A-beta Signaling Pathways

An overview of signaling pathways activated in neurons by soluble A-beta oligomers is shown below.

Interactive Pathways

Presynaptic Neuron
Presynaptic Neuron
beta-CTF
beta-CTF
AICD
AICD
gamma-Secretase
gamma-Secretase
A-beta
A-beta
sAPP beta
sAPP beta
beta-CTF
beta-CTF
BACE
BACE
APP
APP
A-beta Monomers
A-beta Monomers
A-beta Oligomers
A-beta Oligomers
Trans-Golgi Network
Trans-Golgi Network
alpha-Secretase
alpha-Secretase
APP
APP
p3
p3
gamma-Secretase
gamma-Secretase
AICD
AICD
alpha-CTF
alpha-CTF
alpha-CTF
alpha-CTF
sAPP alpha
sAPP alpha
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RAGE
RAGE
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p75NTR
p75NTR
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TRAF-6
TRAF-6
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NRIF
NRIF
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NRAGE
NRAGE
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TRAF-6
TRAF-6
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p62
p62
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TNF RI
TNF RI
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TRADD
TRADD
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FADD
FADD
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Pro-Caspase-8
Pro-Caspase-10
Pro-Caspase-8
Pro-Caspase-10
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RIP1
RIP1
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TRADD
TRADD
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TRAF-2
TRAF-2
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mGluR5
mGluR5
PrPc
PrPc
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Fyn
Fyn
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Gq/1
Gq/1
NR1/NR2B
NR1/NR2B
AMPA R
NMDA R
AMPA R
NMDA R
alpha 7 nAChR
alpha 7 nAChR
NR1/NR2A
NR1/NR2A
p38
p38
JNK
JNK
NFkappaB
NFkappaB
c-Jun
c-Jun

Caspase
Cascade
Activation

Caspase
Cascade
Activation

NFkappaB
NFkappaB

Caspase
Cascade
Activation

Caspase
Cascade
Activation

Neuronal
Death

Neuronal
Death

Postsynaptic Neuron
Postsynaptic Neuron
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ASK1
ASK1
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JNK
JNK

Tau Cleavage and
Hyperphosphorylation

Tau Cleavage and
Hyperphosphorylation

Microtubules
Microtubules
PLC
PLC
Ca2+
Ca2+
Calpain
Calpain
Cytochrome c
Cytochrome c
Caspase 3
Caspase 3
Akt
Akt
GSK-3 beta
GSK-3 beta
Calcineurin
Calcineurin
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STEP
STEP
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LTD
Induction

LTD
Induction

Dendritic
Spine Loss

Dendritic
Spine Loss

Neuronal
Death

Neuronal
Death

[Ca2+]
[Ca2+]
[Ca2+]
[Ca2+]
CaM Kinase II
CaM Kinase II
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CREB
CREB
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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.

A-beta Signaling Pathways background image 1