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  1. AU="Fazaludeen, Mohammad Feroze"
  2. AU="Larsen, Mikko"
  3. AU=Haverkos Bradley M.
  4. AU="Kuklin, Artem V"
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  1. Article ; Online: Particulate matter from car exhaust alters function of human iPSC-derived microglia.

    Jäntti, Henna / Jonk, Steffi / Gómez Budia, Mireia / Ohtonen, Sohvi / Fagerlund, Ilkka / Fazaludeen, Mohammad Feroze / Aakko-Saksa, Päivi / Pebay, Alice / Lehtonen, Šárka / Koistinaho, Jari / Kanninen, Katja M / Jalava, Pasi I / Malm, Tarja / Korhonen, Paula

    Particle and fibre toxicology

    2024  Volume 21, Issue 1, Page(s) 6

    Abstract: Background: Air pollution is recognized as an emerging environmental risk factor for neurological diseases. Large-scale epidemiological studies associate traffic-related particulate matter (PM) with impaired cognitive functions and increased incidence ... ...

    Abstract Background: Air pollution is recognized as an emerging environmental risk factor for neurological diseases. Large-scale epidemiological studies associate traffic-related particulate matter (PM) with impaired cognitive functions and increased incidence of neurodegenerative diseases such as Alzheimer's disease. Inhaled components of PM may directly invade the brain via the olfactory route, or act through peripheral system responses resulting in inflammation and oxidative stress in the brain. Microglia are the immune cells of the brain implicated in the progression of neurodegenerative diseases. However, it remains unknown how PM affects live human microglia.
    Results: Here we show that two different PMs derived from exhausts of cars running on EN590 diesel or compressed natural gas (CNG) alter the function of human microglia-like cells in vitro. We exposed human induced pluripotent stem cell (iPSC)-derived microglia-like cells (iMGLs) to traffic related PMs and explored their functional responses. Lower concentrations of PMs ranging between 10 and 100 µg ml
    Conclusions: Our study indicates that traffic-related air pollutants alter the function of human microglia and warrant further studies to determine whether these changes contribute to adverse effects in the brain and on cognition over time. This study demonstrates human iPSC-microglia as a valuable tool to study functional microglial responses to environmental agents.
    MeSH term(s) Humans ; Particulate Matter/toxicity ; Particulate Matter/analysis ; Microglia/chemistry ; Induced Pluripotent Stem Cells/chemistry ; Automobiles ; Reactive Oxygen Species ; Vehicle Emissions/toxicity ; Vehicle Emissions/analysis ; Neurodegenerative Diseases
    Chemical Substances Particulate Matter ; Reactive Oxygen Species ; Vehicle Emissions
    Language English
    Publishing date 2024-02-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 2170936-1
    ISSN 1743-8977 ; 1743-8977
    ISSN (online) 1743-8977
    ISSN 1743-8977
    DOI 10.1186/s12989-024-00564-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Human iPSC-derived microglia carrying the LRRK2-G2019S mutation show a Parkinson's disease related transcriptional profile and function.

    Ohtonen, Sohvi / Giudice, Luca / Jäntti, Henna / Fazaludeen, Mohammad Feroze / Shakirzyanova, Anastasia / Gómez-Budia, Mireia / Välimäki, Nelli-Noora / Niskanen, Jonna / Korvenlaita, Nea / Fagerlund, Ilkka / Koistinaho, Jari / Amiry-Moghaddam, Mahmood / Savchenko, Ekaterina / Roybon, Laurent / Lehtonen, Šárka / Korhonen, Paula / Malm, Tarja

    Scientific reports

    2023  Volume 13, Issue 1, Page(s) 22118

    Abstract: LRRK2-G2019S is one of the most common Parkinson's disease (PD)-associated mutations and has been shown to alter microglial functionality. However, the impact of LRRK2-G2019S on transcriptional profile of human induced pluripotent stem cell-derived ... ...

    Abstract LRRK2-G2019S is one of the most common Parkinson's disease (PD)-associated mutations and has been shown to alter microglial functionality. However, the impact of LRRK2-G2019S on transcriptional profile of human induced pluripotent stem cell-derived microglia-like cells (iMGLs) and how it corresponds to microglia in idiopathic PD brain is not known. Here we demonstrate that LRRK2-G2019S carrying iMGL recapitulate aspects of the transcriptional signature of human idiopathic PD midbrain microglia. LRRK2-G2019S induced subtle and donor-dependent alterations in iMGL mitochondrial respiration, phagocytosis and cytokine secretion. Investigation of microglial transcriptional state in the midbrains of PD patients revealed a subset of microglia with a transcriptional overlap between the in vitro PD-iMGL and human midbrain PD microglia. We conclude that LRRK2-G2019S iMGL serve as a model to study PD-related effects in human microglia.
    MeSH term(s) Humans ; Induced Pluripotent Stem Cells ; Microglia ; Parkinson Disease/genetics ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Mutation ; Gene Expression
    Chemical Substances Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; LRRK2 protein, human (EC 2.7.11.1)
    Language English
    Publishing date 2023-12-13
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-49294-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Genotyping and Frequency of

