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Impaired parvalbumin interneurons in the retrosplenial cortex as the cause of sex-dependent vulnerability in Alzheimer’s disease [GeoMx]

ABSTRACT: Impaired parvalbumin interneurons in the retrosplenial cortex as the cause of sex-dependent vulnerability in Alzheimer’s disease [GeoMx]

PROVIDER: PRJNA1164202 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30771000_1.fastq.gz	Fastqsanger.gz
	SRR30771000_2.fastq.gz	Fastqsanger.gz
	SRR30771100_1.fastq.gz	Fastqsanger.gz
	SRR30771100_2.fastq.gz	Fastqsanger.gz
	SRR30771001_1.fastq.gz	Fastqsanger.gz

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Impaired parvalbumin interneurons in the retrosplenial cortex as the cause of sex-dependent vulnerability in Alzheimer’s disease [GeoMx]

Project description:Alzheimer’s disease is a debilitating neurodegenerative disorder with no cure and few treatment options. In early stages of Alzheimer’s disease, impaired metabolism and functional connectivity of the retrosplenial cortex strongly predict future cognitive impairments. Therefore, understanding Alzheimer’s disease-related deficits in the retrosplenial cortex is critical for understanding the origins of cognitive impairment and identifying early treatment targets. Using the 5xFAD mouse model, we discovered early, sex-dependent alterations in parvalbumin-interneuron transcriptomic profiles. This corresponded with impaired parvalbumin-interneuron activity, which was sufficient to induce cognitive impairments and dysregulate retrosplenial functional connectivity. In fMRI scans from patients with mild cognitive impairment and Alzheimer’s disease, we observed a similar sex-dependent dysregulation of retrosplenial cortex functional connectivity and, in post-mortem tissue from subjects with Alzheimer’s disease, a loss of parvalbumin interneurons. Reversal of cognitive deficits by stimulation of parvalbumin interneurons in the retrosplenial cortex suggests that this may serve as a promising novel therapeutic strategy.

2025-04-13 | GSE277793 | GEO

Impaired parvalbumin interneurons in the retrosplenial cortex as the cause of sex-dependent vulnerability in Alzheimer’s disease [Xenium]

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Disruption of KCC2 in parvalbumin-positive interneurons causes fatal epilepsy in mice

Project description:Since many years, we are interested in the regulation of the intraneuronal chloride concentration. We were the first group reporting a full knockout of the KCl-co-transporter KCC2, which dies immediately after birth due to respiratory failure. Notably, KCC2 loss-of-function mutations are associated with inherited febrile seizures, severe genetic generalized epilepsy and epilepsy of infancy with migrating focal seizures. Here, we used our floxed line to study the consequences of the disruption of KCC2 within parvalbumin-positive interneurons in mice. Remarkably, this leads to the disinhibition of PV-positive interneurons as evidenced by a decrease of E-S-Coupling and an increase in the sIPSC frequency. Nevertheless, these mice develop fatal epilepsy with progressive loss of parvalbumin-positive interneurons thus increasing network excitability.

2022-11-02 | E-MTAB-11147 | biostudies-arrayexpress

Impaired parvalbumin interneurons in the retrosplenial cortex as the cause of sex-dependent vulnerability in Alzheimer’s disease [Xenium]

Project description:Impaired parvalbumin interneurons in the retrosplenial cortex as the cause of sex-dependent vulnerability in Alzheimer’s disease [Xenium]

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DOT1L deletion impairs the development of cortical Parvalbumin-expressing interneurons

Project description:Our group has reported that the histone methyltransferase DOT1L is necessary for proper cortical plate development and layer distribution of glutamatergic neurons, however, its specific role on cortical interneuron development has not yet been explored. Here, we demonstrate that DOT1L affects interneuron development in a cell-autonomous manner. Deletion of Dot1l in MGE-derived interneuron precursor cells results in an overall reduction and altered distribution of GABAergic interneurons in the cortical plate at postnatal day (P) 0. Furthermore, we observed an altered proportion of GABAergic interneurons in the cortex and striatum at P21 with a significant decrease in Parvalbumin (PVALB)-expressing interneurons. Altogether, our results indicate that reduced numbers of cortical interneurons upon DOT1L deletion results from altered postmitotic differentiation/maturation.

