High Frequency Oscillations in a Rat Model of Alzheimer’s Disease
Abstract number :
3.023
Submission category :
1. Basic Mechanisms / 1C. Electrophysiology/High frequency oscillations
Year :
2022
Submission ID :
2205050
Source :
www.aesnet.org
Presentation date :
12/5/2022 12:00:00 PM
Published date :
Nov 22, 2022, 05:27 AM
Authors :
Lin Li, PhD – University of North Texas; Udaya Kumar, PhD – Neurology – University of California Los Angeles; Sally Frautschy, PhD – University of California Los Angeles; Greg Cole, PhD – University of California Los Angeles; Hedieh Shahpasand-Kroner, PhD – University of California Los Angeles; Jerome Engel, MD, PhD – Neurology – University of California Los Angeles; Anatol Bragin, PhD – Neurology – University of California Los Angeles
Rationale: The aim of this study is to characterize high frequency oscillations (HFOs) in a rat model of Alzheimer Disease (AD) with seizures.
Methods: Brain electrical activity was recorded from 5-10 month old transgenic AD rats (FAD+, n=6) and their littermates (FAD-, n=6) prior to development of significant pathology.
Results: Results showed that local field potential spikes were observed in all FAD+ rats but not in their littermates. Although HFOs (100-600Hz) were present in both groups of animals: the percentage of HFOs which were pathological (Fast Ripples, FRs) was significantly higher in the FAD+ group than in the FAD- group (p=0.031). FRs occurred in the hippocampus, prefrontal cortex, anterior thalamus, striatum and co-occurred within a time window of ±10ms, indicating the existence of a common driver or functional connectivity between these areas. Although generalized seizures were only detected in FAD+ group, the study was insufficiently powered to determine transgene effects for seizure frequency
Conclusions: Our data demonstrate that epilepsy-like pathological HFOs occur in the AD/seizure rat model, and we hypothesize that the neuronal substrate of epileptogenicity in AD is similar to that described in non-AD models of epilepsy and for patients with mesial temporal lobe epilepsy.
Funding: This study was supported by the National Institutes of Health, USA, R01-NS033310 (J.E), U54- NS100064 (J.E), University of North Texas Faculty Research Award 1600733 (LL). VA Merit BX003485 (SAF), VA MERIT RX000669 (FS), DOD AZ14016 (SAF), Oskar Fisher Foundation, Dr. James Truchard (GMC and SAF), and NIH R01 AG066212 (SAF).
Basic Mechanisms