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Poornemaa Natarajan

Bio: Poornemaa Natarajan is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Proteome & Mitochondrion. The author has an hindex of 1, co-authored 1 publications receiving 11 citations.

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TL;DR: The comprehensive mitochondrial proteome of cortical astrocytes and neurons is determined, identifying about 150 significantly enriched mitochondrial proteins for each cell type, including transporters, metabolic enzymes, and cell-type-specific antioxidants.

31 citations


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TL;DR: Recently, it was shown that mitochondria and metabolism remodeling are causally linked to neurogenesis as mentioned in this paper, which has important implications for our understanding of neurodevelopmental diseases and possibly human brain evolution.

32 citations

Journal ArticleDOI
Changjing Wang1, Tongtong Yang1, Meiyu Liang1, Junxia Xie1, Ning Song1 
TL;DR: In this article, the authors discuss the role of α-synuclein (α-syn) pathology in Parkinson's disease and conclude that replenishing the glial cells is a valuable therapeutic approach.
Abstract: Parkinson’s disease (PD) is a common neurodegenerative disorder that primarily affects the elderly. While the etiology of PD is likely multifactorial with the involvement of genetic, environmental, aging and other factors, α-synuclein (α-syn) pathology is a pivotal mechanism underlying the development of PD. In recent years, astrocytes have attracted considerable attention in the field. Although astrocytes perform a variety of physiological functions in the brain, they are pivotal mediators of α-syn toxicity since they internalize α-syn released from damaged neurons, and this triggers an inflammatory response, protein degradation dysfunction, mitochondrial dysfunction and endoplasmic reticulum stress. Astrocytes are indispensable coordinators in the background of several genetic mutations, including PARK7, GBA1, LRRK2, ATP13A2, PINK1, PRKN and PLA2G6. As the most abundant glial cells in the brain, functional astrocytes can be replenished and even converted to functional neurons. In this review, we discuss astrocyte dysfunction in PD with an emphasis on α-syn toxicity and genetic modulation and conclude that astrocyte replenishment is a valuable therapeutic approach in PD.

19 citations

Journal ArticleDOI
01 Feb 2022-Neuron
TL;DR: In this article , the authors discuss the importance of the starter cell for shaping the outcome of neuronal reprogramming and propose a code of conduct to avoid artifacts and pitfalls, and point out next challenges for less invasive cell replacement therapies for humans.

19 citations

Journal ArticleDOI
TL;DR: In this article, a review of the regulatory properties of proneural genes encoding basic-helix-loophelix (bHLH) transcription factors (TFs) is presented, focusing on the murine cerebral cortex.
Abstract: Historically, the mammalian brain was thought to lack stem cells as no new neurons were found to be made in adulthood. That dogma changed ∼25 years ago with the identification of neural stem cells (NSCs) in the adult rodent forebrain. However, unlike rapidly self-renewing mature tissues (e.g., blood, intestinal crypts, skin), the majority of adult NSCs are quiescent, and those that become 'activated' are restricted to a few neurogenic zones that repopulate specific brain regions. Conversely, embryonic NSCs are actively proliferating and neurogenic. Investigations into the molecular control of the quiescence-to-proliferation-to-differentiation continuum in the embryonic and adult brain have identified proneural genes encoding basic-helix-loop-helix (bHLH) transcription factors (TFs) as critical regulators. These bHLH TFs initiate genetic programs that remove NSCs from quiescence and drive daughter neural progenitor cells (NPCs) to differentiate into specific neural cell subtypes, thereby contributing to the enormous cellular diversity of the adult brain. However, new insights have revealed that proneural gene activities are context-dependent and tightly regulated. Here we review how proneural bHLH TFs are regulated, with a focus on the murine cerebral cortex, drawing parallels where appropriate to other organisms and neural tissues. We discuss upstream regulatory events, post-translational modifications (phosphorylation, ubiquitinylation), protein-protein interactions, epigenetic and metabolic mechanisms that govern bHLH TF expression, stability, localization, and consequent transactivation of downstream target genes. These tight regulatory controls help to explain paradoxical findings of changes to bHLH activity in different cellular contexts.

16 citations