A-beta Pathways: Uptake & Degradation

Click on one of the boxes below to see how these cells affect A-beta uptake and degradation.

MARCO
MARCO
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MEGF10
MEGF10
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SR-B1
SR-B1
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LRP-1
LRP-1
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LRP-2
LRP-2
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ApoE
ApoE
LDL R
LDL R
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AQP4
AQP4
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ACE
ACE
InsulysinIDE
InsulysinIDE
MMP-2
MMP-2
MMP-9
MMP-9
Neprilysin
Neprilysin
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ECE
ECE
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A-beta
A-beta

A-beta uptake
& degradation

A-beta uptake
& degradation

Astrocyte
Astrocyte
A-beta Plaque
A-beta Plaque
A-beta Oligomers
A-beta Oligomers
A-beta Monomer
A-beta Monomer
MARCO
MARCO
FPRL1
FPRL1
CD47
CD47
CD45
CD45
CD36/SR-B3
CD36/SR-B3
RAGE
RAGE
SR-AI/MSR
SR-AI/MSR
TLR4
TLR4
MD-2
MD-2
CD14
CD14
ApoE
ApoE
LDL R
LDL R
Integrin alpha
M/CD11b
Integrin alpha
M/CD11b
Complement
Component C3
Complement
Component C3
CD40/TNFRSF5
CD40/TNFRSF5
CD40 Ligand/TNFSF5
CD40 Ligand/TNFSF5
P2Y(2)R
P2Y(2)R

A-beta uptake
& degradation

A-beta uptake
& degradation

ACE
ACE
Insulysin/IDE
Insulysin/IDE
MMP-2
MMP-2
MMP-9
MMP-9
NEP
NEP
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ECE
ECE
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A-beta
A-beta
Microglia
Microglia
alpha 2-Macroglobulin
alpha 2-Macroglobulin
APP
APP
CD36/SR-B3
CD36/SR-B3
TLR4
TLR4
MD-2
MD-2
CD-14
CD-14
CD45
CD45
CD40/TNFRSF5
CD40/TNFRSF5
CD40 Ligand/TNFSF5
CD40 Ligand/TNFSF5
CX3CL1/Fractalkine
CX3CL1/Fractalkine
CX3CR1
CX3CR1
CCL2/JE/MCP-1
CCL2/JE/MCP-1
CCR2
CCR2

A-beta uptake
& degradation

A-beta uptake
& degradation

Macrophage
Macrophage
Insulysin/IDE
Insulysin/IDE
MMP-9
MMP-9
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ECE
ECE
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A-beta
A-beta

Overview of A-beta Uptake & Degradation

Amyloid-beta protein (A-beta) is the proposed causative agent of Alzheimer's disease (AD). One of the neuropathological hallmarks of AD is the accumulation of senile plaques in the brain. Senile plaques represent extracellular deposits of aggregated A-beta. Prior to its deposition as senile plaques, A-beta oligomerizes to exert pathological actions on neuron function and viability. AD therapies that are in the advanced stages of development mostly target A-beta production, aggregation, or clearance. Although most clinical trials focus on the treatment of symptomatic patients, it has been suggested that earlier intervention or disease prevention would be a more effective strategy. Research studies have investigated receptors that are involved in the uptake of A-beta (i.e. APP, CD36, FPRL, LDL R, LRP1, alpha-2-Macroglobulin, MARCO, SR-A1, and RAGE) and enzymes that are known to degrade A-beta (i.e. ACE, Cystatin C, ECE, Insulysin/IDE, MMPs, and Neprilysin). In fact, a recent report suggested that a combinatorial therapy designed to block A-beta production and enhance A-beta clearance might represent the most effective approach.

To learn more, please visit our APP Cleavage and Amyloid-beta Degradation Research Area.