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These changes are linked to parvalbumin\u2010positive () interneuron dysfunction and neuronal loss driven by amyloid\u2010beta () and hyperphosphorylated tau (hp\u2010), though underlying mechanisms remain unclear. To investigate this relationship, we employed a Laminar Neural Mass Model integrating excitatory and inhibitory populations. Synaptic coupling from  interneurons to pyramidal cells was progressively reduced to mimic \u2010induced neurotoxicity. Additional parameter variations simulated alternate mechanisms, including hp\u2010tau pathology. Simulated dipole activity was analyzed in the time\u2010frequency domain and compared to the literature. Simulating  interneuron dysfunction reproduced AD's biphasic progression: early hyperexcitability with elevated gamma and alpha power, followed by oscillatory slowing and reduced spectral power. Alternative mechanisms, such as increased excitatory drive, did not replicate this trajectory. To account for late\u2010stage hypoactivity and reduced firing rates, we incorporated pyramidal cell disruption consistent with hp\u2010 neurotoxicity. While not essential for local oscillatory changes, this addition aligns the model with empirical markers of advanced AD and supports whole\u2010brain modeling. These findings highlight  interneuron dysfunction as a primary mechanism of early electrophysiological disruption in AD, with pyramidal cell loss contributing to late\u2010stage hypoactivity, offering a mechanistic model for excitation\u2013inhibition imbalance across progression.<\/jats:p>","DOI":"10.1002\/hbm.70428","type":"journal-article","created":{"date-parts":[[2026,1,14]],"date-time":"2026-01-14T10:36:58Z","timestamp":1768387018000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Fast Interneuron Dysfunction in Laminar Neural Mass Model Reproduces Alzheimer's Oscillatory Biomarkers"],"prefix":"10.1002","volume":"47","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1580-8750","authenticated-orcid":false,"given":"Roser","family":"Sanchez\u2010Todo","sequence":"first","affiliation":[{"name":"Brain Modeling Department, Neuroelectrics Barcelona  Barcelona Spain"},{"name":"Center of Brain and Cognition, 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