Medical

New study links Alzheimer's disease with liver function and diet

New research suggests obesity that affects the liver could play a part in the long-term onset of Alzheimer's and dementia
New research suggests obesity that affects the liver could play a part in the long-term onset of Alzheimer's and dementia
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New research suggests obesity that affects the liver could play a part in the long-term onset of Alzheimer's and dementia
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New research suggests obesity that affects the liver could play a part in the long-term onset of Alzheimer's and dementia

Scientists have presented new research pointing to the liver as a potential culprit in the onset of Alzheimer's disease. Presented at the Alzheimer's Association International Conference, the research suggests that a compound produced in the liver can confer neurocognitive protections, and when the liver cannot effectively produce those compounds then cognitive deficits can result in the brain.

Molecules called plasmalogens were the primary focus of the new research. These are a class of lipids generated in the liver, and certain types have been found to be critical for effective synaptic function in the brain. The study set out to measure whether reduced levels of several specific types of plasmalogens corresponded with an increased risk of Alzheimer's or mild cognitive decline.

Over 1,500 human subjects were examined, split into three categories: those clinically diagnosed with Alzheimer's disease, those with clinically diagnosed mild cognitive impairment, or those healthy and cognitively normal. The results showed statistically significant differences in plasmalogen levels between all three groups with lower levels associated with higher rates of Alzheimer's or cognitive decline.

"This research shows that an age-related deficiency of plasmalogens could lead to an increased risk of Alzheimer's disease, because the liver cannot make enough of them," says Mitchel Kling, one of the researchers on the project.

The study isn't the first to implicate the liver as playing a role in the onset of Alzheimer's disease. A compelling study from 2011 found that one of the primary genes suspected in production of the pathogenic amyloid beta protein is mostly expressed in the liver. This study hypothesized that the proteins that are thought to be responsible for many cognitive deficits seen in Alzheimer's actually originate in the liver and then travel to the brain via the bloodstream.

Another study, similarly focused on the liver, found that an enzyme the organ produces generates fundamental neuroprotective effects, and when a person's liver isn't effectively producing it brain metabolism can suffer. This particular study was also examining a liver-generated lipid, much like the recent work.

Perhaps the most interesting implication suggested by this growing body of research is that dietary effects on the liver may play a role in the subsequent development of Alzheimer's and cognitive impairment. A recent study does back up this possible hypothesis, finding an association between non-alcoholic fatty liver disease and increased risk of Alzheimer's.

"[The new research] highlights a potential relationship between conditions such as obesity and diabetes and Alzheimer's – as the liver has to work harder to break down fatty acids over time," explains Kling. "This could lead to the eventual destruction of the peroxisomes that create plasmalogens which thus, increases the risk of Alzheimer's."

It is still early days for much of this research but it offers intriguing pathways suggesting scientists could do well by looking outside of the brain when trying to find new ways to approach and treat Alzheimer's disease.

"Moving forward, we're examining the connections between plasmalogens, other lipids, and cognition, in addition to gene expression in the liver and the brain," says Kling. "While we're in the early stages of discovering how the liver, lipids, and diet are related to Alzheimer's disease and neurodegeneration, it's been promising."

The results of this new study was presented at the recent Alzheimer's Association International Conference (AAIC) 2018 in Chicago.

Source: Penn Medicine News

6 comments
william02
Does anybody know yet if taking statins could lower plasmalogens, along with other lipids, and therefor not help with preventing Alzheimers?
dmeisner@gmail.com
It would be great to learn more about *what* dietary changes can affect this. The link to the research abstract was a bit hard to understand (except that alcohol does not seem to be a factor).
Observer101
It mentions "non-alcoholic fatty liver".... I wonder what it says about the use of alcohol? Some studies say a mild use of alcohol is good for the heart, so I must wonder if the same would be good for the liver?
b@man
Whatever they come up will be reversed in a few years, so there is no sense in taking any of it to heart... especially since doctors are the 3rd leading cause of death, right behind heart disease and cancer.
LynnWood
Non Alcoholic fatty liver disease tracks alongside the the increase of sugar consumption, corresponding to the amount of sugar ingested because of sugar being added to almost every processed food. The liver fat deposits can be reduced by eliminating sugar from the diet, meaning, a diet of fresh and natural food with no added sugar, no processed foods. Thus the implications of this research are anathema to our processed food and pharmaceutical industries. So, expect this line of enquiry to be labelled crackpot and ended.
nehopsa
@LynnWood: exactly. That is how the system operates. At some later point there will be crack down on comments like here and YT also - possibly for "spreading alarmist news" that are "unsupported by science"...or just transgressing a "copyright". Mind you, you are a disturber of peace! In the meantime, the best you can do for your preventable Alzheimer is eliminate all sugars, eliminate all starchy food, all processed food, eat raw and rich. ..and watch some relevant YT while they are still available. Alzheimer is so tightly linked to metabolic insulin resistance syndrome it can be considered "diabetes type III".