    Nuglozeh, Edem / Fazaludeen, Mohammad Feroze / Hasona, Nabil / Malm, Tarja / Mayor, Luisito B / Al-Hazmi, Awdah / Ashankyty, Ibraheem

    Indian journal of clinical biochemistry : IJCB

    2018  Volume 34, Issue 4, Page(s) 444–450

    Abstract: Non-synonymous single-nucleotide polymorphism (SNPs) in the gene for proprotein convertase subtilisin/kexin type 9 ( ...

    Abstract Non-synonymous single-nucleotide polymorphism (SNPs) in the gene for proprotein convertase subtilisin/kexin type 9 (
    Language English
    Publishing date 2018-07-30
    Publishing country India
    Document type Journal Article
    ZDB-ID 1033583-3
    ISSN 0974-0422 ; 0970-1915
    ISSN (online) 0974-0422
    ISSN 0970-1915
    DOI 10.1007/s12291-018-0763-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Jg. 1995 - 2021: Lesesall (2.OG)
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  4. Article ; Online: Microglia-like Cells Promote Neuronal Functions in Cerebral Organoids.

    Fagerlund, Ilkka / Dougalis, Antonios / Shakirzyanova, Anastasia / Gómez-Budia, Mireia / Pelkonen, Anssi / Konttinen, Henna / Ohtonen, Sohvi / Fazaludeen, Mohammad Feroze / Koskuvi, Marja / Kuusisto, Johanna / Hernández, Damián / Pebay, Alice / Koistinaho, Jari / Rauramaa, Tuomas / Lehtonen, Šárka / Korhonen, Paula / Malm, Tarja

    Cells

    2021  Volume 11, Issue 1

    Abstract: Human cerebral organoids, derived from induced pluripotent stem cells, offer a unique in vitro research window to the development of the cerebral cortex. However, a key player in the developing brain, the microglia, do not natively emerge in cerebral ... ...

    Abstract Human cerebral organoids, derived from induced pluripotent stem cells, offer a unique in vitro research window to the development of the cerebral cortex. However, a key player in the developing brain, the microglia, do not natively emerge in cerebral organoids. Here we show that erythromyeloid progenitors (EMPs), differentiated from induced pluripotent stem cells, migrate to cerebral organoids, and mature into microglia-like cells and interact with synaptic material. Patch-clamp electrophysiological recordings show that the microglia-like population supported the emergence of more mature and diversified neuronal phenotypes displaying repetitive firing of action potentials, low-threshold spikes and synaptic activity, while multielectrode array recordings revealed spontaneous bursting activity and increased power of gamma-band oscillations upon pharmacological challenge with NMDA. To conclude, microglia-like cells within the organoids promote neuronal and network maturation and recapitulate some aspects of microglia-neuron co-development in vivo, indicating that cerebral organoids could be a useful biorealistic human in vitro platform for studying microglia-neuron interactions.
    MeSH term(s) Adolescent ; Adult ; Aged ; Cell Differentiation ; Female ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Male ; Microglia/metabolism ; Middle Aged ; Neurogenesis/genetics ; Neurons/metabolism ; Organoids/metabolism ; Young Adult
    Language English
    Publishing date 2021-12-30
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11010124
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Single-Cell RNA-Seq Analysis of Olfactory Mucosal Cells of Alzheimer's Disease Patients.

    Lampinen, Riikka / Fazaludeen, Mohammad Feroze / Avesani, Simone / Örd, Tiit / Penttilä, Elina / Lehtola, Juha-Matti / Saari, Toni / Hannonen, Sanna / Saveleva, Liudmila / Kaartinen, Emma / Fernández Acosta, Francisco / Cruz-Haces, Marcela / Löppönen, Heikki / Mackay-Sim, Alan / Kaikkonen, Minna U / Koivisto, Anne M / Malm, Tarja / White, Anthony R / Giugno, Rosalba /
    Chew, Sweelin / Kanninen, Katja M

    Cells

    2022  Volume 11, Issue 4

    Abstract: Olfaction is orchestrated by olfactory mucosal cells located in the upper nasal cavity. Olfactory dysfunction manifests early in several neurodegenerative disorders including Alzheimer's disease, however, disease-related alterations to the olfactory ... ...

