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Beneficial effect of an adenosine A2AR antagonist in the APPswe/PS1dE9 mouse model of Alzheimer’s Disease

ABSTRACT: Beneficial effect of an adenosine A2AR antagonist in the APPswe/PS1dE9 mouse model of Alzheimer’s Disease

ORGANISM(S): Mus musculus

PROVIDER: GSE113141 | GEO | 2019/05/18

REPOSITORIES: GEO

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Beneficial effect of an adenosine A2AR antagonist in the APPswe/PS1dE9 mouse model of Alzheimer’s Disease

Project description:Beneficial effect of an adenosine A2AR antagonist in the APPswe/PS1dE9 mouse model of Alzheimer’s Disease

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Beneficial Effect of a Selective Adenosine A<sub>2A</sub> Receptor Antagonist in the APPswe/PS1dE9 Mouse Model of Alzheimer's Disease.

Project description:Consumption of caffeine, a non-selective adenosine A2A receptor (A2AR) antagonist, reduces the risk of developing Alzheimer's disease (AD) and mitigates both amyloid and Tau lesions in transgenic mouse models of the disease. While short-term treatment with A2AR antagonists have been shown to alleviate cognitive deficits in mouse models of amyloidogenesis, impact of a chronic and long-term treatment on the development of amyloid burden, associated neuroinflammation and memory deficits has never been assessed. In the present study, we have evaluated the effect of a 6-month treatment of APPsw/PS1dE9 mice with the potent and selective A2AR antagonist MSX-3 from 3 to 9-10 months of age. At completion of the treatment, we found that the MSX-3 treatment prevented the development of memory deficits in APP/PS1dE9 mice, without significantly altering hippocampal and cortical gene expressions. Interestingly, MSX-3 treatment led to a significant decrease of Aβ1-42 levels in the cortex of APP/PS1dE9 animals, while Aβ1-40 increased, thereby strongly affecting the Aβ1-42/Aβ1-40 ratio. Together, these data support the idea that A2AR blockade is of therapeutic value for AD.

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MiR-431 attenuates synaptic plasticity and memory deficits in APPswe/PS1dE9 mice

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MiR-431 attenuates synaptic plasticity and memory deficits in APPswe/PS1dE9 mice

Project description:Synaptic plasticity impairment plays a critical role in the pathogenesis of Alzheimer’s disease (AD), and emerging evidence has shown that microRNAs (miRNAs) are alternative biomarkers and therapeutic targets for synaptic dysfunctions in AD. In this study, we found that the level of miR-431 was downregulated in the plasma of amnestic mild cognitive impairment (aMCI) and AD patients. In addition, it was decreased in the hippocampus and plasma of APPswe/PS1dE9 (APP/PS1) mice. Lentivirus mediated miR-431 overexpression in the hippocampus CA1 ameliorated synaptic plasticity and memory deficits of APP/PS1 mice, while it didn't affect the Aβ levels. Smad4 was identified as a target of miR-431, and Smad4 knockdown modulated the expression of synaptic proteins including SAP102, and protected against synaptic plasticity and memory dysfunctions in APP/PS1 mice. Furthermore, Smad4 overexpression reversed the protective effects of miR-431, indicating that miR-431 attenuated synaptic impairment at least partially by Smad4 inhibition. Thus, these results indicated that miR-431/Smad4 might be a potential therapeutic target for AD treatment.

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Differentiated embryonic neurospheres from familial Alzheimer’s disease model show Innate Immune and Glial Cell Responses

Project description:Proteins involved in the Alzheimer’s disease (AD), such as amyloid precursor protein (APP) and presenilin-1 (PS1), play critical roles in early development of the central nervous system (CNS), as well as in innate immune and glial cell responses. However, it is unknown whether these alterations start on development of the CNS of carriers of APPswe and PS1dE9 mutations , associated with familial AD. Using microarray technology we studied the genome-wide gene expression profiles in the differentiated neural progenitor cells (NPCs) from wild-type (WT) and APPswe/PS1dE9 embryo telencephalon. Differential gene expression analysis indicated the occurrence of strong innate immune and glial cell responses in APPswe/PS1dE9 neurospheres, involving mainly microglial cells, inflammatory mediators and chemokines. APPswe/PS1dE9 cells expressed up to 100-fold more CCL12, CCL5, CCL3, C3, CX3CR1, TLR2 and TNF-alpha, which was confirmed by real time PCR. The expression of activated microglia marker Iba-1 was also 20-fold upregulated in APPswe/PS1dE9 cells. The secretome of APPswe/PSldE9 differentiated NPCs increased the chemoattraction of peripheral blood mononuclear cells (PBMCs) compared to the secretome of WT cells. Taken together, our results demonstrated that neurogenic niche obtained from differentiation of embryonic APPswe/PS1dE9 neurospheres is an excellent model for AD in vitro, since this culture spontaneously presents several alterations observed in the adult-brain with this pathology. Moreover, our data strengthen pathophysiological hypotheses that propose an early neurodevelopmental origin for familial AD.

2023-09-30 | GSE227002 | GEO

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