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Preclinical studies on neuronal impairments associated with progressive amyloidosis have demonstrated some A\u03b2\u2010dependent neuronal dysfunction including modulation of gamma\u2010aminobutyric acid\u2010ergic signaling. The present work focuses on the early stage of disease progression and uses TgF344\u2010<jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>rats that recapitulate a broad repertoire of<jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\u2010like pathologies to investigate the neuronal network functioning using simultaneous intracranial recordings from the hippocampus (<jats:styled-content style=\"fixed-case\">HPC<\/jats:styled-content>) and the medial prefrontal cortex (<jats:styled-content style=\"fixed-case\">mPFC<\/jats:styled-content>), followed by pathological analyses of gamma\u2010aminobutyric acid (<jats:styled-content style=\"fixed-case\">GABA<jats:sub>A<\/jats:sub><\/jats:styled-content>) receptor subunits \u03b11<jats:sub>,<\/jats:sub>\u03b15, and \u03b4, and glutamic acid decarboxylases (<jats:styled-content style=\"fixed-case\">GAD<\/jats:styled-content>65 and<jats:styled-content style=\"fixed-case\">GAD<\/jats:styled-content>67). Concomitant to amyloid deposition and tau hyperphosphorylation, low\u2010gamma band power was strongly attenuated in the<jats:styled-content style=\"fixed-case\">HPC<\/jats:styled-content>and<jats:styled-content style=\"fixed-case\">mPFC<\/jats:styled-content>of TgF344\u2010<jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>rats in comparison to those in non\u2010transgenic littermates. In addition, the phase\u2010amplitude coupling of the neuronal networks in both areas was impaired, evidenced by decreased modulation of theta band phase on gamma band amplitude in TgF344\u2010<jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>animals. Finally, the gamma coherence between<jats:styled-content style=\"fixed-case\">HPC<\/jats:styled-content>and<jats:styled-content style=\"fixed-case\">mPFC<\/jats:styled-content>was attenuated as well. These results demonstrate significant neuronal network dysfunction at an early stage of<jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\u2010like pathology. This network dysfunction precedes the onset of cognitive deficits and is likely driven by A\u03b2 and tau pathologies.<\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p><jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc14136-fig-0006-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><jats:p><jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/onlinelibrary.wiley.com\/journal\/10.1111\/(ISSN)1471-4159\/homepage\/special_issues.htm#Vascular Dementia\">This article is part of the Special Issue \u201cVascular Dementia\u201d<\/jats:ext-link>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jnc.14136","type":"journal-article","created":{"date-parts":[[2017,8,4]],"date-time":"2017-08-04T16:12:38Z","timestamp":1501863158000},"page":"669-679","source":"Crossref","is-referenced-by-count":106,"title":["Early\u2010stage attenuation of phase\u2010amplitude coupling in the hippocampus and medial prefrontal cortex in a transgenic rat model of Alzheimer's disease"],"prefix":"10.1111","volume":"144","author":[{"given":"Paolo","family":"Bazzigaluppi","sequence":"first","affiliation":[{"name":"Physical Sciences Sunnybrook Research Institute Toronto Ontario Canada"},{"name":"Fundamental Neurobiology Krembil Research Institute Toronto Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tina L.","family":"Beckett","sequence":"additional","affiliation":[{"name":"Physical Sciences Sunnybrook Research Institute Toronto Ontario 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