Electrophysiological and Molecular Imaging of Early Alzheimer’s Disease Progression
Our research investigates how neuronal and network dysfunction emerge across the biological progression of Alzheimer’s disease (AD). Using a multimodal approach integrating electrophysiological techniques, including EEG and MEG, with molecular and structural neuroimaging, we aim to characterize how abnormal neural activity relates to AD pathology. By identifying mechanisms such as network hyperexcitability and dysfunction, we seek to uncover novel biomarkers and therapeutic targets to slow disease progression and prevent cognitive decline in AD and related dementias.
Excitatory–Inhibitory Imbalance and Response to Amyloid Immunotherapy
While amyloid-targeting therapies have shown promise in slowing cognitive decline in early Alzheimer’s disease, variability in treatment response highlights the need to understand additional biological factors that influence outcomes. Our research examines the role of excitatory–inhibitory (E/I) imbalance and neuronal hyperexcitability in shaping the efficacy and safety of amyloid immunotherapies. By integrating neurophysiological measures, molecular biomarkers, and clinical outcomes, we aim to define mechanisms that contribute to treatment response and advance precision approaches for Alzheimer’s disease therapy.
Sleep Dysfunction and Neural Circuit Alterations in Alzheimer’s Disease
Sleep disturbances are among the earliest clinical features associated with Alzheimer’s disease and may play a critical role in disease progression. Our research examines the bidirectional relationship between abnormal sleep physiology and AD pathology, focusing on how amyloid-β and tau accumulation disrupt neural circuits and alter sleep-wake regulation. We investigate excitatory–inhibitory (E/I) imbalance as a potential mechanism linking protein pathology, synaptic dysfunction, and epileptic activity, with the goal of identifying modifiable targets to improve sleep and influence early disease mechanisms.