Renée I. Seinstra

Ferroptosis inhibition protects against α-synuclein-related neuronal cell death

Nad’a Majerníková, Maria João da Costa Caiado, Renée I. Seinstra, Suzanne Couzijn et autres

Parkinson's disease (PD), characterized by α-synuclein (α-syn) pathology, affects millions of people worldwide. While current treatments mainly symptomatically address the motor aspects of PD, they lack efficacy in delaying or halting the degenerative process. Ferroptosis, a type of programmed cell death characterized …

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Condensate-Driven Triglyceride Depletion Links α-Synuclein to Mitochondrial Dysfunction

Tao Zhang, María Eugenia Goya, Alejandro Herron-Bedoya, Jorien C. van der Weerd et autres

Summary Inclusions of α-Synuclein (αSyn) characterize multiple age-related neurodegenerative diseases, including Parkinson’s disease (PD) and Multiple System Atrophy (MSA). While interactions between αSyn and lipids are known to contribute to αSyn pathobiology, the precise cellular mechanisms that link lipids to αSyn toxicity …

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In Vivo Nanodiamond Quantum Sensing of Free Radicals in Caenorhabditis elegans Models

Siyu Fan, Yue Zhang, Anna P. Ainslie, Renée I. Seinstra et autres

Free radicals are believed to play a secondary role in the cell death cascade associated with various diseases. In Huntington's disease (HD), the aggregation of polyglutamine (PolyQ) not only contributes to the disease but also elevates free radical levels. However, measuring free …

Rebalancing the motor circuit restores movement in a Caenorhabditis elegans model for TDP-43 toxicity

Mandy Koopman, Lale Güngördü, Leen Janssen, Renée I. Seinstra et autres

Amyotrophic lateral sclerosis can be caused by abnormal accumulation of TAR DNA-binding protein 43 (TDP-43) in the cytoplasm of neurons. Here, we use a C. elegans model for TDP-43-induced toxicity to identify the biological mechanisms that lead to disease-related phenotypes. By applying …

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Rebalancing the motor circuit restores movement in a Caenorhabditis elegans model for TDP-43-toxicity

Mandy Koopman, Lale Güngördü, Leen Janssen, Renée I. Seinstra et autres

Abstract Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia are caused by the abnormal accumulation of TAR DNA-binding protein 43 (TDP-43) in the cytoplasm of neurons. How TDP-43 accumulation leads to disease symptoms is not well-characterized. Here, we use a C. elegans model …

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Neuronal overexpression of human TDP-43 in Caenorhabditis elegans causes a range of sensorimotor phenotypes

Mandy Koopman, Lale Güngördü, Renée I. Seinstra, Ellen A. A. Nollen

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Neuronal overexpression of hTDP-43 in Caenorhabditis elegans impairs different neuronally controlled behaviors and decreases fecundity

Mandy Koopman, Lale Güngördü, Renée I. Seinstra, Ellen A. A. Nollen

disrupts chemotaxis and decreases fecundity. The basal slowing response, on the other hand, appears to be preserved in the presence of hTDP-43.

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Neuronal overexpression of hTDP-43 in Caenorhabditis elegans mimics the cellular pathology commonly observed in TDP-43 proteinopathies

Mandy Koopman, Lale Güngördü, Renée I. Seinstra, Wytse Hogewerf et autres

) pan-neuronally. We show that disease-related (hyper)phosphorylation and cytosolic localisation of hTDP-43 are present in hTDP-43 worms and that these features can be enhanced by adjusting the environmental temperature.

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Neuronal overexpression of hTDP-43 in Caenorhabditis elegans impairs motor function

Mandy Koopman, Lale Güngördü, Renée I. Seinstra, Ellen A. A. Nollen

) pan-neuronally. Our data reveal that impaired locomotion includes more than the common deficits in crawling capacity and the presence of early-onset paralysis. We show that reduced thrashing, abnormal coiling, and decreased pharyngeal pumping are also observed, in a temperature-dependent fashion.

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Rebalancing the Motor Circuit Restores Movement in a Caenorhabditis elegans Model for TDP-43 Toxicity

Mandy Koopman, Lale Güngördü, Leen Janssen, Renée I. Seinstra et autres

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Preserving protein homeostasis prevents motor impairment in DNA Damage Response-compromised C. elegans

Wouter Huiting, Alejandra Duque‐Jaramillo, Renée I. Seinstra, Harm H. Kampinga et autres

ABSTRACT To maintain genome integrity, cells rely on a complex system of DNA repair pathways and cell cycle checkpoints, together referred to as the DNA damage response (DDR). Impairments in DDR pathways are linked to cancer, but also to a wide range …

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The cellular modifier MOAG‐4/SERF drives amyloid formation through charge complementation

Anita Pras, Bert Houben, Francesco A. Aprile, Renée I. Seinstra et autres

While aggregation‐prone proteins are known to accelerate aging and cause age‐related diseases, the cellular mechanisms that drive their cytotoxicity remain unresolved. The orthologous proteins MOAG‐4, SERF1A, and SERF2 have recently been identified as cellular modifiers of such proteotoxicity. Using a peptide array …

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