Landmark study presents evidence Alzheimer’s disease begins in the liver
An impressive new study is presenting robust evidence showing the toxic proteins thought to be the cause of Alzheimer’s disease may be produced in the liver and travel through the blood before landing in the brain causing neuron damage.
For several decades it has been generally accepted that Alzheimer’s disease is caused by the accumulation of amyloid proteins in the brain. These proteins form toxic aggregations known as plaques and it is these plaques that damage the brain.
The big challenge in investigating this liver-amyloid hypothesis is that amyloid is also produced in the brain. Most mouse models used in Alzheimer’s research involve engineering the animals to overexpress amyloid production in the central nervous system, which only really resembles the minority of humans suffering from hereditary early-onset Alzheimer’s. The vast majority of people developing the disease instead experience what is known as sporadic Alzheimer’s, where the disease develops in older age, with no familial or genetic history.
The breakthrough in this new research is the development of a new animal model of Alzheimer’s disease. Here, the researchers engineered a mouse to produce human amyloid proteins solely in the liver, and this allowed for novel observations into how these proteins can enter the bloodstream and travel to the brain.
John Mamo, lead researcher on the project from Curtin University in Australia, says this new study offers clear evidence of a “blood-to-brain pathway.” Using the newly developed mouse model the study shows how amyloid produced in the liver can move to the brain and cause damage leading to pathological signs similar to those seen with Alzheimer’s disease.
“As we predicted, the study found that mouse models producing lipoprotein-amyloid in the liver suffered inflammation in the brain, accelerated brain cell death and memory loss,” says Mamo. “This ‘blood-to-brain pathway’ is significant because if we can manage the levels in blood of lipoprotein-amyloid and prevent their leakage into the brain, this opens up potential new treatments to prevent Alzheimer’s disease and slow memory loss.”
If this liver-amyloid hypothesis is further validated in future studies a number of other outcomes could arise. Alzheimer’s disease risk may be estimated at a young age by evaluating an individual’s propensity for synthesizing amyloid in the liver. Plus,dietary interventions could hypotheticallybe deployed to improve liver health and decrease a person’s risk of developing Alzheimer’s.
“While further studies are now needed, this finding shows the abundance of these toxic protein deposits in the blood could potentially be addressed through a person’s diet.