相关实验视频

Updated: Jun 10, 2026

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
04:41

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 15, 2010

协同神经完整性的PLD1-依赖性调节:对认知性和阿尔茨海默氏症病原性的影响

Sravan Gopalkrishnashetty Sreenivasmurthy, Shaneilahi M Budhwani, Sanjana Mohanty

    bioRxiv : the preprint server for biology
    |March 4, 2026
    PubMed
    概括

    脂酶D1 (PLD1) 失调影响神经退行性疾病. 减弱PLD1改善了阿尔茨海默氏症患者的突触功能和认知能力.

    更多相关视频

    Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology14:57

    Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

    Published on: March 23, 2011

    Evaluation of Synapse Density in Hippocampal Rodent Brain Slices07:44

    Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

    Published on: October 6, 2017

    相关概念视频

    Long-term Potentiation01:35

    Long-term Potentiation

    Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
    Long-term Depression01:05

    Long-term Depression

    Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
    Long-term Potentiation01:25

    Long-term Potentiation

    Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
    Hebbian LTP
    LTP can occur when presynaptic neurons...
    Long-term Depression01:03

    Long-term Depression

    Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
    Calcium Ion Concentration Mechanism
    If over time, all...
    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...