The discovery of a gene mutation that has immunized a woman in Colombia against early Alzheimer’s, it could set the direction for the research. Which protein leads to the pathological forgetfulness?
Healthy Brain Cells
It is spooky what happens in Belmira, a small village in Colombia: again and again, relatively young people develop already suffering from Alzheimer’s already, with just over 40 years. The cause is a genetic inheritance, the so-called Presenilin 1 Mutation, which makes those Affected especially prone to the early onset of the disease.
A patient under a Thousand
Now a team of researchers has discovered Joseph Arbodela-Velasquez from Harvard Medical School among 1200 surveyed, Colombians, carry this mutation in a particular patient. You had the gene mutation, but showed, unlike all the others – with over 70 no cognitive failures.
The researchers suggest that this is due to another gene mutation. They published their observations in the journal Nature Medicine. The woman, who remained until old age, mentally fit, as it was only a two-fold copy of a gene mutation, which is also under the name of Christchurch-Mutation (Apolipoprotein E 3ch) is known.
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Green tea against Alzheimer’s disease?
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Green tea against Alzheimer’s disease?
A-Beta and Tau – what is cause, what effect?
Apolipoproteins E are proteins, which are involved by different mechanisms in the pathogenesis of Alzheimer’s disease. They play in particular a role in the accumulation of Alzheimer-typical Plaques in the brain tissue.
Of these Plaques, there are Essentially two forms: Amyloid-Beta (A-Beta) and Tau Protein, which occurs in the Form of tiny fibers, called fibrils. For many years, Alzheimer’s researchers speculate whether a treatment of the disease should be primarily directed against A-Beta or the Tau.
Against Alzheimer’s, immune patient from Colombia is now for the researchers especially interesting, because their brain showed significant A-Beta Plaques, but surprisingly few Tau fibrils. At the same time but she had almost no memory loss. Also, the loss of nerve cells was not critical.
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This would indicate that the Alzheimer’s typical amyloid-Beta Plaques are perhaps the reason for the dreaded course of the disease, so aging also with A-Beta in the brain mentally fit. At the same time there is evidence to suggest that A-Beta is the key, the Tau needs to damage to the nerve cells in a sustainable manner.
The suspicion that A-Beta, not the only forgetful, was already come by the time between 1986 and 1990 nuns-studies in the USA. At the time of the epidemiologist David A. Snowdon, the Catholic nuns had examined, which were between 75 and 106 years old, and many of the significant A-Beta Plaques are found, although these women were up to a high age and mentally capable.
And also, the pharmaceutical industry has, after 25 years of intensive research is now a strong doubt as to whether Alzheimer’s combat, when you attack the A-Beta. 2018 ended up two very advanced clinical trials for Alzheimer’s drugs, directed against A-Beta in a harsh disappointment.
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Hope for a drug
There is still a long way to curing Alzheimer’s, and the current state of knowledge is still part of basic research. The Harvard researchers have developed at least a hypothesis that could point the way.
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Alzheimer’s
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Alzheimer’s
You have found out that the rare double mutation of the Colombian patient relates to certain protein receptors on the surface of brain cells. These receptors, in turn, are both for the accumulation of A-Beta, as well as for the inclusion of the Tau through the nerve cells.
Now the researchers hope, an already self-developed antibody applied that binds to the Receptor and so the absorption of harmful Tau could break. It would be a Tau-Blocker for the cell surface, which acts similar to the Colombian-born observed in double gene mutation.
How is the antibody into the brain?
It won’t be easy, however. “You have to be […] aware of the fact that an antibody against APEO [Apolipoprotein E] also blocks its biological function,” says Dr. Christian Haas, Professor of metabolic biochemistry at the Ludwig-Maximilian-University of Munich.
He refers to the fact that the body makes this substance, among other things, to protect the brain. “In addition, APOE is an extremely common Protein in the blood stream, so there is a risk that antibodies are absorbed in the blood, and considerable difficulties will have to get into the brain.”
His colleague Dr. Marc Aurel Busche by the British Institute for dementia research remains nevertheless optimistic: “the Blockade of The […] spread of Tau in the brain [should be] a major goal of therapy,” says Alzheimer’s researcher. Physician tested already Anti-Tau therapies are in clinical trials.
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Villages of forgetfulness in Colombia
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