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Barrett, G. M.

Publications and source records attributed to Barrett, G. M..

2 recordsLinked to original sources

Open-Source Tools to Analyze Temporal and Spatial Properties of Local Field Potentials

Analysis of local field potentials (LFPs) is important for understanding how ensemble neurons function as a network in a specific region of the brain. Despite the availability of tools for analyzing LFP data, there are some missing features such as analysis of high frequency oscillations (HFOs) and spatial properties. In addition, accessibility of most tools is restricted due to closed source code and/or high costs. To overcome these issues, we have developed two freely available tools that make temporal and spatial analysis of LFP data easily accessible. The first tool, hfoGUI (High Frequency Oscillation Graphical User Interface), allows temporal analysis of LFP data and scoring of HFOs such as ripples and fast ripples which are important in understanding memory function and neurological disorders. To complement the temporal analysis tool, a second tool, SSM (Spatial Spectral Mapper), focuses on the spatial analysis of LFP data. The SSM tool maps the spectral power of LFPs as a function of subjects position in a given environment allowing investigation of spatial properties of LFP signal. Both hfoGUI and SSM are open-source tools that have unique features not offered by any currently available tools, and allow visualization and spatio-temporal analysis of LFP data.

neuroscience↗

Attenuation of Aβ-associated hyperactivity reduces Aβ and tau pathology along the entorhinal cortex-hippocampal network

High levels of the amyloid-beta (A{beta}) peptide have been shown to disrupt neuronal function and induce hyperexcitability but it is unclear what effects A{beta}-associated hyperexcitability may have on tauopathy pathogenesis or propagation in vivo. Using a novel transgenic mouse line to model the impact of hAPP/A{beta} accumulation on tauopathy in the entorhinal cortex-hippocampal (EC-HIPP) network, we demonstrate that hAPP aggravates EC tau aggregation and accelerates pathological tau spread into the hippocampus. In vivo recordings revealed a strong role for hAPP/A{beta}, but not tau, in the emergence of EC neuronal hyperactivity and impaired theta rhythmicity. Chemogenetic attenuation of A{beta}-associated hyperactivity led to reduced hAPP/A{beta} accumulation and reduction of pathological tau in downstream hippocampus. These data strongly support the hypothesis that in Alzheimers disease (AD), A{beta}-associated hyperactivity accelerates the progression of pathological tau along vulnerable neuronal circuits, and demonstrates the utility of chronic, neuromodulatory approaches in ameliorating AD pathology in vivo.

neuroscience↗