Deciphering the molecular mechanism of REST regulation through DEGs and TFs in Alzheimer’s disease DOI Open Access

Ajmal Nassar,

Madhavan Nampoothiri, Prasada Chowdari Gurram

и другие.

Journal of Applied Pharmaceutical Science, Год журнала: 2023, Номер unknown

Опубликована: Янв. 1, 2023

Bibliometric analysis and visualization of research on nanotechnology in dentistry from 1999 to 2022Namrata Dagli, Bhavin Patel, Rushabh Nihad Adnan, Rahnuma Ahmad, Mainul Haque, Santosh Kumar

Язык: Английский

New perspectives on heterogeneity in astrocytic reactivity in neuroinflammation DOI Creative Commons

Daniel Santos,

Sarah Lima, L. Moreira

и другие.

Brain Behavior & Immunity - Health, Год журнала: 2025, Номер 44, С. 100948 - 100948

Опубликована: Янв. 31, 2025

The inflammatory response is a fundamental aspect of all insults to the central nervous system (CNS), which includes acute trauma, infections, and chronic neurodegenerative conditions. As methods for investigating astrocytes have progressed, recent findings indicate that can react diverse spectrum affecting system. Astrocytes respond external internal stimuli from in process called glial reactivity. Astrocyte reactivity, previously considered uniform functionally inactive, currently very event different processes. These differences occur due nature, intensity stimulus, brain region involved range subtle changes astrocytic morphology protein expression alteration, gene transcription profile shifts, variations secretory pattern molecules. elucidation roles both normal pathological conditions has led increased interest notion various astrocyte subtypes may exist, each contributing with distinct functions. Our study will prioritize characterization patterns context development progression diseases, particularly Alzheimer's Parkinson's. In addition, we investigate astrocyte's during bacterial viral given potential enhance specific therapeutic interventions based on reactivity profiles astrocytes.

Язык: Английский

Процитировано

0

Modulation of neuroplasticity and neuroinflammation by exosomal proteins and microRNA in depression: A review DOI Creative Commons

Rajni Daksh,

Priyanka Sharma,

Saumya Khanna

и другие.

International Journal of Biological Macromolecules, Год журнала: 2025, Номер unknown, С. 142829 - 142829

Опубликована: Апрель 1, 2025

Exosomes are tiny extracellular membrane vesicles produced by various biological sources that have gained significant attention due to their theranostic potential. They carry macromolecules such as proteins, DNA, and RNA (including miRNAs) involved in intercellular communication within the central nervous system (CNS). This review summarizes role of exosomes miRNAs aspects depression, emphasizing therapeutic potential depression applications drug delivery systems. modulating critical pathways neurogenesis, synaptic plasticity, blood-brain barrier integrity, neuroinflammation, neural development. reduce neuroinflammation suppressing cytokine production immune activation. Furthermore, facilitate neuronal repair which is important for restoring circuitry, cognitive abilities, emotional mental stability affected depression. Moreover, exosomal emerging targets both diagnostic treatment perspectives treatment. The regulate gene expressions associated with functions health serve biomarkers novel approaches. In conclusion, may play a crucial will enhance probability successful

Язык: Английский

Процитировано

0

Spermidine as an epigenetic regulator of autophagy in neurodegenerative disorders DOI Creative Commons
Sairaj Satarker,

Joel Wilson,

Kiran Kumar Kolathur

и другие.

European Journal of Pharmacology, Год журнала: 2024, Номер 979, С. 176823 - 176823

Опубликована: Июль 18, 2024

Autophagy is an abnormal protein degradation and recycling process that impaired in various neurological diseases like Alzheimer's disease (AD), Parkinson's (PD), Huntington's disease. Spermidine a natural polyamine found plant- meat-based diets can induce autophagy, decreased neurodegenerative diseases. It acts on epigenetic enzymes E1A-binding p300, HAT Iki3p Sas3p, α-tubulin acetyltransferase 1 modulate autophagy. Histone modifications acetylation, phosphorylation, methylation could influence epigenetically regulated disorders with many miRNAs. Polyamine regulation plays essential role the pathogenesis of AD PD. Therefore, this review, we discuss miRNAs involved autophagy spermidine as enhancer. The alterations spermidine-mediated Beclin-1, LC3-II, p62 genes other PD-associated impact these With ever-growing data such promising effects feel it be target area worth further detailed studies.

