An Update on Dkk1 as a Therapeutic Target in Alzheimer's Disease
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25

Sep

2018

25

Sep

2018

An Update on Dkk1 as a Therapeutic Target in Alzheimer’s Disease

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Six years ago, researchers reported that dkk1 appears to be involved in the destruction of synapses in Alzheimer’s disease. More recent work expands the understanding of dkk1 in this context, placing it in a positive feedback loop related to amyloid-β, in which synaptic damage drives more synaptic damage. The researchers provide evidence to suggest that dkk1 protein can be a therapeutic target for treatments that slow the progression of Alzheimer’s disease. Fortunately, there is an existing approved drug that might be used to produce a proof of concept in human patients, so it seems likely that we will be hearing more from this line of research in the years ahead.

Overproduction of the protein beta-amyloid is strongly linked to development of Alzheimer’s disease but many drugs targeting beta-amyloid have failed in clinical trials. Beta-amyloid attacks and destroys synapses – the connections between nerve cells in the brain – resulting in memory problems, dementia, and ultimately death. In a new study researchers found that when beta-amyloid destroys a synapse, the nerve cells make more beta-amyloid driving yet more synapses to be destroyed.

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Article originally posted at
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