Some researchers have found that the outer fabric of the brain that contains the protein beta amyloid misfolded can move and infect the brain. Abnormal protein deposits have been recognized as closely related to the genesis of neuro degenerative disease called Alzheimer’s disease.
The research was supported by the ERA-NET NEURON (Network of European Funding for Neuroscience Research), which has subsidized the project MIPROTRAN involved in this study. ERA-NET NEURON, for its part, has received nearly 3 million under the ERA-NET funding scheme of the Sixth Framework Programme (FP6). The study was recently published in the journal Science.
Alzheimer’s disease is the most common form of dementia that begins at an advanced stage of life, and in which the symptoms gradually worsen. The disease is incurable, and scientists still groping in the dark with regard to its causes. It is usually diagnosed in people over 65 years of age although the less common form of early Alzheimer’s can occur much earlier. There are more than 27 million patients worldwide and it is expected that the disease will affect 1 person in 85 worldwide by 2050.
In this latest study, which aimed to gain a greater understanding of the disease, scientists Hertie Institute for Clinical Brain Research at the University of Tübingen (UT) and the German Centre for Neurodegenerative Diseases (DZNE) injected brain tissue containing amyloid from the abdomen of mice older younger mice.
Several months after injection, the younger mice showed signs of the presence of amyloid in the brain.
Both Alzheimer’s disease a vascular disease of the brain called the cerebral beta-amyloid angiopathy are characterized by the accumulation of a protein fragment known as Abeta. In Alzheimer’s disease, the misfolded Abeta is deposited mainly in so-called amyloid plaques, while nell’angiopatia brain beta-amyloid, the protein Abeta accumulates on the walls of blood vessels, interfering with their function and, in some cases, causing rupture resulting in intra-cerebral hemorrhage.
In 2006, researchers in Tubingen under the guidance of Professor Mathias Jucker, reported that the injection of diluted extracts of tissue of Alzheimer’s disease, Abeta-landen or tissue of the mice in the brains of mice transgenic (genetically modified produce the human form of Abeta) aggregation stimulates the brain in mice.
In this study, the researchers found that the deposition of Abeta can be induced in the brain of transgenic mice by intraperitoneal administration of extracts of mouse brain containing misfolded Abeta. They also found that the time needed to induce the deposition of amyloid in the brain was much longer for treatment than the device directly to the brain. But in both cases, the deposition of amyloid-induced changes also caused several neurodegenerative and neuroinflammatory commonly observed in the brains of people with Alzheimer’s disease and brain beta-amyloid angiopathy.
“The discovery that there are mechanisms that allow the transport of aggregates of Abeta from the periphery to the brain raises the question of whether the aggregation and propagation of the protein, which could be involved in other neurodegenerative brain diseases, can be induced by agents originating in the periphery , “commented Professor Jucker.
He and his colleagues also suggests that the amyloid protein may have similar qualities to prions. Prions are made mainly of protein and can be transmitted to cause brain disorders such as Creutzfeldt-Jakob disease. They claim, however, that “despite this remarkable observation and the apparent mechanistic similarities between Alzheimer’s and prion diseases, there is no evidence that Alzheimer’s disease or amyloid angiopathy are transmitted between mammals and human prion diseases in the same way.”
These findings provide new insights into the pathogenic mechanisms underlying Alzheimer’s disease, they say, adding that further studies could lead to outline new strategies for prevention and treatment.
