Light microscopic and heterogeneity analysis of astrocytes in the common marmoset brain

Muñoz, Yorka; Cuevas-Pacheco, Francisco; Quesseveur, Gaël; Murai, Keith K.

doi:10.1002/jnr.24967

Cited by 4 publications

(2 citation statements)

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“…The primate plexiform layer contains GFAP + interlaminar astrocytes, which represent a group of distinct primate‐specific glial cells characterized by their long, fine, unbranched processes (often greater than 300 μm in length) extending toward layers II−IV (Falcone et al., 2019; Munoz et al., 2021; Oberheim et al., 2009). We found that 30.1% (± 4.6%) of GFAP + interlaminar astrocytes express RAI1, with their somas juxtaposed to, and their long processes extending away from, the pial surface (Figure 3a; a reconstructed RAI1 + /GFAP + interlaminar astrocyte is shown on the left).…”

Section: Resultsmentioning

confidence: 99%

Comparative analyses of the Smith−Magenis syndrome protein RAI1 in mice and common marmoset monkeys

Chang,

Lee,

Haque

et al. 2024

J of Comparative Neurology

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Retinoic acid‐induced 1 (RAI1) encodes a transcriptional regulator critical for brain development and function. RAI1 haploinsufficiency in humans causes a syndromic autism spectrum disorder known as Smith−Magenis syndrome (SMS). The neuroanatomical distribution of RAI1 has not been quantitatively analyzed during the development of the prefrontal cortex, a brain region critical for cognitive function and social behaviors and commonly implicated in autism spectrum disorders, including SMS. Here, we performed comparative analyses to uncover the evolutionarily convergent and divergent expression profiles of RAI1 in major cell types during prefrontal cortex maturation in common marmoset monkeys (Callithrix jacchus) and mice (Mus musculus). We found that while RAI1 in both species is enriched in neurons, the percentage of excitatory neurons that express RAI1 is higher in newborn mice than in newborn marmosets. By contrast, RAI1 shows similar neural distribution in adult marmosets and adult mice. In marmosets, RAI1 is expressed in several primate‐specific cell types, including intralaminar astrocytes and MEIS2‐expressing prefrontal GABAergic neurons. At the molecular level, we discovered that RAI1 forms a protein complex with transcription factor 20 (TCF20), PHD finger protein 14 (PHF14), and high mobility group 20A (HMG20A) in the marmoset brain. In vitro assays in human cells revealed that TCF20 regulates RAI1 protein abundance. This work demonstrates that RAI1 expression and protein interactions are largely conserved but with some unique expression in primate‐specific cells. The results also suggest that altered RAI1 abundance could contribute to disease features in disorders caused by TCF20 dosage imbalance.

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Section: Resultsmentioning

confidence: 99%

Comparative analyses of the Smith−Magenis syndrome protein RAI1 in mice and common marmoset monkeys

Chang,

Lee,

Haque

et al. 2024

J of Comparative Neurology

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“…However, numerous specialized subtypes have been described in distinct brain areas such as the Bergman glia in the cerebellum ( De Zeeuw and Hoogland, 2015 ), the Müller glia in the retina, or the interlaminar astrocytes in the neo-cortex ( Colombo, 2018 ) or in specific localization such as the perivascular astrocytes or the subpial astrocytes. The morphology, density, overlap, and diversity of astrocytes can vary depending on brain areas and species ( Oberheim et al, 2009 ; Batiuk et al, 2020 ; Muñoz et al, 2021 ). The classic description of the astrocyte, representing mainly protoplasmic ones, is the following:…”

Section: Introductionmentioning

confidence: 99%

The Multifaceted Neurotoxicity of Astrocytes in Ageing and Age-Related Neurodegenerative Diseases: A Translational Perspective

et al. 2022

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In a healthy physiological context, astrocytes are multitasking cells contributing to central nervous system (CNS) homeostasis, defense, and immunity. In cell culture or rodent models of age-related neurodegenerative diseases (NDDs), such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), numerous studies have shown that astrocytes can adopt neurotoxic phenotypes that could enhance disease progression. Chronic inflammatory responses, oxidative stress, unbalanced phagocytosis, or alteration of their core physiological roles are the main manifestations of their detrimental states. However, if astrocytes are directly involved in brain deterioration by exerting neurotoxic functions in patients with NDDs is still controversial. The large spectrum of NDDs, with often overlapping pathologies, and the technical challenges associated with the study of human brain samples complexify the analysis of astrocyte involvement in specific neurodegenerative cascades. With this review, we aim to provide a translational overview about the multi-facets of astrocyte neurotoxicity ranging from in vitro findings over mouse and human cell-based studies to rodent NDDs research and finally evidence from patient-related research. We also discuss the role of ageing in astrocytes encompassing changes in physiology and response to pathologic stimuli and how this may prime detrimental responses in NDDs. To conclude, we discuss how potentially therapeutic strategies could be adopted to alleviate or reverse astrocytic toxicity and their potential to impact neurodegeneration and dementia progression in patients.

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