Mercoledì 22 Gennaio 2025, ore 13
Edificio Asclepio U8 Aula 8
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Alzheimer’s disease (AD), is a neurodegenerative disorder characterized by synaptic and memory loss, chronic neuroinflammation and neuronal death. Although the accumulation of β-amyloid (Aβ) aggregates has been long considered the major culprit, in recent years neuroinflammation has emerged as the other central player in the pathogenesis and progression of AD. The hallmarks of AD—Aβ plaques, and tau neurofibrillary tangles made of hyperphosphorylated tau protein aggregates—trigger a cascade of immune responses in the brain, primarily mediated by microglia and astrocytes. Activated microglia, initially protective by clearing Aβ and damaged neurons, may become dysregulated, releasing pro-inflammatory cytokines and reactive oxygen species that exacerbate neuronal damage.
Similarly, astrocytic activation contributes to chronic inflammation, impairing synaptic function and blood-brain barrier integrity. However, emerging evidence highlights also a bidirectional relationship between neuroinflammation and Aβ/tau pathology, by which chronic inflammation would amplify Aβ accumulation and tau, creating an uncontrollable vicious cycle. Genetic predispositions, such as mutations in immune-related genes, have been found to increase AD susceptibility; gut microbiota dysbiosis predisposes to AD, likely through an activation of the immune system. All this evidence has recently placed immune cells at the forefront as attractive therapeutic targets in the fight against AD.
Claudia Balducci
Claudia Balducci began her scientific career as a Research Assistant at The Scripps Research Institute in La Jolla, San Diego (1995-1997), where she worked on animal models of cocaine self-administration. In 1997, she contributed as a Consultant at The Psychiatry Institute in Chicago, assisting in the development of a drug self-administration system for rodents.
From 1998 to 2003, she undertook a fellowship at the Mario Negri Institute in Milan, focusing on cognitive dysfunctions in Alzheimer’s Disease (AD) models within the Department of Neuroscience. This was followed by a PhD, sponsored by the Open University in London (2004-2009), during which she investigated the emerging role of β-amyloid oligomers in AD, significantly contributing to demonstrate their mechanisms of action. Her work led to the
development of an oligomer-induced acute mouse model widely used in neurodegenerative research.
From 2010 to 2016, she held the position of Senior Scientist at the Mario Negri Institute, where she explored the interplay between cognitive deficits and neuroinflammation in AD, with a particular focus on multi-target therapeutic strategies.
Since 2016, she leads the "Neurobiology of Cognitive Disorders in Neurodegenerative Diseases" unit as Lab Unit Head.