Konstantin Yenkoyan’s Post

The inducible overexpression of the transcription factor Neurogenin 2 (NGN2) has proven to be an extremely useful tool in neurodegenerative disease research. Using the inducible NGN2 approach, neurons can be generated in just 14 days in vitro, expediting research in neurodegenerative disease. The team at Bioneer are happy once again to have collaborated with the group of Prof. Kristine Freude at the University of Copenhagen to help generate a series of inducible NGN2 iPSC lines for an allelic series of Huntington's Disease iPSCs, to help expedite Huntington's Disease Research (article below). If you are interested in knowing more about how Bioneer can help make inducible NGN2 iPSC lines to assist you research, please reach out to Dale Shelton for more details. #NGN2 #Huntingtonsdisease #Huntingtons #iPSC https://lnkd.in/d-VjXCqf

reMYND NV announces the publication in the prestigious journal Science of research detailing the identification of first-in-class small-molecule septin modulators with neuroprotective efficacy. 2 key takeaways: 👉 reMYND’s septin modulator program demonstrated neuroprotective qualities in Alzheimer’s disease models  👉 the findings provide support for deregulated calcium signalling as a key-driver of neurodegeneration 

📃Scientific paper: Lamp1 Deficiency Enhances Sensitivity to α-Synuclein and Oxidative Stress in Drosophila Models of Parkinson Disease Abstract: International audience; Parkinson disease (PD) is a common neurodegenerative condition affecting people predominantly at old age that is characterized by a progressive loss of midbrain dopaminergic neurons and by the accumulation of α-synuclein-containing intraneuronal inclusions known as Lewy bodies. Defects in cellular degradation processes such as the autophagy-lysosomal pathway are suspected to be involved in PD progression. The mammalian Lysosomal-associated membrane proteins LAMP1 and LAMP2 are transmembrane glycoproteins localized in lysosomes and late endosomes that are involved in autophagosome/lysosome maturation and function. Here, we show that the lack of Drosophila Lamp1, the homolog of LAMP1 and LAMP2, severely increased fly susceptibility to paraquat, a pro-oxidant compound known as a potential PD inducer in humans. Moreover, the loss of Lamp1 also exacerbated the progressive locomotor defects induced by the expression of PD-associated mutant α-synuclein A30P (α-synA30P) in dopaminergic neurons. Remarkably, the ubiquitous re-expression of Lamp1 in a mutant context fully suppressed all these defects and conferred significant resistance towards both PD factors above that of wild-type flies. Immunostaining analysis showed that the brain levels of α-synA30P were unexpectedly decreased in young adult Lamp1-deficient flies expressing this protein in comparison to non-mutant controls. This suggests that Lamp1 could neutralize α-synuclein toxicit... Continued on ES/IODE ➡️ https://etcse.fr/Z8Ug ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

NEW from AD/PD 2024 | LEADS: shedding light on early-onset #Alzheimersdisease 🎥 🧠 In this video, Melissa E Murray, PhD, Mayo Clinic, provides insights into the Longitudinal Early-Onset #Alzheimers Disease Study (LEADS). This is a longitudinal, observational study enrolling #cognitively impaired and normal individuals aged 40-65 to study the development of early-onset Alzheimer’s disease (AD) The study assesses #clinical, #imaging, #biomarker, and #genetic characteristics. While autosomal dominant cases with PSEN1/2 and APP mutations are relatively well studied, much remains unknown about sporadic early-onset AD 🧬 LEADS will bring together numerous sites internationally to track #biomarkers in these individuals, gain a better understanding of the #genetic and #biological processes involved in sporadic cases, and to bring more awareness to early onset AD 🌟 Learn more 👉 https://lnkd.in/egsNMN3X #VJDementia

