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JANSSEN M. KOTAH

BSc, MSc, PhD

I am a Filipino neuroscientist 🇵🇭 currently based in the Netherlands. My PhD
work with the Aniko Korosi and Paul Lucassen lab at the University of Amsterdam
involved the use of mouse models to study long term consequences of early-life
stress exposure on later-life challanges, such as aging, inflammation, and
amyloid-β neuropathology. I am currently a postdoc in the lab of prof. Bart
Eggen, studying microglial profiles in the context of neurodegenerative
conditions such as Alzheimer's disease and multiple sclerosis.

While my bachelors degree was in psychology, during my masters in the Neurasmus
program, I was able to acquire a more neurobiological background. During my PhD,
I was able to supplement this with a variety of wet lab experiments involving
behavioral neuroscience and molecular neurobiology. Currently, I am doing a more
bioinformatics-focused postdoc, as I use single cell and spatial transcriptomic
approaches to study the human brain.

My hope is to someday use this combination of wet and dry lab skills to
contribute to building neuroscience in the Philippines.




SELECTED PUBLICATIONS

 1. Early-life stress lastingly impacts microglial transcriptome and function
    under basal and immune-challenged conditions
    Kitty Reemst, Laura Kracht, Janssen M. Kotah, Reza Rahimian, Astrid A.S.
    Irsen, Gonzalo Congrains Sotomayor, Laura N. Verboon, Nieske Brouwer, Sophie
    Simard, Gustavo Turecki, Naguib Mechawar, Susanne M. Kooistra, Bart J.L.
    Eggen, and Aniko Korosi
    Translational psychiatry, Dec 2022
    
    Abs DOI
    
    Early-life stress (ELS) leads to increased vulnerability to psychiatric
    disorders including depression later in life. Neuroinflammatory processes
    have been implicated in ELS-induced negative health outcomes, but how ELS
    impacts microglia, the main tissue-resident macrophages of the central
    nervous system, is unknown. Here, we determined the effects of ELS-induced
    by limited bedding and nesting material during the first week of life
    (postnatal days [P]2–9) on microglial (i) morphology; (ii) hippocampal gene
    expression; and (iii) synaptosome phagocytic capacity in male pups (P9) and
    adult (P200) mice. The hippocampus of ELS-exposed adult mice displayed
    altered proportions of morphological subtypes of microglia, as well as
    microglial transcriptomic changes related to the tumor necrosis factor
    response and protein ubiquitination. ELS exposure leads to distinct gene
    expression profiles during microglial development from P9 to P200 and in
    response to an LPS challenge at P200. Functionally, synaptosomes from
    ELS-exposed mice were phagocytosed less by age-matched microglia. At P200,
    but not P9, ELS microglia showed reduced synaptosome phagocytic capacity
    when compared to control microglia. Lastly, we confirmed the ELS-induced
    increased expression of the phagocytosis-related gene GAS6 that we observed
    in mice, in the dentate gyrus of individuals with a history of child abuse
    using in situ hybridization. These findings reveal persistent effects of ELS
    on microglial function and suggest that altered microglial phagocytic
    capacity is a key contributor to ELS-induced phenotypes.

 2. Spatially resolved gene signatures of white matter lesion progression in
    multiple sclerosis
    Astrid M. Alsema, Marion H. C. Wijering, Anneke Miedema, Janssen M.
    Kotah, Mirjam Koster, Merel Rijnsburger, Hilmar R. J. Weering, Helga E.
    Vries, Wia Baron, Susanne M. Kooistra, and Bart J. L. Eggen
    Nat Neurosci, Nov 2024
    
    Abs DOI
    
    Multiple sclerosis (MS) is an inflammatory disease of the central nervous
    system characterized by myelin loss and progressive neurodegeneration. To
    understand MS lesion initiation and progression, we generate spatial gene
    expression maps of white matter (WM) and grey matter (GM) MS lesions. In
    different MS lesion types, we detect domains characterized by a distinct
    gene signature, including an identifiable rim around active WM lesions.
    Expression changes in astrocyte-specific, oligodendrocyte-specific and
    microglia-specific gene sets characterize the active lesion rims.
    Furthermore, we identify three WM lesion progression trajectories,
    predicting how normal-appearing WM can develop into WM active or mixed
    active-inactive lesions. Our data shed light on the dynamic progression of
    MS lesions.

 3. Early-life stress and amyloidosis in mice share pathogenic pathways
    involving synaptic mitochondria and lipid metabolism
    Janssen M. Kotah, Mandy S. J. Kater, Niek Brosens, Sylvie L. Lesuis, Roberta
    Tandari, Thomas M. Blok, Luca Marchetto, Ella Yusaf, Frank T. W.
    Koopmans, August B. Smit, Paul J. Lucassen, Harm J. Krugers, Mark H. G.
    Verheijen, and Aniko Korosi
    Alzheimers Dement, Mar 2024
    
    Abs DOI
    
    INTRODUCTION: Early-life stress (ES) increases the risk for Alzheimer’s
    disease (AD). We and others have shown that ES aggravates amyloid-beta (Aβ)
    pathology and promotes cognitive dysfunction in APP/PS1 mice, but underlying
    mechanisms remain unclear. METHODS: We studied how ES affects the
    hippocampal synaptic proteome in wild-type (WT) and APP/PS1 mice at early
    and late pathological stages, and validated hits using electron microscopy
    and immunofluorescence. RESULTS: The hippocampal synaptosomes of both
    ES-exposed WT and early-stage APP/PS1 mice showed a relative decrease in
    actin dynamics-related proteins and a relative increase in mitochondrial
    proteins. ES had minimal effects on older WT mice, while strongly affecting
    the synaptic proteome of advanced stage APP/PS1 mice, particularly the
    expression of astrocytic and mitochondrial proteins. DISCUSSION: Our data
    show that ES and amyloidosis share pathogenic pathways involving synaptic
    mitochondrial dysfunction and lipid metabolism, which may underlie the
    observed impact of ES on the trajectory of AD.

Email is usually the easiest way to reach me, but feel free to reach out on
social media as well.
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