2023-08-01 | GSE221994 | GEO

Discrete hippocampal projections are differentially regulated by parvalbumin and somatostatin interneurons

Project description:People with schizophrenia show hyperactivity in the ventral hippocampus (vHipp) and we have previously demonstrated distinct behavioral roles for vHipp cell populations. Here, we test the hypothesis that parvalbumin (PV) and somatostatin (SST) interneurons differentially innervate and regulate hippocampal pyramidal neurons based on their projection target. First, we use eGRASP to show that PV-positive interneurons form a similar number of synaptic connections with pyramidal cells regardless of their projection target while SST-positive interneurons preferentially target nucleus accumbens (NAc) projections. To determine if these anatomical differences result in functional changes, we used in vivo opto-electrophysiology to show that SST cells also preferentially regulate the activity of NAc-projecting cells. These results suggest vHipp interneurons differentially regulate that vHipp neurons that project to the medial prefrontal cortex (mPFC) and NAc. Characterization of these cell populations may provide potential molecular targets for the treatment schizophrenia and other psychiatric disorders associated with vHipp dysfunction.

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A postnatal molecular switch drives the activity-dependent maturation of parvalbumin interneurons [CUT&RUN]

Project description:Cortical neurons are specified during embryonic development but often only acquire their mature properties at relatively late stages of postnatal development. This delay in terminal differentiation is particularly prominent for fast-spiking parvalbumin-expressing (PV+) interneurons, which play critical roles in regulating the activity of the cerebral cortex. We found that the terminal differentiation of PV+ interneurons is triggered by neuronal activity and mediated by the transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1a). Developmental loss of PGC-1a prevents PV+ interneurons from acquiring their unique structural, electrophysiological, synaptic, and metabolic features and disrupts PV+ interneuron subtype specification. PGC-1a exerts its function as a master regulator of the differentiation of PV+ interneurons by directly controlling gene expression through a transcriptional complex that includes ERRg and Mef2c. Our results uncover a molecular switch that translates neural activity into transcriptional programs promoting the maturation of PV+ interneurons at the appropriate developmental stage.

2025-07-15 | GSE256442 | GEO

A postnatal molecular switch drives the activity-dependent maturation of parvalbumin interneurons [scRNA-seq]

2025-07-15 | GSE256441 | GEO

Transcriptomic changes in parvalbumin positive interneurons from cortex and striatum.

Project description:This experiment was designed to compare the transcriptomic differences between two parvalbumin (PV) interneuron population of the mouse brain. These two populations have the same embryological origin and share several neurochemical and electrophysiological properties, but differ in their ability to express the glial cell line-derived neurotrophic factor GDNF (negative in cortex and positive in striatum). Two different reporters for PV expressing cells were used: i) a constitutive tdTomato gene inserted in the Pvalb locus, and ii) a PV-Cre; tdTomato model in which fluorescent cells are PV cells expressing Cre recombinase. The comparative gene expression analysis between PV neurons captured from striatum and cortex allowed unraveling differential molecular characteristics of GDNF-synthesizing striatal PV interneurons and their potential role in endogenous GDNF modulation. The specific expression of several genes of interest in the striatal PV interneurons has been validated by other methods (real-time RT-PCR, in situ hibridization, immunohistochemistry).

2020-07-16 | GSE100300 | GEO

DOT1L deletion impairs the development of cortical Parvalbumin-expressing interneurons

Project description:DOT1L deletion impairs the development of cortical Parvalbumin-expressing interneurons

| PRJNA917294 | ENA