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Related Concept Videos

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...
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 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...
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...

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Updated: May 12, 2026

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
07:55

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

Published on: October 17, 2015

NeuroAiD® (MLC601) and amyloid precursor protein processing.

Y A Lim1, L A Murray, M K P Lai

  • 1Memory, Aging and Cognition Centre, National University Health System, National University of Singapore, Singapore.

Cerebrovascular Diseases (Basel, Switzerland)
|April 4, 2013
PubMed
Summary
This summary is machine-generated.

MLC601 modulates amyloid precursor protein (APP) processing by increasing beneficial sAPPα and decreasing full-length APP. This suggests MLC601 may be a therapeutic strategy for Alzheimer's disease and poststroke dementia.

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Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
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Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain
10:08

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain

Published on: August 28, 2012

Related Experiment Videos

Last Updated: May 12, 2026

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
07:55

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

Published on: October 17, 2015

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
09:31

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain
10:08

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain

Published on: August 28, 2012

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Amyloid precursor protein (APP) processing involves α-secretase (non-amyloidogenic) and β-secretase (amyloidogenic) pathways.
  • The amyloidogenic pathway produces amyloid-beta (Aβ), a key component of senile plaques in Alzheimer's disease (AD).
  • Elevated Aβ levels are also observed in stroke patients, suggesting a role in secondary neurotoxicity.

Purpose of the Study:

  • To investigate the effects of MLC601 (NeuroAiD®) on the regulation of APP processing.
  • To determine if MLC601 influences the production of sAPPα and the levels of full-length APP.

Main Methods:

  • Experiments were conducted using the human neuroblastoma cell line SH-SY5Y.
  • Cells were treated with various concentrations of MLC601.
  • Assessed levels of lactate dehydrogenase (LDH), full-length APP, and secreted sAPPα.

Main Results:

  • MLC601 (1-1,000 µg/ml) significantly reduced LDH release, indicating reduced cell death.
  • Higher MLC601 concentrations (5,000-10,000 µg/ml) increased LDH release.
  • MLC601 (100-1,000 µg/ml) significantly increased sAPPα secretion.
  • MLC601 (1,000 µg/ml) significantly decreased full-length APP levels.

Conclusions:

  • MLC601 acts as a modulator of APP processing.
  • MLC601 demonstrates potential as a therapeutic strategy for poststroke dementia and AD.