Microglia in Alzheimer's Disease: The Role of Stem Cell-Microglia Interaction in Brain Homeostasis
- PDF / 644,154 Bytes
- 8 Pages / 595.276 x 790.866 pts Page_size
- 34 Downloads / 205 Views
REVIEW
Microglia in Alzheimer’s Disease: The Role of Stem Cell‑Microglia Interaction in Brain Homeostasis Saeid Bagheri‑Mohammadi1,2,3 Received: 25 June 2020 / Revised: 28 September 2020 / Accepted: 27 October 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Microglia as resident cells of the brain can regulate neural development and maintenance of neuronal networks. Any types of pathologic events or changes in brain homeostasis are involved in the activation of microglia. This activation depends on the context, type of the stressor, or pathology. Due to the release of a plethora of substances such as chemokines, cytokines, and growth factors, microglia able to influence the pathologic outcome. In Alzheimer’s disease (AD) condition, the deposition of amyloid‐β (Aβ) result in provokes the phenotypic activation of microglia and their elaboration of pro-inflammatory molecules. New investigations reveal that cellular therapy with stem cells might have therapeutic effects in preventing the pathogenesis of AD. Although many strategies have focused on the use of stem cells to regenerate damaged neurons, new researches have demonstrated the immune-regulatory feature of stem cells which can modulate the activity state of microglia as well as mediates neuroinflammation. Hence, understanding the molecular mechanisms involved in the brain homeostasis by the protective features of mesenchymal stem cells (MSCs) could lead to remedial treatment for AD. Keywords Alzheimer’s disease · Cell therapy · Stem cells · Microglia · Mesenchymal stem cells
Introduction Alzheimer’s disease (AD), one of the most prevalent neuronal disorders worldwide, clinically is characterized by impairments in memory, cognition, and intellectual disabilities. The extracellular plaques composed predominately of the amyloid‐β (Aβ) peptide, intra-neuronal tangles of hyper-phosphorylated tau, and synaptic and neuronal loss are the neuropathological hallmarks of the AD in the brain of patients [1, 2]. Moreover, inflammation in brain tissue plays a significant role in the neurodegeneration process. In the last 10 years, there was dramatic increase in the AD prevalence due to the advancing age of the human population, female sex, and genetic risk factors; to this end, it * Saeid Bagheri‑Mohammadi bagherimohammadi‑[email protected] 1
Department of Physiology and Neurophysiology Research Center, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2
Department of Physiology, Faculty of Medicine, Kashan University of Medical Sciences, Kashan, Iran
3
Departments of Applied Cell Sciences, Faculty of Medicine, Kashan University of Medical Sciences, Kashan, Iran
is estimated that in the future, there will be more people affected by this neuronal disorder in the world [3, 4]. Hence, this shows that there are no effective therapeutic strategies available to prevent, treat, or manage AD [4]. Based on studies, it has been approved that microglia play important roles in the developmental process in
Data Loading...
