Early social deficits in TgF344-AD rats are accompanied by sex-specific parvalbumin-positive interneuron reduction and altered brain oscillations in the hippocampal CA2

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F25%3A00618259" target="_blank" >RIV/67985823:_____/25:00618259 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68407700:21230/25:00382139 RIV/00216208:11120/25:43928262

Výsledek na webu

<a href="https://doi.org/10.1016/j.nbd.2025.106875" target="_blank" >https://doi.org/10.1016/j.nbd.2025.106875</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.nbd.2025.106875" target="_blank" >10.1016/j.nbd.2025.106875</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Early social deficits in TgF344-AD rats are accompanied by sex-specific parvalbumin-positive interneuron reduction and altered brain oscillations in the hippocampal CA2

Popis výsledku v původním jazyce

Social withdrawal and deficits in social cognition are hallmarks of Alzheimer's disease (AD). While early deficits in social behavior and memory have been documented in mouse AD models, they remain understudied in rat models. Early-stage AD is accompanied by dysfunction of parvalbumin-positive (PV+) interneurons, implicating their potential connection to early symptoms. In this study, we employed a 5-trial social memory task to investigate early deficits in social cognition in 6-month-old TgF344-AD male and female rats. We counted the number of PV+ interneurons and recorded local field potentials during social interactions in the hippocampal CA2 – a region critical for social information processing. Our results show decreased social interest and novelty preference in TgF344-AD male and female rats. However, reduced PV+ interneuron numbers were observed only in female rats and specific to the CA2 area. The electrophysiological recordings revealed reduced theta-gamma phase-amplitude coupling in the CA2 during direct social interactions. We conclude that deficits in social cognition accompany early-stage AD in TgF344-AD rats and are potentially linked to PV+ interneuron and brain oscillatory dysfunction in the CA2 region of the hippocampus.

Název v anglickém jazyce

Early social deficits in TgF344-AD rats are accompanied by sex-specific parvalbumin-positive interneuron reduction and altered brain oscillations in the hippocampal CA2

Popis výsledku anglicky

Social withdrawal and deficits in social cognition are hallmarks of Alzheimer's disease (AD). While early deficits in social behavior and memory have been documented in mouse AD models, they remain understudied in rat models. Early-stage AD is accompanied by dysfunction of parvalbumin-positive (PV+) interneurons, implicating their potential connection to early symptoms. In this study, we employed a 5-trial social memory task to investigate early deficits in social cognition in 6-month-old TgF344-AD male and female rats. We counted the number of PV+ interneurons and recorded local field potentials during social interactions in the hippocampal CA2 – a region critical for social information processing. Our results show decreased social interest and novelty preference in TgF344-AD male and female rats. However, reduced PV+ interneuron numbers were observed only in female rats and specific to the CA2 area. The electrophysiological recordings revealed reduced theta-gamma phase-amplitude coupling in the CA2 during direct social interactions. We conclude that deficits in social cognition accompany early-stage AD in TgF344-AD rats and are potentially linked to PV+ interneuron and brain oscillatory dysfunction in the CA2 region of the hippocampus.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Neurobiology of Disease

ISSN

0969-9961

e-ISSN

1095-953X

Svazek periodika

208

Číslo periodika v rámci svazku

May

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

14

Strana od-do

106875

Kód UT WoS článku

001452981000001

EID výsledku v databázi Scopus

2-s2.0-105000036160