Язык: Английский

Процитировано

3

Recent advances in the molecular signaling pathways of Substance P in Alzheimer's disease: Link to neuroinflammation associated with toll-like receptors DOI Creative Commons
Prasada Chowdari Gurram, Sairaj Satarker, Madhavan Nampoothiri

и другие.

Biochemical and Biophysical Research Communications, Год журнала: 2024, Номер 733, С. 150597 - 150597

Опубликована: Авг. 23, 2024

A significant quantity of substance P (SP) and its receptor, the neurokinin 1 (NK1) receptors are found in brain. SP is a neuropeptide distributed central nervous system functions as neurotransmitter, neuromodulator, neurotrophic factor. The concentrations brain cerebrospinal fluid fluctuate individuals with Alzheimer's disease (AD). an endogenous ligand for NK1 enhancing expression toll-like (TLR) vice versa. So, both pathways interconnected, where activation one pathway activates second pathway. Researchers have observed interaction TLR pathophysiology AD. Thus, this review discusses various TLRs involved regulating amyloid processing Further, AD pathology, can regulate non-amyloidogenic Recent studies also demonstrated capacity voltage-gated potassium channel currents, emphasizing SP's neuroprotective ability. Therefore, we corroborate findings linking SP, NK1R,

Язык: Английский

Процитировано

3

Identification of the abnormalities in astrocytic functions as potential drug targets for neurodegenerative disease DOI

Valtteri Syvänen,

Jari Koıstınaho, Šárka Lehtonen

и другие.

Expert Opinion on Drug Discovery, Год журнала: 2024, Номер 19(5), С. 603 - 616

Опубликована: Фев. 26, 2024

Historically, astrocytes were seen primarily as a supportive cell population within the brain; with neurodegenerative disease research focusing exclusively on malfunctioning neurons. However, perform numerous tasks that are essential for maintenance of central nervous system`s complex processes. Disruption these functions can have negative consequences; hence, it is unsurprising to observe growing amount evidence role in development and progression diseases. Targeting astrocytic may serve potential disease-modifying drug therapy future.

Язык: Английский

Процитировано

2

Astrocytic transcription factors REST, YY1, and putative microRNAs in Parkinson’s disease and advanced therapeutic strategies DOI Creative Commons

Ajmal Nassar,

Triveni Kodi, Sairaj Satarker

и другие.

Gene, Год журнала: 2023, Номер 892, С. 147898 - 147898

Опубликована: Окт. 11, 2023

Transcription factors (TF) and microRNAs are regulatory in astrocytes linked to several Parkinson's disease (PD) progression causes, such as disruption of glutamine transporters concomitant disrupted uptake inflammation. REST, a crucial TF, has been documented an epigenetic repressor that limits the expression neuronal genes non-neural cells. REST activity is significantly its corepressors astrocytes, specifically histone deacetylases (HDACs), CoREST, MECP2. Another REST-regulating YY1, studied interaction with investigated. In this review, molecular processes support astrocytic control YY1 terms regulation glutamate transporter EAAT2 were addressed more detailed comprehensive manner. Both TFs' function how astrocyte abnormalities cause PD still mystery. Moreover, (short non-coding RNAs) key regulators have correlated numerous PD. The identification miRs engaged dysfunction triggers shown. term "Gut-brain axis" refers two systems' mutual communication. Gut microbial dysbiosis, which mediates imbalance gut-brain axis, might contribute neurodegenerative illnesses through altered regulation. New treatment approaches modify axis prevent repercussions also investigated review.

Язык: Английский

Процитировано

4

Epigenetic Alterations in Alzheimer’s Disease: Impact on Insulin Signaling and Advanced Drug Delivery Systems DOI Creative Commons
Alosh Greeny, Ayushi Nair,

Prashant Sadanandan

и другие.

Biology, Год журнала: 2024, Номер 13(3), С. 157 - 157

Опубликована: Фев. 28, 2024

Alzheimer’s disease (AD) is a neurodegenerative condition that predominantly affects the hippocampus and entorhinal complex, leading to memory lapse cognitive impairment. This can have negative impact on an individual’s behavior, speech, ability navigate their surroundings. AD one of principal causes dementia. One most accepted theories in AD, amyloid β (Aβ) hypothesis, assumes buildup peptide Aβ root cause AD. Impaired insulin signaling periphery central nervous system has been considered effect pathophysiology Further, researchers shifted focus epigenetic mechanisms are responsible for dysregulating major biochemical pathways intracellular processes directly or indirectly causing The prime encompass DNA methylation, histone modifications, non-coding RNA, majorly impairing both centrally peripherally, thus In this review, we provide insights into involved such as methylation deacetylation. We decipher how alter peripheral brain signaling, pathophysiology. addition, review also discusses need newer drug delivery systems targeted drugs explores nanoparticles, vesicular systems, networks, other nano formulations sheds light future approaches used delivery.

