A-beta Signaling Pathways
An overview of signaling pathways activated in neurons by soluble A-beta oligomers is shown below.
Get Print CopyPro-Caspase-10
Pro-Caspase-10
AMPA Receptor Antagonists
AMPA Receptor Blockers
AMPA Receptor Compounds
AMPA Receptor Inhibitors
AMPA Receptor Modulators
AMPA Receptor Peptides
GRIN1/NMDAR1
NMDA Receptor Agonists
NMDA Receptor Antagonists
NMDA Receptor Ligand Sets
Glutamate Ligand Sets
Glutamate Receptor Inhibitors
Glutamate Receptor Compounds
NMDA R
NMDA R
AMPA Receptor Antagonists
AMPA Receptor Blockers
AMPA Receptor Compounds
AMPA Receptor Inhibitors
AMPA Receptor Modulators
AMPA Receptor Peptides
GRIN1/NMDAR1
NMDA Receptor Agonists
NMDA Receptor Antagonists
NMDA Receptor Ligand Sets
Glutamate Ligand Sets
Glutamate Receptor Inhibitors
Glutamate Receptor Compounds
Nicotinic (a7) Receptor Agonists
Nicotinic (a7) Receptor Antagonists
Nicotinic (a7) Receptor Modulators
Additional Nicotinic (a7) Receptor Products
Additional Nicotinic Receptor Agonists
Additional Nicotinic Receptor Antagonists
Other Nicotinic Receptor Agonists
Other Nicotinic Receptor Modulators
Nicotinic (a7) Receptor Agonists
Nicotinic (a7) Receptor Antagonists
Nicotinic (a7) Receptor Modulators
Additional Nicotinic (a7) Receptor Products
Additional Nicotinic Receptor Agonists
Additional Nicotinic Receptor Antagonists
Other Nicotinic Receptor Agonists
Other Nicotinic Receptor Modulators
Caspase
Cascade
Activation
Caspase
Cascade
Activation
Caspase
Cascade
Activation
Caspase
Cascade
Activation
Neuronal
Death
Neuronal
Death
Tau Cleavage and
Hyperphosphorylation
Tau Cleavage and
Hyperphosphorylation
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LTD
Induction
LTD
Induction
Dendritic
Spine Loss
Dendritic
Spine Loss
Neuronal
Death
Neuronal
Death
LTP
Induction
LTP
Induction
Microtubule
Disintegration
Microtubule
Disintegration
Tau Aggregation
Tau Aggregation
NFT Formation
NFT Formation
Overview of A-beta Signaling
Alzheimer’s disease (AD) is a complex, neurodegenerative disorder that is characterized by neuroinflammation, neuronal cell death, the accumulation of amyloid plaques and neurofibrillary tangles (NFTs), and cortical and hippocampal atrophy. A key trigger of AD is believed to be the beta-Amyloid protein (A-beta), which is formed by the sequential enzymatic processing of Amyloid Precursor Protein (APP) by beta- and gamma-secretases. A-beta released into the extracellular space can aggregate to form oligomers, protofibrils, fibrils, and senile plaques. Soluble A-beta oligomers have been shown to be toxic to neuronal synapses. However, the molecular mechanisms underlying its cytotoxic effects appear to be very complex. A-beta oligomers interact with several putative receptors at excitatory synapses, stimulating intracellular signaling pathways that culminate in the inhibition of long-term potentiation (LTP), facilitation of long-term depression (LTD), and synapse loss. Additionally, A-beta oligomers can activate caspases, causing neuronal cell death, and induce cleavage and hyperphosphorylation of Tau, leading to the formation of NFTs.
To learn more A-beta, please visit our APP Cleavage and Amyloid-beta Degradation Research Area.
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