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Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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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...
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...
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Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
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Amyloid Fibrils03:03

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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...

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Related Experiment Video

Updated: Jun 18, 2026

A High-content Assay for Monitoring AMPA Receptor Trafficking
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Published on: January 28, 2019

MAPK, beta-amyloid and synaptic dysfunction: the role of RAGE.

Nicola Origlia1, Ottavio Arancio, Luciano Domenici

  • 1Institute of Neuroscience, CNR-Pisa, 56100 Pisa, Italy. origlia@in.cnr.it

Expert Review of Neurotherapeutics
|November 12, 2009
PubMed
Summary

Alzheimer's disease (AD) involves beta-amyloid peptide (Abeta) accumulation. Inhibiting the receptor for advanced glycation end products (RAGE) may halt neuronal dysfunction and cognitive decline in AD.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Alzheimer's disease (AD) is linked to beta-amyloid peptide (Abeta) accumulation.
  • Oligomeric soluble Abeta contributes to synaptic dysfunction and cognitive impairment in AD.
  • The receptor for advanced glycation end products (RAGE) binds Abeta and affects mitogen-activated protein kinases (MAPKs).

Purpose of the Study:

  • To review evidence for RAGE signaling as a therapeutic target in Alzheimer's disease.
  • To explore the role of RAGE-mediated MAPK alterations in AD pathogenesis.
  • To justify a novel therapeutic strategy focused on RAGE inhibition.

Main Methods:

  • Review of genetic and biological studies on Abeta and AD.
  • Analysis of research on RAGE, Abeta, and MAPK signaling pathways.
  • Synthesis of evidence linking MAPK phosphorylation to neurodegeneration in AD.

Main Results:

  • Abeta accumulation is a key factor in Alzheimer's disease etiology.
  • RAGE acts as a cell surface receptor for Abeta, influencing MAPK phosphorylation.
  • Abeta-induced changes in MAPKs contribute to synaptic dysfunction, cognitive decline, and neuroinflammation in AD.

Conclusions:

  • RAGE signaling plays a critical role in the neurodegenerative processes of AD.
  • Inhibiting RAGE signaling presents a promising therapeutic approach for AD.
  • Targeting RAGE may help arrest or halt the progression of neuronal dysfunction in Alzheimer's disease.