Alzheimer’s, Parkinson’s, Frontotemporal Lobar Degeneration, and Amyotrophic Lateral Sclerosis Start in Pediatric Ages: Ultrafine Particulate Matter and Industrial Nanoparticles Are Key in the Early-Onset Neurodegeneration: Time to Invest in Preventive Medicine

Toxics, Год журнала: 2025, Номер 13(3), С. 178 - 178

Опубликована: Фев. 28, 2025

Billions of people are exposed to fine particulate matter (PM2.5) levels above the USEPA’s annual standard 9 μg/m3. Common emission sources anthropogenic, producing complex aerosolized toxins. Ultrafine (UFPM) and industrial nanoparticles (NPs) have major detrimental effects on brain, but USA does not measure UFPM a routine basis. This review focuses development progression common neurodegenerative diseases, as diagnosed through neuropathology, among young residents in Metropolitan Mexico City (MMC). MMC is one most polluted megacities world, with population 22 million residents, many whom unaware brain caused by their atmosphere. Fatal diseases (such Alzheimer’s Parkinson’s) that begin childhood populations living air environments preventable. We conclude UFPM/NPs capable disrupting neural homeostasis give rise relentless processes throughout entire life highly MMC. The paradigm reaching old age neurodegeneration no longer supported. Neurodegenerative changes start early pediatric ages irreversible. It time invest preventive medicine.

Язык: Английский

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Molecular Pathways of Neuronal Apoptosis in Neurodegenerative Diseases and Intervention Strategies

BIO Web of Conferences, Год журнала: 2025, Номер 166, С. 01006 - 01006

Опубликована: Янв. 1, 2025

Neurodegenerative diseases are a group of progressive conditions characterized by the dysfunction and death neurons, leading to cognitive motor impairments. A key process in pathogenesis these is neuronal apoptosis, which regulated complex array molecular pathways. This paper provides an overview intrinsic extrinsic apoptotic pathways, highlighting critical role caspases executing cell death. It also discusses additional such as endoplasmic reticulum stress, DNA damage response, autophagy, contribute initiation progression apoptosis neurodegenerative diseases.

Язык: Английский

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Parishin A ameliorates cognitive decline by promoting PS1 autophagy in Alzheimer’s disease

Frontiers in Aging Neuroscience, Год журнала: 2025, Номер 17

Опубликована: Март 20, 2025

Introduction Alzheimer’s disease (AD) is a common neurodegenerative in the elderly. Its pathological features include: A lot of misfolding and abnormal aggregation amyloid protein (Aβ); Autophagy disorder, oxidative stress, neuroinflammation, phosphorylated tau synaptic dysfunction. Modern pharmacological studies have found that Paisinhin (PA) has beneficial effects on prevention treatment central nervous system diseases. This study aims to explore role mechanism PA AD through autophagy pathway, lay scientific foundation for development clinical strategies AD. Methods N2A APP cells were treated with different concentrations PA. Cell viability was detected by CCK-8 method. Western blotting expression levels proteins related production, Tau levels. flow transfecting Lc3 double fluorescent plasmid. After Aβ injected into hippocampus WT mice intraperitoneally, learning memory ability tested new object recognition, y maze water maze. The stress level kit. inflammatory factors RT-qpcr. Results not affected at PA, but PS1 significantly decreased 40μM. can obviously improve accumulation AD, some extent save inhibition CQ. Behavioral shown also impairments caused injections. In addition, vivo experiments, levels, inflammation salvage dysfunctions synapses. reduces total . Discussion Our provides first evidence improves Aβ-induced mice. effect appears be mediated promoting reducing stress. It may regulating inflammation, improving abnormally tau, salvaging damaged function, providing valuable insights potential applications

Язык: Английский

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GPR50 regulates neuronal development as a mitophagy receptor

Cell Death and Disease, Год журнала: 2024, Номер 15(8)

Опубликована: Авг. 15, 2024

Abstract Neurons rely heavily on high mitochondrial metabolism to provide sufficient energy for proper development. However, it remains unclear how neurons maintain oxidative phosphorylation (OXPHOS) during Mitophagy plays a pivotal role in maintaining quality and quantity. We herein describe that G protein-coupled receptor 50 (GPR50) is novel mitophagy receptor, which harbors the LC3-interacting region (LIR) required under stress conditions. Although does not localize mitochondria normal culturing conditions, GPR50 recruited depolarized membrane upon stress, marks portion recruits assembling autophagosomes, eventually facilitating fragments be engulfed by autophagosomes. Mutations Δ502-505 T532A attenuate GPR50-mediated disrupting binding of LC3 recruitment GPR50. Deficiency causes accumulation damaged disrupts OXPHOS, resulting insufficient ATP production excessive ROS generation, impairing neuronal GPR50-deficient mice exhibit impaired social recognition, rescued prenatal treatment with mitoQ, mitochondrially antioxidant. The present study identifies as OXPHOS developing neurons.

Язык: Английский

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Autophagy in Oligodendrocyte Lineage Cells Controls Oligodendrocyte Numbers and Myelin Integrity in an Age-dependent Manner

Neuroscience Bulletin, Год журнала: 2024, Номер 41(3), С. 374 - 390

Опубликована: Сен. 16, 2024

Язык: Английский

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