According to a new study in mice, a probable cause of Alzheimer’s disease is the leakage from blood into the brain of fat-carrying particles transporting toxic proteins.
“We identified the probable ‘blood-to-brain pathway’ that can lead to Alzheimer’s disease, the most prevalent form of dementia globally,” said study’s senior author Professor John Mamo, director of the Curtin Health Innovation Research Institute at Curtin University.
“While we previously knew that the hallmark feature of people living with Alzheimer’s disease was the progressive accumulation of toxic protein deposits within the brain called beta-amyloid, we did not know where the amyloid originated from, or why it deposited in the brain.”
“Our research shows that these toxic protein deposits that form in the brains of people living with Alzheimer’s disease most likely leak into the brain from fat carrying particles in blood, called lipoproteins.”
“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.”
Building on previous research that showed beta-amyloid is made outside the brain with lipoproteins, Professor Mamo and his colleagues tested the blood-to-brain pathway by genetically engineering mouse models to produce human amyloid-only liver that make lipoproteins.
“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,” Professor Mamo said.
“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 and some drugs that could specifically target lipoprotein amyloid, therefore reducing their risk or slowing the progression of Alzheimer’s disease.”
The study was published online in the journal PLoS Biology.
V. Lam et al. 2021. Synthesis of human amyloid restricted to liver results in an Alzheimer disease-like neurodegenerative phenotype. PLoS Biol 19 (9): e3001358; doi: 10.1371/journal.pbio.3001358
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