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Zaal Kokaia

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Articles

AVHANDLINGAR.SE: Neuroinflammation during stroke and Gaucher’s disease : How monocyte-derived macrophages and microglia shape the inflammatory environment of the brain

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By Zaal Kokaia, Emanuela Monni, Arne Lindgren, Henrik Ahlenius
| avhandlingar.se
Nyckelord: MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Sammanfattning: The human brain is a complex and finely tuned organ, constantly monitored and maintained by its resident immune cells. Among these, microglia are the primary regulators of the brain immune environment under physiological conditions, and monocyte-derived macrophages contribute mainly to pathological states such as ischemic stroke and neuronopathic Gaucher’s disease (GD).
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DNA methylation governs the sensitivity of repeats to restriction by the HUSH-MORC2 corepressor - Nature Communications

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By Jon Matas-Fuentes, Patricia Gerdes, Raquel Garza, Anita Adami, Elisabet Englund, Zaal Kokaia, Johan Jakobsson
| Nature Verified
Abstract The human silencing hub (HUSH) complex binds to transcripts of LINE-1 retrotransposons (L1s) and other genomic repeats, recruiting MORC2 and other effectors to remodel chromatin. How HUSH and MORC2 operate alongside DNA methylation, a central epigenetic regulator of repeat transcription, remains largely unknown. Here we interrogate this relationship in human neural progenitor cells (hNPCs), a somatic model of brain development that tolerates removal of DNA methyltransferase DNMT1.
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Customized Brain Cells for Stroke Patients Using Pluripotent Stem Cells

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By Irene Llorente, Zaal Kokaia, S. Thomas Carmichael
| stroke.ahajournals.org
Regenerative medicine in stroke involves therapies that induce tissue repair and recovery. This is a distinct approach from reducing stroke damage: restoring blood flow, reducing cell death, or limiting secondary progression of injury. These 3 areas have a very concise or limited focus: restoring blood flow involves lysing or removing clots. Reducing cell death means neuroprotection. Limiting secondary damage involves modulating process of inflammation or delayed apoptosis.
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