    Abstract Olfaction is orchestrated by olfactory mucosal cells located in the upper nasal cavity. Olfactory dysfunction manifests early in several neurodegenerative disorders including Alzheimer's disease, however, disease-related alterations to the olfactory mucosal cells remain poorly described. The aim of this study was to evaluate the olfactory mucosa differences between cognitively healthy individuals and Alzheimer's disease patients. We report increased amyloid-beta secretion in Alzheimer's disease olfactory mucosal cells and detail cell-type-specific gene expression patterns, unveiling 240 differentially expressed disease-associated genes compared to the cognitively healthy controls, and five distinct cell populations. Overall, alterations of RNA and protein metabolism, inflammatory processes, and signal transduction were observed in multiple cell populations, suggesting their role in Alzheimer's disease-related olfactory mucosa pathophysiology. Furthermore, the single-cell RNA-sequencing proposed alterations in gene expression of mitochondrially located genes in AD OM cells, which were verified by functional assays, demonstrating altered mitochondrial respiration and a reduction of ATP production. Our results reveal disease-related changes of olfactory mucosal cells in Alzheimer's disease and demonstrate the utility of single-cell RNA sequencing data for investigating molecular and cellular mechanisms associated with the disease.
    MeSH term(s) Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Humans ; Olfactory Mucosa/metabolism ; RNA ; Sequence Analysis, RNA
    Chemical Substances Amyloid beta-Peptides ; RNA (63231-63-0)
    Language English
    Publishing date 2022-02-15
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11040676
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: PSEN1ΔE9, APPswe, and APOE4 Confer Disparate Phenotypes in Human iPSC-Derived Microglia.

    Konttinen, Henna / Cabral-da-Silva, Mauricio E Castro / Ohtonen, Sohvi / Wojciechowski, Sara / Shakirzyanova, Anastasia / Caligola, Simone / Giugno, Rosalba / Ishchenko, Yevheniia / Hernández, Damián / Fazaludeen, Mohammad Feroze / Eamen, Shaila / Budia, Mireia Gómez / Fagerlund, Ilkka / Scoyni, Flavia / Korhonen, Paula / Huber, Nadine / Haapasalo, Annakaisa / Hewitt, Alex W / Vickers, James /
    Smith, Grady C / Oksanen, Minna / Graff, Caroline / Kanninen, Katja M / Lehtonen, Sarka / Propson, Nicholas / Schwartz, Michael P / Pébay, Alice / Koistinaho, Jari / Ooi, Lezanne / Malm, Tarja

    Stem cell reports

    2019  Volume 13, Issue 4, Page(s) 669–683

    Abstract: Here we elucidate the effect of Alzheimer disease (AD)-predisposing genetic backgrounds, APOE4, PSEN1ΔE9, and APPswe, on functionality of human microglia-like cells (iMGLs). We present a physiologically relevant high-yield protocol for producing iMGLs ... ...

    Abstract Here we elucidate the effect of Alzheimer disease (AD)-predisposing genetic backgrounds, APOE4, PSEN1ΔE9, and APPswe, on functionality of human microglia-like cells (iMGLs). We present a physiologically relevant high-yield protocol for producing iMGLs from induced pluripotent stem cells. Differentiation is directed with small molecules through primitive erythromyeloid progenitors to re-create microglial ontogeny from yolk sac. The iMGLs express microglial signature genes and respond to ADP with intracellular Ca
    MeSH term(s) Alzheimer Disease/etiology ; Alzheimer Disease/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Apolipoprotein E4/genetics ; Apolipoprotein E4/metabolism ; Calcium/metabolism ; Cell Differentiation/genetics ; Cells, Cultured ; Chemokines/metabolism ; Cytokines/metabolism ; Hematopoiesis ; Humans ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/metabolism ; Inflammation Mediators/metabolism ; Microglia/cytology ; Microglia/metabolism ; Mutation ; Phagocytosis ; Phenotype ; Presenilin-1/genetics ; Presenilin-1/metabolism ; Proteolysis
    Chemical Substances APP protein, human ; Amyloid beta-Protein Precursor ; Apolipoprotein E4 ; Chemokines ; Cytokines ; Inflammation Mediators ; PSEN1 protein, human ; Presenilin-1 ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2019-09-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2720528-9
    ISSN 2213-6711 ; 2213-6711
    ISSN (online) 2213-6711
    ISSN 2213-6711
    DOI 10.1016/j.stemcr.2019.08.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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