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Descripción
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| Early identification and detection of AD during its long preclinical phase is a key opportunity to future disease prevention and successful therapeutic interventions. My central hypothesis is that a prevalent indication of early AD developments is in the alteration of the excitatory and inhibitory mechanisms that regulate neural activity. This imbalance may affect brain function first, only locally in the MCI phase - e.g., in medial temporal structures - then more lobally in AD, when neural signalling between multiple brain regions is severe ly altered. The core hypothesis is that abe1nnt neural activity - which origin remains unknown - precedes A-B deposition and marks the early pathogenesis of AD. A-B is a potent modulator of neural communication via excitatory synaptic transmission. The production of A-B in the hea lthy brain is regulated by neural activity. One possible hypothesis is that the excess ive deposits of A-B in the AD brain are a consequence of primari ly perturbed neural activity, rather than viceversa. To summarize, l hypothes ize that the well-studied, long process of A-B acc umulation in the AD brain reinforces an unstable regime of pathogenesis initiated by a form of abnormal neural activity. This latter primarily affects medial temporal regions before it propagates globally, as mediated by the inte r-connectivity of brain networks. | |
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Internacional
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Si |
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Tipo de proyecto
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Proyectos y convenios en convocatorias públicas competitivas |
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Entidad financiadora
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AXA |
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Nacionalidad Entidad
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FRANCIA |
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Tamaño de la entidad
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Gran Empresa (>250) |
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Fecha concesión
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18/01/2017 |