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1.
Neural Regen Res ; 20(3): 740-750, 2025 Mar 01.
Article in English | MEDLINE | ID: mdl-38886939

ABSTRACT

Lipid droplets serve as primary storage organelles for neutral lipids in neurons, glial cells, and other cells in the nervous system. Lipid droplet formation begins with the synthesis of neutral lipids in the endoplasmic reticulum. Previously, lipid droplets were recognized for their role in maintaining lipid metabolism and energy homeostasis; however, recent research has shown that lipid droplets are highly adaptive organelles with diverse functions in the nervous system. In addition to their role in regulating cell metabolism, lipid droplets play a protective role in various cellular stress responses. Furthermore, lipid droplets exhibit specific functions in neurons and glial cells. Dysregulation of lipid droplet formation leads to cellular dysfunction, metabolic abnormalities, and nervous system diseases. This review aims to provide an overview of the role of lipid droplets in the nervous system, covering topics such as biogenesis, cellular specificity, and functions. Additionally, it will explore the association between lipid droplets and neurodegenerative disorders. Understanding the involvement of lipid droplets in cell metabolic homeostasis related to the nervous system is crucial to determine the underlying causes and in exploring potential therapeutic approaches for these diseases.

2.
Int J Mol Sci ; 25(1)2023 Dec 21.
Article in English | MEDLINE | ID: mdl-38203282

ABSTRACT

Synaptic plasticity enhances or reduces connections between neurons, affecting learning and memory. Postsynaptic AMPARs mediate greater than 90% of the rapid excitatory synaptic transmission in glutamatergic neurons. The number and subunit composition of AMPARs are fundamental to synaptic plasticity and the formation of entire neural networks. Accordingly, the insertion and functionalization of AMPARs at the postsynaptic membrane have become a core issue related to neural circuit formation and information processing in the central nervous system. In this review, we summarize current knowledge regarding the related mechanisms of AMPAR expression and trafficking. The proteins related to AMPAR trafficking are discussed in detail, including vesicle-related proteins, cytoskeletal proteins, synaptic proteins, and protein kinases. Furthermore, significant emphasis was placed on the pivotal role of the actin cytoskeleton, which spans throughout the entire transport process in AMPAR transport, indicating that the actin cytoskeleton may serve as a fundamental basis for AMPAR trafficking. Additionally, we summarize the proteases involved in AMPAR post-translational modifications. Moreover, we provide an overview of AMPAR transport and localization to the postsynaptic membrane. Understanding the assembly, trafficking, and dynamic synaptic expression mechanisms of AMPAR may provide valuable insights into the cognitive decline associated with neurodegenerative diseases.


Subject(s)
Central Nervous System Depressants , Receptors, AMPA , Central Nervous System , Neurons , Cognition , Learning
3.
Int J Mol Sci ; 23(5)2022 Feb 25.
Article in English | MEDLINE | ID: mdl-35269692

ABSTRACT

Due to aging of the world's population, stroke has become increasingly prevalent, leading to a rise in socioeconomic burden. In the recent past, stroke research and treatment have become key scientific issues that need urgent solutions, with a sharp focus on stem cell transplantation, which is known to treat neurodegenerative diseases related to traumatic brain injuries, such as stroke. Indeed, stem cell therapy has brought hope to many stroke patients, both in animal and clinical trials. Mesenchymal stem cells (MSCs) are most commonly utilized in biological medical research, due to their pluripotency and universality. MSCs are often obtained from adipose tissue and bone marrow, and transplanted via intravenous injection. Therefore, this review will discuss the therapeutic mechanisms of MSCs and extracellular vehicles (EVs) secreted by MSCs for stroke, such as in attenuating inflammation through immunomodulation, releasing trophic factors to promote therapeutic effects, inducing angiogenesis, promoting neurogenesis, reducing the infarct volume, and replacing damaged cells.


