相关实验视频

Updated: Jun 22, 2026

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation
09:16

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Published on: June 26, 2018

7.6K

酸会损害人类和老鼠大脑中的α-synuclein播种活动

Saumya Digraskar, George Dobbins, Piyali Das

    bioRxiv : the preprint server for biology
    |August 12, 2025
    PubMed
    概括

    甲酸处理有效地降低了固定大脑样本中对α-syn聚合物的职业暴露风险. 这种方法使病理性α-syn的播种活动失活,而不会影响其本病理学.

    更多相关视频

    Generation of Alpha-Synuclein Preformed Fibrils from Monomers and Use In Vivo09:44

    Generation of Alpha-Synuclein Preformed Fibrils from Monomers and Use In Vivo

    Published on: June 2, 2019

    21.7K
    Technique for Intranasal Administration of α-Synuclein Aggregates04:49

    Technique for Intranasal Administration of α-Synuclein Aggregates

    Published on: November 8, 2024

    574

    相关概念视频

    Neural Regulation01:37

    Neural Regulation

    Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
    Amyloid Fibrils03:03

    Amyloid Fibrils

    Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
    Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
    Alzheimer Disease l: Introduction01:29

    Alzheimer Disease l: Introduction

    Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
    Alzheimer Disease ll: Pathophysiology01:23

    Alzheimer Disease ll: Pathophysiology

    Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
    Parkinson Disease ll: Pathophysiology01:24

    Parkinson Disease ll: Pathophysiology

    Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...