Methamphetamine Increases Tubulo-Vesicular Areas While Dissipating Proteins from Vesicles Involved in Cell Clearance DOI Open Access
Gloria Lazzeri, Paola Lenzi, Carla L. Busceti

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(17), P. 9601 - 9601

Published: Sept. 4, 2024

Cytopathology induced by methamphetamine (METH) is reminiscent of degenerative disorders such as Parkinson’s disease, and it characterized membrane organelles arranged in tubulo-vesicular structures. These areas, appearing clusters vesicles, have never been defined concerning the presence specific organelles. Therefore, present study aimed to identify relative absolute area membrane-bound following a moderate dose (100 µM) METH administered catecholamine-containing PC12 cells. Organelles antigens were detected immunofluorescence, they further quantified plain electron microscopy situ stoichiometry. This analysis indicated an increase autophagosomes damaged mitochondria along with decrease lysosomes healthy mitochondria. Following METH, severe dissipation hallmark proteins from their own vesicles was measured. In fact, amounts LC3 p62 reduced within autophagy vacuoles compared whole cytosol. Similarly, LAMP1 Cathepsin-D reduced. findings suggest loss compartmentalization confirm competence cell clearing during catecholamine degeneration. Such entropy consistent energy stores, which routinely govern appropriate subcellular compartmentalization.

Language: Английский

Evolving Landscape of Parkinson’s Disease Research: Challenges and Perspectives DOI Creative Commons
Rumiana Koynova, Janet M. Sasso, Qiongqiong Angela Zhou

et al.

ACS Omega, Journal Year: 2025, Volume and Issue: 10(2), P. 1864 - 1892

Published: Jan. 8, 2025

Parkinson's disease (PD) is a progressive neurodegenerative disorder that primarily affects movement. It occurs due to gradual deficit of dopamine-producing brain cells, particularly in the substantia nigra. The precise etiology PD not fully understood, but it likely involves combination genetic and environmental factors. therapies available at present alleviate symptoms do stop disease's advancement. Research endeavors are currently directed inventing disease-controlling aim inherent mechanisms PD. biomarker breakthroughs hold enormous potential: earlier diagnosis, better monitoring, targeted treatment based on individual response could significantly improve patient outcomes ease burden this disease. research an active evolving field, focusing understanding mechanisms, identifying biomarkers, developing new treatments, improving care. In report, we explore data from CAS Content Collection outline progress We analyze publication landscape offer perspective into latest expertise advancements. Key emerging concepts reviewed strategies fight evaluated. Pharmacological targets, risk factors, as well comorbid diseases explored, clinical usage products against with their production pipelines trials for drug repurposing examined. This review aims comprehensive overview advancing current about PD, define challenges, assess growth prospects stimulate efforts battling

Language: Английский

Citations

3
Large-scale proteomic analyses of incident Parkinson’s disease reveal new pathophysiological insights and potential biomarkers DOI

Yi‐Han Gan,

Lingzhi Ma, Yi Zhang

et al.

Nature Aging, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 20, 2025

Language: Английский

Citations

1
Metabolomics in Parkinson’s Disease and Correlation with Disease State DOI Creative Commons
Elena A. Ostrakhovitch, Kenjiro Ono, Tritia R. Yamasaki

et al.

Metabolites, Journal Year: 2025, Volume and Issue: 15(3), P. 208 - 208

Published: March 18, 2025

Changes in the level of metabolites, small molecules that are intermediates produced by metabolism or catabolism, associated with developing diseases. Metabolite signatures body fluids such as plasma, cerebrospinal fluid, urine, and saliva Parkinson’s disease. Here, we discuss alteration metabolites TCA cycle, pentose phosphate pathway, kynurenic network, redox system. We also summarize efforts many research groups to differentiate between metabolite profiles characterize PD motor progression dyskinesia, gait balance, non-motor symptoms depression cognitive decline. Understanding how changes lead may allow for identification individuals at earliest stage disease development new therapeutic strategies.

Language: Английский

Citations

1
Transforming neurodegenerative disorder care with machine learning: Strategies and applications DOI
Aya Galal, Ahmed A. Moustafa, Mohamed Salama

et al.

Neuroscience, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Language: Английский

Citations

0
Lysophosphatidylcholine promoting α-Synuclein aggregation in Parkinson’s disease: disrupting GCase glycosylation and lysosomal α-Synuclein degradation DOI Creative Commons

Chunyan Mu,

Kaiquan Shao,

Mingyu Su

et al.

npj Parkinson s Disease, Journal Year: 2025, Volume and Issue: 11(1)

Published: March 15, 2025

In Parkinson's Disease (PD), elevated serum lysophosphatidylcholine (LPC) levels correlate with disease progression. However, the mechanisms by which abnormal LPC elevation contributes to PD-related neurotoxicity remain poorly understood. This study aims investigate pathogenic role of in dopaminergic neuronal damage and elucidates its underlying mechanisms. Our results showed induces α-synuclein aggregation, exacerbating cognitive dysfunction. activates Cleaved-Caspase3 via orphan receptor GPR35-ERK signaling pathway, inhibits GRASP65 expression, disrupts polarized structure Golgi apparatus. disruption impairs glycosylation function glucocerebrosidase (GCase), preventing transport lysosomes leading glucosylceramide (GlcCer) accumulation, a scaffold for aggregation. also autophagolysosomal pathway lysosomal acidification, toxic accumulation. Restoring GCase glycosylation, limiting GlcCer synthesis, or blocking ERK mitigates these effects. highlights LPC's promoting aggregation dysfunction, advancing our understanding PD pathology.

Language: Английский

Citations

0
Methamphetamine Increases Tubulo-Vesicular Areas While Dissipating Proteins from Vesicles Involved in Cell Clearance DOI Open Access
Gloria Lazzeri, Paola Lenzi, Carla L. Busceti

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(17), P. 9601 - 9601

Published: Sept. 4, 2024

Cytopathology induced by methamphetamine (METH) is reminiscent of degenerative disorders such as Parkinson’s disease, and it characterized membrane organelles arranged in tubulo-vesicular structures. These areas, appearing clusters vesicles, have never been defined concerning the presence specific organelles. Therefore, present study aimed to identify relative absolute area membrane-bound following a moderate dose (100 µM) METH administered catecholamine-containing PC12 cells. Organelles antigens were detected immunofluorescence, they further quantified plain electron microscopy situ stoichiometry. This analysis indicated an increase autophagosomes damaged mitochondria along with decrease lysosomes healthy mitochondria. Following METH, severe dissipation hallmark proteins from their own vesicles was measured. In fact, amounts LC3 p62 reduced within autophagy vacuoles compared whole cytosol. Similarly, LAMP1 Cathepsin-D reduced. findings suggest loss compartmentalization confirm competence cell clearing during catecholamine degeneration. Such entropy consistent energy stores, which routinely govern appropriate subcellular compartmentalization.

Language: Английский

Citations

0