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In a study of older rats, USC researchers reported that two weeks of cinaciguat treatment restored features of aging liver cells and reduced blood amyloid beta by about half. LDL levels also fell to levels seen in younger rats, but the findings have not been tested in people and do not show that the drug prevents Alzheimer’s disease or heart disease.
Researchers at the Keck School of Medicine of USC report that an experimental drug, cinaciguat, restored key features of aging liver cells in older rats and cut blood levels of amyloid beta by about 50% after two weeks. The study also found that LDL cholesterol fell to levels seen in younger animals, but it does not establish that the treatment prevents Alzheimer’s disease or heart disease in people.
The study, published in the Journal of Biological Chemistry, focused on liver sinusoidal endothelial cells, or LSECs. These cells line small blood vessels in the liver and have tiny openings that allow molecules in the blood to reach hepatocytes, neighboring cells that process and remove substances. In aging animals, those openings can become smaller or disappear, potentially making the liver less effective at clearing some compounds.
USC researchers treated older rats for two weeks and compared them with untreated older rats and younger animals. They reported that cinaciguat reopened the microscopic pores in LSECs and improved their function. Amyloid beta concentrations in treated rats fell by roughly half, to levels comparable to those in young rats; untreated older rats did not show a similar change.
The team also measured low-density lipoprotein (LDL), a blood particle associated with fatty deposits in arteries when levels are high. Researchers had included LDL as a comparison measure and did not expect it to respond because LDL particles are small enough to leave the bloodstream without passing through the LSEC openings. Instead, they reported that LDL levels in treated older rats also returned to levels seen in younger animals. The supplied report does not provide the full numerical LDL results or explain the mechanism behind that change.
A Liver Route to Amyloid Beta
The findings point to a possible research approach that targets the liver’s role in clearing substances from blood, rather than trying to act directly on the brain. Amyloid beta is associated with Alzheimer’s disease and can form plaques in the brain, but a fall in blood levels in rats does not show that brain amyloid changed, that memory improved, or that Alzheimer’s risk declined.
The study may matter because the liver is accessible to drug delivery in ways the brain is not. The report notes that the blood-brain barrier restricts what can enter the brain and has complicated efforts to develop some brain-directed treatments. However, whether improving liver function can meaningfully affect human brain disease remains an open research question. The LDL result likewise suggests an additional effect worth investigating, not evidence that cinaciguat reduces cardiovascular events.
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How Aging Changes Liver Filters
LSECs act as a specialized interface between blood and the liver’s hepatocytes. Their pores help larger molecules reach the cells that process them. The researchers’ account is that age-related loss of these openings may impair the liver’s handling of substances including amyloid beta, allowing more to remain in circulation.
The study builds on earlier observations that aging can reduce the liver’s ability to remove amyloid beta. It also draws on epidemiological findings cited by corresponding author Laurie DeLeve, who said age is a major risk factor for Alzheimer’s disease and atherosclerosis, and liver damage is associated with Alzheimer’s risk. Those associations provide context, but they do not prove that liver changes cause either disease or that treating them will prevent it.
The experiment was conducted in rats, not humans. The source describes cinaciguat as experimental and does not report clinical testing for this purpose. The reported changes in cell structure and blood measurements are early findings, not established patient benefits.
“We need to do further translational work to see whether our findings might point to new therapies.”
— Laurie DeLeve, corresponding author and professor at the Keck School of Medicine of USC
Human Benefits Remain Unknown
It is not yet clear whether cinaciguat can produce similar effects in humans, what dose or treatment duration might be suitable, or whether the changes persist after treatment stops. The report does not describe human safety data for this use, long-term outcomes, or effects on cognition, brain amyloid, Alzheimer’s diagnosis, heart disease, or stroke.
The reason LDL fell is also unresolved in the supplied account, particularly because the researchers did not expect the LSEC pores to govern LDL movement. The study’s size, detailed measurements and any potential adverse effects are not specified in the source material. These gaps limit what can be concluded from the reported results.
Testing the Liver Findings in People
The researchers say further translational work is needed to determine whether the findings could lead to therapies. Follow-up research would need to establish how cinaciguat affects liver cells and blood measurements over time, clarify the LDL result, and assess safety before any conclusions about human treatment could be drawn.
No human trial, timetable or planned clinical milestone is identified in the available report. For now, the study supports further investigation of the liver’s role in clearing circulating substances; it does not support using cinaciguat to prevent or treat Alzheimer’s disease or cardiovascular disease.
Key Questions
What did the researchers find?
In older rats, two weeks of cinaciguat treatment restored features of liver sinusoidal endothelial cells and reduced blood amyloid beta by about 50%. The researchers also reported LDL levels comparable to those in younger animals.
Does this show cinaciguat can prevent Alzheimer’s disease?
No. The experiment measured changes in rats and does not show that the drug changes brain amyloid, improves cognition, or prevents Alzheimer’s disease in animals or people.
Has the treatment been tested in people?
The report describes a study in rats and says further translational work is needed. It does not report human trials for this purpose.
Why did the researchers examine liver cells?
The liver filters blood, and the study investigated whether age-related changes in tiny openings in liver cells could interfere with clearing substances such as amyloid beta. The results suggest a possible connection that requires further testing.
Why did LDL levels change?
The researchers did not expect LDL to respond because the particles can leave the bloodstream without passing through the liver-cell openings they studied. The supplied report does not establish why LDL fell, so the mechanism remains unclear.
Source: sciencedaily.com
