EVOS M5000 in Neuroscience & Neurodegeneration

Curated literature review of independent peer-reviewed studies that used the EVOS M5000 Imaging System. Each paper is summarised by cell type, imaging technique, and disease area, with links to Google Scholar, PubMed, PMC and DOI where available. Plankton & Zoom does not host paywalled content.

From TDP-43 proteinopathies and C9orf72 ALS/FTD to Huntington’s disease and spinal cord injury, the EVOS M5000 supports neuronal imaging in a range of neurodegeneration models. Each paper below was identified outside the manufacturer’s reference list. These papers were identified by searching the open-access literature and verifying that the full text explicitly mentions the EVOS M5000 Imaging System as a microscope; they are not part of the manufacturer’s curated citation list.

Targeting the integrated stress response or Ataxin-2 alleviates neurodegeneration in PolyGR models of C9orf72 associated frontotemporal dementia and amyotrophic lateral sclerosis.

Cell type: Neurons / iPSC / Drosophila neurons

Imaging technique: Fluorescence microscopy

Disease area: C9orf72 FTD / ALS

Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are fatal, early-onset neurodegenerative diseases. The most common genetic cause of FTD and ALS is a G4C2 hexanucleotide repeat expansion in the C9orf72 gene. This mutation leads to the production of toxic dipeptide repeat proteins (DPRs), via repeat...

Acta Neuropathol Commun PMID 42087256 — PMC13251143

Google Scholar | PubMed | PMC | DOI

Striatal Neuron Excitability Is Regulated by Huntingtin in the Adult Brain.

Cell type: Striatal neurons (mouse brain)

Imaging technique: Fluorescence / cell excitability imaging

Disease area: Huntington disease

Huntington's disease (HD) is a hereditary neurodegenerative disease that typically presents during midlife and is characterized by a combination of motor, cognitive, and psychiatric symptoms. HD is fatal and arises from a mutation in the huntingtin (HTT) gene, which results in decreased neuronal health followed by...

eNeuro PMID 42209021 — PMC13249443

Google Scholar | PubMed | PMC | DOI

Uric Acid Released from Poly (Lactic-co-Glycolic Acid) Nanoparticles Mitigates Glutamate-Induced Excitotoxicity of Spinal Cord Neurons.

Cell type: Spinal cord neurons

Imaging technique: Fluorescence imaging (excitotoxicity assays)

Disease area: Spinal cord injury

Spinal cord injury (SCI) is often compounded by secondary damage caused by glutamate-induced excitotoxicity (GIE), where excessive glutamate release results in neuronal damage by overstimulation of glutamate receptors. This process leads to mitochondrial dysfunction, oxidative stress, and neuronal death. Uric acid (UA)...

ASN Neuro PMID 42405595 — PMC13349032

Google Scholar | PubMed | PMC | DOI

Short RNA chaperones promote aggregation-resistant TDP-43 conformers to mitigate neurodegeneration.

Cell type: Neurons / iPSC / Drosophila / TDP-43

Imaging technique: Fluorescence microscopy

Disease area: ALS / TDP-43 proteinopathies

Aberrant aggregation of the prion-like RNA binding protein TDP-43 drives several fatal neurodegenerative proteinopathies, including amyotrophic lateral sclerosis (ALS). In this work, we define how short, specific RNAs solubilize TDP-43. These short RNAs engage and stabilize the TDP-43 RNA recognition motifs, which allo...

Science PMID 42096556 — PMC13155378

Google Scholar | PubMed | PMC | DOI

Correction of the molecular phenotype of X-linked Dystonia-Parkinsonism reveals a non-canonical function of BRD4.

Cell type: Neuronal cells / patient-derived cells

Imaging technique: Fluorescence microscopy

Disease area: X-linked Dystonia-Parkinsonism

Transcription and mRNA processing are tightly coupled regulatory layers on gene expression, and their perturbations underly human disorders. X-linked Dystonia-Parkinsonism (XDP) is a unique example of a human disease connecting aberrant mRNA processing and the basal transcription machinery. XDP is a rare, monogenic fat...

Nat Commun PMID 42086561 — PMC13144358

Google Scholar | PubMed | PMC | DOI