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Alteration of the microRNA network during the progression of Alzheimer’s disease

ABSTRACT: We report the high-throughput profiling of microRNAs (miRNAs) from the prefrontal cortex of controls, early and late-stages Alzheimer's disease subjects. We show miRNA expression changes between the two groups and down-regulation of miR-132-3p in the late-stages group.

ORGANISM(S): Homo sapiens

PROVIDER: GSE48552 | GEO | 2013/07/25

SECONDARY ACCESSION(S): PRJNA210613

REPOSITORIES: GEO

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Alteration of the microRNA network during the progression of AlzheimerM-bM-^@M-^Ys disease

Project description:We report the high-throughput profiling of microRNAs (miRNAs) from the prefrontal cortex of controls, early and late-stages Alzheimer's disease subjects. We show miRNA expression changes between the two groups and down-regulation of miR-132-3p in the late-stages group. Deep-sequencing of microiRNAs in 6 controls/early-stages and 6 late-stages Alzheimer's disease patients

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Project description:The process of generating new neurons at the hippocampal neurogenic niche, also referred to as adult hippocampal neurogenesis (AHN), is impaired in Alzheimer’s disease (AD). MicroRNA-132 (miR-132), the most consistently downregulated microRNA (miRNA) in AD, was recently identified as a potent regulator of AHN, exerting multilayered proneurogenic effects in adult neural stem cells (NSCs) and their progeny. Supplementing miR-132 in AD mouse brain restores AHN and relevant memory deficits, yet the exact mechanisms involved are still unknown. Here, we identify NACC2 as a novel miR-132 target implicated in both AHN and AD. miR-132 deficiency in mouse hippocampus induces Nacc2 expression and inflammatory signaling in adult NSCs. We show that miR-132-dependent regulation of NACC2 is involved in the initial stages of human NSC differentiation towards astrocytes and neurons. Later, NACC2 function in astrocytic maturation becomes uncoupled from miR-132. We demonstrate that NACC2 is present in reactive astrocytes surrounding amyloid plaques in mouse and human AD hippocampus, and that there is an anticorrelation between miR-132 and NACC2 levels in AD and upon induction of inflammation. Unraveling the molecular mechanisms by which miR-132 regulates neurogenesis and cellular reactivity in AD, will provide valuable insights towards its possible application as a therapeutic target.

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Project description:Ion channel splice array data from cerebellum brain tissue samples collected from Alzheimer's disease patients. Temporal cortex (Alzheimer's disease affected brain tissue structure) and cerebellum (Alzheimer's disease unaffected brain tissue structure) samples from control subjects were compared to temporal cortex and cerebellum of patients with Alzheimer's disease.

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Project description:Ion channel splice array data from temporal cortex brain tissue samples collected from Alzheimer's disease patients. Temporal cortex (Alzheimer's disease affected brain tissue structure) and cerebellum (Alzheimer's disease unaffected brain tissue structure) samples from control subjects were compared to temporal cortex and cerebellum of patients with Alzheimer's disease.

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Project description:Late-onset Alzheimer disease (LOAD) is the most common neurodegenerative disorder worldwide. Recent studies have shown that differential expression in genes (DEG) related to inflammatory response may result associated with disease onset and progression. This study aimed to explore the molecular pathogenesis of LOAD-related inflammation through next-generation sequencing, to assess RNA expression profiles in Alzheimer's disease patients and healthy controls.

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microRNA-132/212 deficiency enhances Ab production and senile plaque deposition in Alzheimer’s disease triple transgenic mice

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