Язык: Английский

Процитировано

1

Bases celulares y moleculares de la cronopatología en la enfermedad de Alzheimer DOI Creative Commons
Bettsy Bell Bosch Rodríguez, Marbelys Guevara Rodríguez

eNeurobiología, Год журнала: 2024, Номер 15(37)

Опубликована: Апрель 19, 2024

Los relojes biológicos son osciladores anticipatorios autónomos que desempeñan un papel fundamental en la organización y procesamiento de información desde el genoma hasta desarrollo los organismos completos. Esta compleja jerárquica determina alteración crónica ritmos circadianos sea factor riesgo importante para una variedad enfermedades, incluyendo las patologías neurodegenerativas. La enfermedad Alzheimer (EA) representa trastorno neurodegenerativo más prevalente nuestra sociedad actual, durante mucho tiempo ha sido asociado con alteraciones (ciclos sueño/ vigilia, variaciones amplitud del ciclo liberación melatonina, cortisol, glucosa e insulina), así como perturbaciones ultradianos (diferentes fases sueño). El estudio cronopatología EA orientado busca relación bidireccional, puede comportarse bien causa o consecuencia, lo permitido revelar nuevas dianas terapéuticas capaces retrasar progresión esta enfermedad. objetivo este artículo consiste describir, a través revisión integral literatura médica, trastornos enfocada aportar bases fisiopatológicas ratificar correlación bidireccional existente.

Процитировано

1

NF‐κB1 promotes miR‐27a‐5p upregulation in acrylamide‐induced toxicity in rats DOI Creative Commons
Lujia Zhang, Liuqing Yang, Jianwei Gao

и другие.

Food Frontiers, Год журнала: 2024, Номер 5(2), С. 607 - 617

Опубликована: Янв. 10, 2024

Abstract Acrylamide (AA) is a neurotoxic and potentially carcinogenic contaminant, usually generated during food processing. MicroRNAs are class of noncoding small RNAs, which serve essential pathogenic roles in linking exposure to toxic contaminants with their pathological outcomes. Our previous research identified miR‐27a‐5p as key regulator AA toxicity, it induces mitochondria‐dependent apoptosis by targeting Btf3 rats. However, the mechanisms regulated exert its effects remain unclear. Here, transcription factors that bind promoter potential regulatory functions investigated cell lines The results showed nuclear factor kappa‐B 1 (NF‐κB1) promising from bioinformatic analysis. luciferase reporter assay demonstrated NF‐κB1 enhances transcriptional activity promoter, whereas cleavage under targets tagmentation successfully verified specific binding sites at −305/−298 bp. Furthermore, inhibition resulted suppression expression associated target pathways, additional validation provided vivo experimentation. Consequently, upregulation induced subsequent intrinsic can be attributed promoter. This event may initial step molecular network underlies toxicity.

Язык: Английский

Процитировано

0

LncRNA 3222401L13Rik Is Up-regulated in Aging Astrocytes and Regulates Neuronal Support Function Through Interaction with Npas3 DOI Creative Commons

Sophie Schroeder,

M. Sadman Sakib, D. Krüger

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Авг. 19, 2024

Abstract Aging is linked to a decline in cognitive functions and significantly increases the risk of neurodegenerative diseases. While molecular changes all central nervous system (CNS) cell types contribute aging-related decline, mechanisms driving disease development or offering protection remain poorly understood. Long non-coding RNAs (lncRNAs) have emerged as key regulators cellular gene expression, yet their roles aging, particularly within glial cells, are not well characterized. In this study, we investigated lncRNA expression profiles non-neuronal cells from aged mice. We identified 3222401L13Rik, previously unstudied enriched being specifically upregulated astrocytes during aging. Knockdown 3222401L13Rik primary revealed its critical role regulating genes essential for neuronal support synapse organization. This function was also conserved human iPSC-derived astrocytes. Additionally, found that mediates effects through interaction with transcription factor Neuronal PAS Domain Protein 3 (Npas3), overexpression Npas3 effectively rescued functional deficits observed lacking 3222401L13Rik. Our findings suggest upregulation aging acts compensatory mechanism enhance synaptic support, potentially delaying onset structural both neurons. Strategies boost earlier life may help mitigate age-associated loss plasticity.

Язык: Английский

Процитировано

0