Microglia are permanent immune cells of the central nervous system.Microglia play an important role in the pathological process of Alzheimer's disease (AD). They are mainly involved in the uptake and clearance of amyloid-β (Aβ), as well as the formation of neuroinflammation. We found that overactivated microglia increase Aβ and Tau, and Aβ and Tau in turn act as activators of microglia. Additionally, various cytokines and proteins, high cholesterol, and telomere shortening are all associated with microglia activation. More activated microglia induce the release of inflammatory and antiinflammatory factors to regulate inflammation, while microglia express multiple homologous receptors that bind to neuroimmunomodulators to prevent microglia overactivation. Moreover, aging of the body promotes neuroinflammation by increasing the response to IFN-γ (interferon-γ), and aging of the microglia themselves promotes AD by inducing the accumulation of large amounts of iron and reducing autophagy by regulating protein levels. Cognitive dysfunction occurs when activated microglia induce an increase in beta oligomers, promoting the production of pro-inflammatory factors that alter the shape, composition, and density of synapses. Based on their correlation, microglia-mediated AD therapy as well as the corresponding targets and drugs are discussed. In contrast to similar reviews, this article also summarizes some novel microglia-mediated AD treatment methods over the recent years. K E Y W O R D S aging, Alzheimer disease, growth and development, microglia 1 | INTRODUCTION 1.1 | Alzheimer diseaseAlzheimer's disease (AD), also known as senile dementia, is a typical neurodegenerative disease, mainly manifested as progressive memory impairment, cognitive dysfunction, language impairment, and personality changes and other neuropsychiatric symptoms, and adversely affects patients' social, professional, and daily lives. With the aging of the population, about one-third of the elderly over the age of 85 years will suffer from AD,

Neonatal hypoxic‐ischemic encephalopathy (HIE) is one of the important complications of neonatal asphyxia, which not only leads to neurological disability but also seriously threatens the life of neonates. Over the years, animal models of HIE have been a research hotspot to find ways to cope with HIE and thereby reduce the risk of neonatal death or disability in moderate‐to‐severe HIE. By reviewing the literature related to HIE over the years, it was found that nonhuman primates share a high degree of homology with human gross neural anatomy. The basic data on nonhuman primates are not yet complete, so it is urgent to mine and develop new nonhuman primate model data. In recent years, the research on nonhuman primate HIE models has been gradually enriched and the content is more novel. Therefore, the purpose of this review is to further summarize the methods for establishing the nonhuman primate HIE model and to better elucidate the relevance of the nonhuman primate model to humans by observing the behavioral manifestations, neuropathology, and a series of biomarkers of HIE in primates HIE. Finally, the most popular and desirable treatments studied in nonhuman primate models in the past 5 years are summarized.

This study aimed to provide a recommendable protocol for the preparation of brain cryosections of rats to reduce and avoid ice crystals. We have designed five different dewatering solutions (Scheme 1: dehydrate with 15%, 20%, and 30% sucrose–phosphate‐buffered saline solution; Scheme 2: 20% sucrose and 30% sucrose; Scheme 3: 30% sucrose; Scheme 4: 10%, 20%, and 30% sucrose; and Scheme 5: the tissue was dehydrated with 15% and 30% sucrose polyacetate I until it sank to the bottom, followed by placement in 30% sucrose polyacetate II) to minimize the formation of ice crystals. Cryosections from different protocols were stained with Nissl staining and compared with each other by density between cells and the distance of intertissue spaces. The time required for the dehydration process from Scheme 1 to Scheme 5 was 24, 23, 24, 24, and 33 h, respectively. Density between cells gradually decreased from Scheme 1 to Scheme 5, and the distance of intertissue spaces was differentiated and irregular in different schemes according to the images of Nissl staining. We recommend the dewatering method of Scheme 4 (the brain tissues were dehydrated in 10%, 20% and 30% sucrose solution in turn until the tissue samples were completely immersed in the solution and then immersed in the next concentration solution for dehydration).

Emergence delirium (ED) is a common complication in elderly patients in post post‐anesthesia care units (PACU), To our knowledge, there is currently no specific treatment for ED in the elderly, especially for patients combined with vital organs dysfunction. This article described an elderly patient with ED was successfully treated with dexmedetomidine. Although dexmedetomidine has been widely used in recent years, there are few articles on the administration of dexmedetomidine in PACU. The purpose of this paper is to review the literature and analyze related hazardous factors for ED in the elderly with complications of emergency abdominal surgery and angiocardiopathy, and to further confirm and explain the effectiveness and validation of dexmedetomidine as a rescue therapy in PACU. Finally, we look forward to more samples being collected to persuasively prove our opinion in this case.

Microglia are the main immune cells in the brain and the first defense barrier of the nervous system. Microglia play a complex role in the process of stroke. A growing number of studies focus on the mechanism of action of drugs functions and how to regulate microglia. Therefore, we talk about the pathophysiological mechanisms of stroke and elaborate on the microglia signaling pathways of drug action in stroke models and how these drugs play a role in stroke treatment in this review. Understanding how drugs modulate proinflammatory and anti-inflammatory responses of microglia may be critical to implementing therapeutic strategies using immune interventions in stroke.