Alzheimer’s Protein can Travel from Blood to Build up in the Brain

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Summary:
           Recent results suggest that the protein amyloid-beta may affect Alzheimer’s disease by moving from the blood to the brain and accumulating there. It’s normally found in small quantities. It was wondered whether quantities of A-beta from the blood could be high enough to form plaques in the brain.

 Scientists conducted an experiment on mice where they had mutated a portion of the brain to produce an increase of A-beta proteins. Results after the experiment showed inflammation, tiny areas of bleeding and a dangerous type of the protein tau in the brains of mice that had been exposed to blood with A-beta inserted. Alzheimer’s symptoms became present. In a healthy brain, there is a balance between A-beta inside and outside. When this is disrupted, however, the brain may get an influx of the protein inside, resulting in plaquing. Testing this theory, drugs or therapies that reduce A-beta in the body might help slow or prevent Alzheimer’s.
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In our physiological psychology course, we’ve discussed the importance of healthy functioning neuronal connections. Alzheimer’s disease, many neurons stop functioning, lose connections with other neurons, and die. Typically, the disease initially destroys neurons and their connections in parts of the brain involved in memory such as the hippocampus. It later affects areas in the cerebral cortex responsible for language, reasoning, and social behavior. As we discussed in class, the prefrontal cortex is responsible for managing memory while it is being used. If the hippocampus is affected by a disease such as this, connections may not be made between the two as a result of a lack of functioning neurons, resulting in widespread brain damage and shrinking. Preventing build-up of A beta should decrease plaquing of the A-beta protein, which may prevent or a least slow the blocking of neuronal connections in the brain, therefore maintaining functioning longer.
Link
https://www.fxncc.com/alzheimers-protein-can-travel-from-blood-to-build-up-in-the-brain/185601/

Comments

  1. Roya NajafaliNovember 14, 2017 at 3:04 PM

    Alzheimer's disease (AD) is a very interesting topic and there is a lot to study on the topic. Tying in cognitive psychology, AD is a degeneration of acetylcholinergic neurons that are found in the hippocampus and senile plaques & neurofibrillary tangles are found in brains of people with AD. Since there are no treatments there are ways to slow down the process, which include drugs that prevent the breakdown of acetylcholine (ex: Cognex), drugs that control excess levels of glutemate (ex: Namenda), vitamin E supplements (for anti-oxidants), and non-steroidal anti-inflammatories (ex: Aleve). This article does have a good argument how A-beta can slow the process. AD promotes a lot of opportunity for research study, but since it isn't able to be fully diagnosed until a brain autopsy is done post death it can be hard to determine 100% that the person does in fact have AD.

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  2. Cory LinkNovember 16, 2017 at 10:31 AM

    It will be interesting to see if since they can produce an overproduction of A-beta that a way to lower production can later be found if it hasn't yet. Many factors go into the development of AD so being able to block or lower A-beta may not sure the disease. But certainly for individuals who suffer from AD due to this overproduction can find this nearly life saving. Perhaps a GABA variant could have the capacity to block this production and minimize or dematerialize plaque production within the brain cells.

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  3. UnknownNovember 16, 2017 at 9:44 PM

    Alzheimer's was a huge topic in a Psychology of aging class I've taken and we actually looked at other studies coming to the same conclusion talking about A-beta increases leading to plaque buildup and being one of the likely many causes of the disease!

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  4. Morgan SagerNovember 16, 2017 at 10:31 PM

    With Alzheimer's disease being in the top 6 causes of death in the U.S; it is very important to study the brain closer to find out why neural connections are being lost and if there is a way to prevent it. This disease contains the same plaques and tangles that Down syndrome has. Some known genes found in Alzheimer's are APP, Presenilin 1 and 2, and APOE e4. I wrote my blog post on the APOE e4 variant which affects the 19th chromosome in our DNA. The APP gene changes is associated with lead exposure. Research to prove this was conducted on monkeys that created elevated plaques and tangles in their brains.

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