Literature DB >> 10705642

The comparison of microglia maturation in CNS of normal human fetuses and fetuses with Down's syndrome.

T Wierzba-Bobrowicz1, E Lewandowska, B Schmidt-Sidor, E Gwiazda.   

Abstract

The study was performed on the tissues derived from the central nervous system (CNS) of 72 normal human fetuses between 8 and 22 week of gestation (GW) and 30 fetuses with genetically confirmed Down's syndrome between 17 and 22 GW. Histochemical, immunocytochemical and ultrastructural examinations of microglial cells in frontal lobe, mesencephalon and cerebellum were carried out. A quantitative evaluation of developing microglia was performed in comparison with astroglial cells by counting the mean number of cells per 1 mm2. The study indicated that microglial cells emerge at the same time in all structures under study, both in normal fetuses and in those with Down's syndrome. It was also found that ameboid microglia (AM) and ramified microglia (RM) emerge at the same time and show the same morphological structure in both groups of fetuses. It was revealed that in the CNS of fetuses with Down's syndrome, the number of ramified microglial cells increased significantly as compared with in normal fetuses. Astroglial cells outnumbered microglial cells in the normal fetal development. Due to the enhanced number of RM cells in the CNS of fetuses with Down's syndrome the quantitative difference between these cells obliterated, and microglial cells in the frontal lobe cortex even outnumbered astroglial cells.

Entities:  

Mesh:

Year:  1999        PMID: 10705642

Source DB:  PubMed          Journal:  Folia Neuropathol        ISSN: 1509-572X            Impact factor:   2.038


  8 in total

1.  Organotypic cultures of free-floating slices of human embryo medulla oblongata.

Authors:  V M Vostrikov; N S Kolomeets; O P Aleksandrova; I V Viktorov; N A Uranova; G T Sukhikh
Journal:  Neurosci Behav Physiol       Date:  2005-01

2.  Challenges and Opportunities for Translation of Therapies to Improve Cognition in Down Syndrome.

Authors:  Sarah E Lee; Monica Duran-Martinez; Sabina Khantsis; Diana W Bianchi; Faycal Guedj
Journal:  Trends Mol Med       Date:  2019-11-07       Impact factor: 11.951

3.  Effects of S100B on Serotonergic Plasticity and Neuroinflammation in the Hippocampus in Down Syndrome and Alzheimer's Disease: Studies in an S100B Overexpressing Mouse Model.

Authors:  Lee A Shapiro; Lynn A Bialowas-McGoey; Patricia M Whitaker-Azmitia
Journal:  Cardiovasc Psychiatry Neurol       Date:  2010-08-22

Review 4.  Neurodevelopment in Down syndrome: Concordance in humans and models.

Authors:  Jenny A Klein; Tarik F Haydar
Journal:  Front Cell Neurosci       Date:  2022-07-15       Impact factor: 6.147

Review 5.  Astroglial and microglial pathology in Down syndrome: Focus on Alzheimer's disease.

Authors:  Octavio García; Lisi Flores-Aguilar
Journal:  Front Cell Neurosci       Date:  2022-09-20       Impact factor: 6.147

Review 6.  Down Syndrome Is a Metabolic Disease: Altered Insulin Signaling Mediates Peripheral and Brain Dysfunctions.

Authors:  Mara Dierssen; Marta Fructuoso; María Martínez de Lagrán; Marzia Perluigi; Eugenio Barone
Journal:  Front Neurosci       Date:  2020-07-08       Impact factor: 4.677

7.  Rescuing Over-activated Microglia Restores Cognitive Performance in Juvenile Animals of the Dp(16) Mouse Model of Down Syndrome.

Authors:  Bruno Pinto; Giovanni Morelli; Mohit Rastogi; Annalisa Savardi; Amos Fumagalli; Andrea Petretto; Martina Bartolucci; Emilio Varea; Tiziano Catelani; Andrea Contestabile; Laura E Perlini; Laura Cancedda
Journal:  Neuron       Date:  2020-10-06       Impact factor: 17.173

8.  RvE1 treatment prevents memory loss and neuroinflammation in the Ts65Dn mouse model of Down syndrome.

Authors:  Eric D Hamlett; Erik Hjorth; Aurélie Ledreux; Anah Gilmore; Marianne Schultzberg; Ann Charlotte Granholm
Journal:  Glia       Date:  2020-01-16       Impact factor: 7.452

  8 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.