📃Scientific paper: Lamp1 Deficiency Enhances Sensitivity to α-Synuclein and Oxidative Stress in Drosophila Models of Parkinson Disease Abstract: International audience; Parkinson disease (PD) is a common neurodegenerative condition affecting people predominantly at old age that is characterized by a progressive loss of midbrain dopaminergic neurons and by the accumulation of α-synuclein-containing intraneuronal inclusions known as Lewy bodies. Defects in cellular degradation processes such as the autophagy-lysosomal pathway are suspected to be involved in PD progression. The mammalian Lysosomal-associated membrane proteins LAMP1 and LAMP2 are transmembrane glycoproteins localized in lysosomes and late endosomes that are involved in autophagosome/lysosome maturation and function. Here, we show that the lack of Drosophila Lamp1, the homolog of LAMP1 and LAMP2, severely increased fly susceptibility to paraquat, a pro-oxidant compound known as a potential PD inducer in humans. Moreover, the loss of Lamp1 also exacerbated the progressive locomotor defects induced by the expression of PD-associated mutant α-synuclein A30P (α-synA30P) in dopaminergic neurons. Remarkably, the ubiquitous re-expression of Lamp1 in a mutant context fully suppressed all these defects and conferred significant resistance towards both PD factors above that of wild-type flies. Immunostaining analysis showed that the brain levels of α-synA30P were unexpectedly decreased in young adult Lamp1-deficient flies expressing this protein in comparison to non-mutant controls. This suggests that Lamp1 could neutralize α-synuclein toxicit... Continued on ES/IODE ➡️ https://etcse.fr/Z8Ug ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📃Scientific paper: Lamp1 Deficiency Enhances Sensitivity to α-Synuclein and Oxidative Stress in Drosophila Models of Parkinson Disease Abstract: International audience; Parkinson disease (PD) is a common neurodegenerative condition affecting people predominantly at old age that is characterized by a progressive loss of midbrain dopaminergic neurons and by the accumulation of α-synuclein-containing intraneuronal inclusions known as Lewy bodies. Defects in cellular degradation processes such as the autophagy-lysosomal pathway are suspected to be involved in PD progression. The mammalian Lysosomal-associated membrane proteins LAMP1 and LAMP2 are transmembrane glycoproteins localized in lysosomes and late endosomes that are involved in autophagosome/lysosome maturation and function. Here, we show that the lack of Drosophila Lamp1, the homolog of LAMP1 and LAMP2, severely increased fly susceptibility to paraquat, a pro-oxidant compound known as a potential PD inducer in humans. Moreover, the loss of Lamp1 also exacerbated the progressive locomotor defects induced by the expression of PD-associated mutant α-synuclein A30P (α-synA30P) in dopaminergic neurons. Remarkably, the ubiquitous re-expression of Lamp1 in a mutant context fully suppressed all these defects and conferred significant resistance towards both PD factors above that of wild-type flies. Immunostaining analysis showed that the brain levels of α-synA30P were unexpectedly decreased in young adult Lamp1-deficient flies expressing this protein in comparison to non-mutant controls. This suggests that Lamp1 could neutralize α-synuclein toxicit... Continued on ES/IODE ➡️ https://etcse.fr/Z8Ug ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📃Scientific paper: Lamp1 Deficiency Enhances Sensitivity to α-Synuclein and Oxidative Stress in Drosophila Models of Parkinson Disease Abstract: International audience; Parkinson disease (PD) is a common neurodegenerative condition affecting people predominantly at old age that is characterized by a progressive loss of midbrain dopaminergic neurons and by the accumulation of α-synuclein-containing intraneuronal inclusions known as Lewy bodies. Defects in cellular degradation processes such as the autophagy-lysosomal pathway are suspected to be involved in PD progression. The mammalian Lysosomal-associated membrane proteins LAMP1 and LAMP2 are transmembrane glycoproteins localized in lysosomes and late endosomes that are involved in autophagosome/lysosome maturation and function. Here, we show that the lack of Drosophila Lamp1, the homolog of LAMP1 and LAMP2, severely increased fly susceptibility to paraquat, a pro-oxidant compound known as a potential PD inducer in humans. Moreover, the loss of Lamp1 also exacerbated the progressive locomotor defects induced by the expression of PD-associated mutant α-synuclein A30P (α-synA30P) in dopaminergic neurons. Remarkably, the ubiquitous re-expression of Lamp1 in a mutant context fully suppressed all these defects and conferred significant resistance towards both PD factors above that of wild-type flies. Immunostaining analysis showed that the brain levels of α-synA30P were unexpectedly decreased in young adult Lamp1-deficient flies expressing this protein in comparison to non-mutant controls. This suggests that Lamp1 could neutralize α-synuclein toxicit... Continued on ES/IODE ➡️ https://etcse.fr/Z8Ug ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📣 We are excited to announce that our manuscript “PARK7/DJ-1 deficiency impairs microglial activation in response to LPS-induced inflammation” has now been published in Journal of Neuroinflammation! 🧠 We would like to thank the reviewers for their valuable feedback which improved our manuscript from its preprint stage to its current form. 🔬In this study we explore how DJ-1 affects microglial transcriptional programs and functions and how it could contribute to Parkinson’s disease pathogenesis. Our findings highlight the critical role of microglia in inflammation 🧠 A huge thanks to collaborators from LIH and LCSB! Check out the full article here 📃 https://lnkd.in/eg6U9daP

The proteomic and biological profiling of mitochondria-containing extracellular vesicles derived from neural progenitor cells (NPCs) of an Alzheimer's disease patient reveals critical insights into neurodegenerative mechanisms. Tingting Chen from the University of Groningen, The Netherlands, shared her groundbreaking research at #TargetingEVs2024, highlighting how these extracellular vesicles could serve as vital indicators of disease progression and potential therapeutic targets in Alzheimer’s. #TargetingEVs #mitovesicles #microvesicles #extracellularvesicles #mitochondria #alzheimersdisease #neurodegeneration

Multiomics and machine learning are two topics we're learning more and more about from our clients. In this study, a group used machine learning to assemble and analyze transcriptomic, proteomic, metabolic and lipidomic data-- giving them new insights into Alzheimer's disease molecular profiles. https://lnkd.in/gFxmUwka