Subject(s)
Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells , Neurodegenerative Diseases , Stroke , Animals , Humans , Neurodegenerative Diseases/therapy , Neurogenesis , Stroke/therapy
4.
Biomark Res ; 10(1): 4, 2022 Jan 15.
Article in English | MEDLINE | ID: mdl-35033201

ABSTRACT

The negatively charged aminophospholipid, phosphatidylserine (PtdSer), is located in the inner leaflet of the plasma membrane in normal cells, and may be exposed to the outer leaflet under some immune and blood coagulation processes. Meanwhile, Ptdser exposed to apoptotic cells can be recognized and eliminated by various immune cells, whereas on the surface of activated platelets Ptdser interacts with coagulation factors prompting enhanced production of thrombin which significantly facilitates blood coagulation. In the case where PtdSer fails in exposure or mistakenly occurs, there are occurrences of certain immunological and haematological diseases, such as the Scott syndrome and Systemic lupus erythematosus. Besides, viruses (e.g., Human Immunodeficiency Virus (HIV), Ebola virus (EBOV)) can invade host cells through binding the exposed PtdSer. Most recently, the Corona Virus Disease 2019 (COVID-19) has been similarly linked to PtdSer or its receptors. Therefore, it is essential to comprehensively understand PtdSer and its functional characteristics. Therefore, this review summarizes Ptdser, its eversion mechanism; interaction mechanism, particularly with its immune receptors and coagulation factors; recognition sites; and its function in immune and blood processes. This review illustrates the potential aspects for the underlying pathogenic mechanism of PtdSer-related diseases, and the discovery of new therapeutic strategies as well.

5.
Front Aging Neurosci ; 12: 227, 2020.
Article in English | MEDLINE | ID: mdl-32848706

ABSTRACT

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by senile plaques (SPs), which are caused by amyloid beta (Aß) deposition and neurofibrillary tangles (NFTs) of abnormal hyperphosphorylated tau protein. The receptor for advanced glycation end products (RAGE) binds to advanced glycation end products deposited during vascular dysfunction. Alzheimer's disease may occur when RAGE binds to Aß and releases reactive oxygen species, further exacerbating Aß deposition and eventually leading to SPs and NFTs. As it is involved in early AD, RAGE may be considered as a more potent biomarker than Aß. Positron emission tomography provides valuable information regarding the underlying pathological processes of AD many years before the appearance of clinical symptoms. Thus, to further reveal the role of RAGE in AD pathology and for early diagnosis of AD, a tracer that targets RAGE is needed. In this review, we first describe the early diagnosis of AD and then summarize the interaction between RAGE and Aß and Tau that is required to induce AD pathology, and finally focus on RAGE-targeting probes, highlighting the potential of RAGE to be used as an effective target. The development of RAGE probes is expected to aid in AD diagnosis and treatment.

6.
Ultrason Sonochem ; 55: 135-148, 2019 Jul.
Article in English | MEDLINE | ID: mdl-30853534

ABSTRACT

In this paper, a coconut milk composite system (glycerin monostearate as an emulsifier) with different maize additives (e.g., maize kernels and starch with different amylose contents) was treated with high-intensity ultrasound irradiation (HIUS, frequency 20 kHz). The stability and structural features of the added coconut milk emulsion were studied. Comparing the mechanical emulsifications, coconut milk with maize kernels was similar to coconut milk with high-amylose maize starch. However, coconut milk with a high proportion of amylopectin had the best stability. After ultrasonic treatment, the particle sizes were found to be smaller than those in the nonultrasound-treated coconut milk, and the particles demonstrated a monomodal size distribution. The electronegativity of the compound system was significantly improved. The electronegativity of the maize kernel and high-amylose maize starch-coconut milk systems was significantly decreased, and this change was beneficial to the stability of the systems. However, ultrasonic treatment did not change the fluid type of the coconut milk compound system (which showed pseudoplastic fluid characteristics). The proportion of amylose in maize had an important influence on the stability of the compound system. The apparent viscosity and crystallization order of the high-amylose maize starch-coconut milk system were high. However, the waxy maize starch system showed high complex viscosity and tended to be liquid with ultrasonic treatment. Ultrasound treatment reduced the particle size of coconut milk and homogenized the distribution of the system. Additionally, the amylase of the system contained amylose encapsulated in the interfacial layer after ultrasound treatment. The tiny gel beads formed by waxy maize starch had a good fusion effect on coconut milk fat/protein droplets. The results indicated that the stability of coconut-grain milk composite systems can be enhanced with the use of maize additives and ultrasound irradiation through space effects, electrostatic effects and continuous phase viscosity.


Subject(s)
Amylose/chemistry , Cocos/chemistry , Sonication , Zea mays/chemistry , Color , Particle Size , Rheology , Surface Tension , Viscosity
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