Focused ultrasound and microbubbles targeting alpha-synuclein pathology-related...
Focused ultrasound and microbubbles targeting alpha-synuclein pathology-related dementia (FUMA)
Over half of Parkinson Disease patients develop cortical dysfunctions leading to Parkinson Disease Dementia (PDD). The cognitive changes are primarily driven by pathological alpha-synuclein (a-syn) protein aggregates with secondar...
ver más
¿Tienes un proyecto y buscas un partner? Gracias a nuestro motor inteligente podemos recomendarte los mejores socios y ponerte en contacto con ellos. Te lo explicamos en este video
Proyectos interesantes
PID2021-127800OA-I00
MARCO METODOLOGICO PARA LA MONITORIZACION ONLINE DE LA DOSIS...
194K€
Cerrado
PGC2018-096335-B-I00
INVESTIGANDO LA AGREGACION AMILOIDE DE ALFA-SINUCLEINA EN LA...
168K€
Cerrado
PID2020-117656RB-I00
DESARROLLO DE NUEVAS HERRAMIENTAS DIAGNOSTICAS Y ESTRATEGIAS...
316K€
Cerrado
nanoIR4AD
Infrared nanospectroscopy to understand and combat Alzheimer...
207K€
Cerrado
CTQ2017-86994-R
DETECCION DE BIOMARCADORES RELACIONADOS CON LA ENFERMEDAD DE...
174K€
Cerrado
Información proyecto FUMA
Duración del proyecto: 40 meses
Fecha Inicio: 2023-04-17
Fecha Fin: 2026-08-31
Líder del proyecto
AARHUS UNIVERSITET
No se ha especificado una descripción o un objeto social para esta compañía.
TRL
4-5
Presupuesto del proyecto
231K€
Fecha límite de participación
Sin fecha límite de participación.
Descripción del proyecto
Over half of Parkinson Disease patients develop cortical dysfunctions leading to Parkinson Disease Dementia (PDD). The cognitive changes are primarily driven by pathological alpha-synuclein (a-syn) protein aggregates with secondary synaptic dysfunctions in the cortex. Microglia plays a key role in synapse maintenance and clearance of aggregated a-syn proteins, however, this is impaired in PD.
Low intensity focused ultrasound (FUS) combined with intravenous microbubbles (MB) can non-invasively increase the permeability of the blood-brain barrier, resulting in a transient and controlled entry of blood-born substances. In animal models of Alzheimer disease, FUS-MB treatments increase microglial-mediated clearance of extra- and intracellular protein aggregates and improve synapse health. In small patient cohorts in the clinic, FUS-MB treatments are safe and results suggest decreased levels of pathological proteins in Alzheimer disease patients.
HYPOTHESIS: FUS-MB applications targeted to the cortex promote cortical a-syn clearance and synapse maintenance which can prevent or slow the development of dementia in PD.
In a mouse model of PDD we will determine the ability of FUS-MB treatment to increase microglial-mediated clearance of a-syn, maintain synapse health, and inhibit the development of cognitive dysfunctions. In addition, we aim to evaluate non-invasive positron emission tomography and magnetic resonance imaging as biomarkers of the effects of FUS-MB treatment. Finally, we will investigate the underlying pathway of potentially beneficial effects of FUS-MB treatments by measuring changes in specific pathways of interest as well as perform an unbiased screen for novel targets.
Both the researcher and supervisor have a background in Parkinson disease research. The researcher brings expertise in FUS-MB treatments of mouse models and the supervisor is an expert in preclinical and clinical neuromodulation, the latter with FUS.