potential therapy for brain disorders. The main goal of this project is to develop a new approach for treating AD using a neural precursor-based non-invasive therapy.

Funded by Texas Alzheimer’s Research & Care Consortium

Identification and Characterization of Alzheimer’s Disease-Associated Protein Misfolding Seeds after Traumatic Brain Injury

Traumatic brain injuries (TBI) can accelerate the development of Alzheimer’s disease (AD) and, therefore, could be considered a risk factor for this neurodegenerative disease. The main objective of this project is to elucidate the molecular mechanisms responsible for the contribution of TBI to the pathogenesis of AD, focusing on tau aggregation.

Funded by USA Department of Defense

PET imaging to detect Alzheimer’s like pathology after brain injury

This proposal focuses on studying the potential use of neuroimaging to identify and diagnose traumatic brain injury by detecting the associated Alzheimer’s brain pathology by imaging tau, amyloid deposition, and brain inflammation. The development of an imaging test to identify pathological abnormalities after TBI would likely allow an improved and earlier therapeutic intervention, diminishing the severity of long-term sequelae, and reducing the probabilities to develop AD later on.

Funded by Alzheimer’s Association

Photodynamic treatment for Alzheimer’s disease based on directed amyloid photo-oxidation

Amyloid-beta aggregates are toxic to neurons and trigger a cascade of events that will lead to AD. We propose to develop red light-activated molecules that bind and produce a chemical modification to amyloid-beta. Modification of amyloid-beta is expected to change its shape, preventing its association and, therefore, its toxicity and capability to induce disease.

Funded by Rice University/UTHealth

Protective role of interleukin33 in abnormal neuronal aging and degeneration

Brain interleukin33 has a neuroprotective role of during aging-related oxidative stress. We aim to explore if interleukin33 deficiency causes aging related neuronal death and senile dementia such as Alzheimer’s disease, affecting amyloid deposition and brain inflammation.

Funded by National Institutes of Health