{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T17:48:06Z","timestamp":1790704086954,"version":"4.1.0"},"reference-count":82,"publisher":"SAGE Publications","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAD"],"published-print":{"date-parts":[[2024,5,14]]},"abstract":"<jats:p>Background: Cognitive deficits observed in Alzheimer\u2019s disease (AD) patients have been correlated with altered hippocampal activity. Although the mechanism remains under extensive study, neurofibrillary tangles and amyloid plaques have been proposed as responsible for brain activity alterations. Aiming to unveil the mechanism, researchers have developed several transgenic models of AD. Nevertheless, the variability in hippocampal oscillatory alterations found in different genetic backgrounds and ages remains unclear. Objective: To assess the oscillatory alterations in relation to animal developmental age and protein inclusion, amyloid-\u03b2 (A\u03b2) load, and abnormally phosphorylated tau (pTau), we reviewed and analyzed the published data on peak power, frequency, and quantification of theta-gamma cross-frequency coupling (modulation index values). Methods: To ensure that the search was as current as possible, a systematic review was conducted to locate and abstract all studies published from January 2000 to February 2023 that involved in vivo hippocampal local field potential recording in transgenic mouse models of AD. Results: The presence of A\u03b2 was associated with electrophysiological alterations that are mainly reflected in power increases, frequency decreases, and lower modulation index values. Concomitantly, pTau accumulation was associated with electrophysiological alterations that are mainly reflected in power decreases, frequency decreases, and no significant alterations in modulation index values. Conclusions: In this study, we showed that electrophysiological parameters are altered from prodromal stages to the late stages of pathology. Thus, we found that A\u03b2 deposition is associated with brain network hyperexcitability, whereas pTau deposition mainly leads to brain network hypoexcitability in transgenic models<\/jats:p>","DOI":"10.3233\/jad-231365","type":"journal-article","created":{"date-parts":[[2024,4,26]],"date-time":"2024-04-26T14:04:20Z","timestamp":1714140260000},"page":"595-607","source":"Crossref","is-referenced-by-count":9,"title":["Meta-Analysis in Transgenic Alzheimer\u2019s Disease Mouse Models Reveals Opposite Brain Network Effects of Amyloid-\u03b2 and Phosphorylated Tau Proteins"],"prefix":"10.1177","volume":"99","author":[{"given":"Carlos Antonio","family":"Garc\u00eda-Carlos","sequence":"first","affiliation":[{"name":"UNAM Division of Neurosciences, Institute of Cellular Physiology, National Autonomous University of M\u00e9xico, M\u00e9xico City, M\u00e9xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gustavo","family":"Basurto-Islas","sequence":"additional","affiliation":[{"name":"UG University of Guanajuato, Le\u00f3n, Guanajuato, M\u00e9xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George","family":"Perry","sequence":"additional","affiliation":[{"name":"UTSA Neuroscience Institute and Department of Biology, College of Sciences, University of Texas at San Antonio, San Antonio, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Siddhartha","family":"Mondrag\u00f3n-Rodr\u00edguez","sequence":"additional","affiliation":[{"name":"UAQ Centre for Applied Biomedical Research \u2013 CIBA, School of Medicine, Autonomous University of Quer\u00e9taro, Quer\u00e9taro, M\u00e9xico"},{"name":"CONAHCYT National Council for Science and Technology, M\u00e9xico City, M\u00e9xico"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","reference":[{"key":"10.3233\/JAD-231365_ref1","doi-asserted-by":"crossref","first-page":"768","DOI":"10.1038\/nature05289","article-title":"A network dysfunction perspective on neurodegenerative disease","volume":"443","author":"Palop","year":"2006","journal-title":"Nature"},{"key":"10.3233\/JAD-231365_ref2","doi-asserted-by":"crossref","first-page":"239","DOI":"10.1007\/BF00308809","article-title":". 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