Published on: April 11, 2013
by Vonda J. Sines for Yahoo News:
California researchers have solved one important mystery regarding how Alzheimer’s disease operates. Their discovery of a link between the illness and an overactive enzyme could eventually lead to a way to prevent the disease.
Scientists at The Scripps Research Institute (TSRI) in California have established a connection between Alzheimer’s and the over-activation of an enzyme dubbed AMPK, according to ScienceDaily. The team, led by Professor Franck Polleux, published its findings in the journal Neuron.
After the California researchers blocked AMPK in mouse models, neurons did not show the loss of synapses typically found in the early phase of Alzheimer’s. Their discovery highlights the potential of developing new therapies to target factors that cause AMPK overactivation in human brains.
The Alzheimer’s Association reports that an estimated 5.2 million Americans have Alzheimer’s disease. Every 68 seconds, another American develops this devastating form of dementia. By 2050, experts expect the frequency to drop to every 33 seconds.
Experts believe both genetics and environmental factors play a role in developing the illness. However, they don’t know the exact cause, according to PubMed Health.
Researchers have long known that small collections of amyloid beta, a protein, can cause early-stage patients to start to lose synapses, which are neuron-to-neuron points of connection. What they haven’t been able to figure out is specifically how the process unfolds.
After multiple research groups found hints that AMPK might be important to Alzheimer’s, Polleux decided to investigate whether an interaction involving amyloid beta and a modification of a protein known as tau with AMPK could cause brain damage in Alzheimer’s patients. One of the California scientists discovered that a calcium influx into neurons jump-starts an enzyme known as CAMKK2, believed to be the main AMPK instigator in neurons.
Further studies using genetically engineered mice that produce too much mutant amyloid beta resulted in a condition resembling Alzheimer’s. After various experiments involving CAMKK2 and AMPK, the eventual California findings suggested that amyloid beta is a contributor to developing Alzheimer’s, by way of AMPK and primarily by enabling tau toxicity.
The researchers are currently conducting more experiments to find any other toxic process that’s related to AMPK overactivation and that might have a role in the progression of Alzheimer’s.
My late father-in-law developed signs of Alzheimer’s at around the same age my husband is now. My husband has short-term memory issues supposedly related to another health condition. However, every time he mixes up the syntax of a sentence or can’t think of the name of a person or of a familiar object, we each wonder the same thing: Could it be Alzheimer’s? Our hope is that the link between Alzheimer’s and an overactive enzyme will lead to even earlier diagnoses, if not a means of prevention.
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Two blood markers, phosphorylated tau 217 (p-tau217) and phosphorylated tau 181 (p-tau181), showed strong diagnostic performances for Alzheimer’s disease and discriminated Alzheimer’s from frontotemporal lobar denervation (FTLD) syndromes and normal cognition, a retrospective study...
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