MiRNA-501-3p and MiRNA-502-3p: A promising biomarker panel for Alzheimer's disease.

Introduction: Alzheimer's disease (AD) lacks a less invasive and early detectable biomarker. Here, we investigated the biomarker potential of miR-501-3p and miR-502-3p using different AD sources.

Methods: MiR-501-3p and miR-502-3p expressions were evaluated in AD cerebrospinal fluid (CSF) exosomes, serum exosomes, familial and sporadic AD fibroblasts and B-lymphocytes by qRT-PCR analysis.

Neural signatures and personalized neuromodulation in a subject experiencing context-dependent inhibitory control deficits.

The ability to override prepotent actions is critical to control impulses and adjust behavior depending on goals and contextual needs. In this study, we investigate the inhibitory control abilities of a patient diagnosed with Klüver-Bucy Syndrome following a left temporal resection. The patient presented with disruptive hypersexuality symptoms akin to compulsions, leading to the inability to control and suppress inappropriate actions.

Integrated multi-omics analyses of synaptosomes revealed synapse-associated novel targets in Alzheimer's disease.

Synapse dysfunction is an early event in Alzheimer's disease (AD) caused by various factors, including amyloid beta, p-tau, inflammation, and aging. However, the precise molecular mechanism underlying synapse dysfunction in AD remains largely unknown. To understand this, we comprehensively analyzed the synaptosomes fraction in post-mortem brain samples from AD patients and cognitively normal individuals.

MicroRNA-based recent research developments in Alzheimer's disease.

Alzheimer's disease (AD) is a chronic neurodegenerative disorder that is characterized by memory and physical impairment in aged individuals. microRNAs (miRNAs) are small, single-stranded noncoding RNAs that induce translational repression by binding to the 3' UTR of a target mRNA. miRNAs play a crucial role in neurological activity by mediating cellular proliferation, synaptic plasticity, apoptosis and more.

Integrated Multi-Omics Analyses of Synaptosomes Revealed Synapse-Centered Novel Targets in Alzheimer's Disease.

Synapse dysfunction is an early event in Alzheimer's disease (AD) caused by various factors such as Amyloid beta, p-tau, inflammation, and aging. However, the exact molecular mechanism of synapse dysfunction in AD is largely unknown. To understand this, we comprehensively analyzed the synaptosome fraction in postmortem brain samples from AD patients and cognitively normal individuals.

MiRNA-501-3p and MiRNA-502-3p: A Promising Biomarker Panel for Alzheimer's Disease.

Introduction: Alzheimer's disease (AD) lacks a less invasive and early detectable biomarker. Here, we investigated the biomarker potential of miR-501-3p and miR-502-3p using different AD sources.

Methods: MiR-501-3p and miR-502-3p expressions were evaluated in AD CSF exosomes, serum exosomes, familial and sporadic AD fibroblasts and B-lymphocytes by qRT-PCR analysis.

MicroRNAs and synapse turnover in Alzheimer's disease.

Alzheimer's Disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-beta plaques and neurofibrillary tangles in the brain, leading to synaptic dysfunction and cognitive decline. Healthy synapses are the crucial for normal brain function, memory restoration and other neurophysiological function. Synapse loss and synaptic dysfunction are two primary events that occur during AD initiation.

Role of MicroRNA-502-3p in Human Diseases.

MicroRNAs (miRNAs) are non-coding RNAs that play a major role in gene regulation in several diseases. MicroRNA-502-3p (MiR-502-3p) has been previously characterized in a variety of human diseases such as osteoporosis, diabetes, tuberculosis, cancers, and neurological disorders. Our studies recently explored the new role of miR-502-3p in regulating synapse function in Alzheimer's disease (AD).