Team:Linkoping Sweden/AlzheimersDisease
Most people have heard of Alzheimer’s disease and could probably name some symptom, like memory loss or confusion. Then again some people would also just clump together those symptoms with getting older, as if it is a normal part of aging. And since there are an increasing number of older people today than ever before, due to the average lifespan is getting longer and longer thanks to improving life conditions, more people should experience the side effects of growing older. But cognitive brain disease is not a normal part of aging. It is not a side effect, it is a disease that we should be able to prevent people from getting.
In 2015 around 46.8 million people on Earth was living with Alzheimer’s disease and a new brain is affected by the disease every 3.2 seconds.[1] By 2050 it is estimated that around 106.8 million people will be affected by the disease which is excluding the people who are secondary effected by the disease through a loved one who is sick. [2] Alzheimer’s is a kind of dementia where the patient suffers from memory lost, problem with thinking and strange behavior which means that the patient's needs constant care, and patience. The disease’s course takes time, once a person has been diagnosed with Alzheimer’s they are expected to have an average lifespan of 4-8 years. [3]
It can take time before the symptoms can get noticeable but it will almost always get worse over time. The use of the word almost here is due to the fact that people get affected by the disease in different ways and it is often hard to generalize when everything about the disease is so personal. But one thing we can generalize is that there are typically three stages: early stage, middle stage and late-stage, or mild, moderate and severe stages. [4] The hard part is to determine in which stage a patient is in at the time of diagnosis.
The majority of patients gets the disease when they are 65 years or older. But there are exceptions, types of early onset Alzheimer’s where people are in their 40s or 50s. This kind of Alzherimer’s is often much harder to diagnose since it is easily mistaken for stress. [5]
Now let’s look a little closer at the disease, more exactly where it is formed and why. In our brains we have cells called neurons which is basically the essence of our brain. They connect to each other by sending signals between them. In and around these cells we have proteins that help with signaling and just basic cell functioning. Two of those proteins are Amyloid Beta and Tau. In a healthy individual the body gets rid of these precursor proteins by breaking them down. In Alzheimer's disease these protein fragments accumulates into insoluble clots, called plaques. They form around the neurons and prevent them from communicating with each other with prevent signals to getting through until the neuron stops trying and shrivels. [6] Tau on the other hand is in the neuron and part of the stabilization along the part that sends the signals. In Alzheimer’s disease Tau gets loose from the structure and form tangles in the cell. Since the Tau stabilized the structure it begins to fall apart when Tau is gone so the cells ultimately dies. [6]
The exact reason why these proteins start to aggregate is still unknown and apart of the unsolved riddles about this disease.
Another question is the genetic part of the disease. Less than 2 % of Alzheimer cases can be associated with a dominant inherent gene. In half of these cases, where the disease developed earlier than at 60 years old, a mutation in the gene has been found. A total of 200 mutations in three different genes, which all lead to Alzheimer’s, has been discovered. The known gene mutations are all so called autosomalt dominant which means that if one of the parents have the disease caused by the dominant gene there is a 50% chance that the child will also develop it. [7]
Sources
(1) Alzheimer Sverige. Fakta om sjukdomarna [Internet]. Lund: Alzheimer Sverige; 2017. [cited 16 Aug 2017]. Available from: http://www.alzheimersverige.se/fakta-om-sjukdomarna/ (2) Brookmeyer R, Johnson E, Ziegler-Graham K, Arrighi H. Forecasting the global burden of Alzheimer’s disease [Internet]. Baltimore: Department of Biostatistics; 2007. [cited 31 Aug 2017] Available from: http://alzheimerstoday.elsevier.com/Content/PDF/Forecasting_the_global_burden_of_Alzheimers_disease.pdf (3) Alzheimer’s association. What Is Alzheimer’s? [Internet]. Chicago: Alzheimer’s association; 2017. [cited 31 Aug 2017]. Available from:https://www.alz.org/alzheimers_disease_what_is_alzheimers.asp (4) Alzheimer’s association. Stages of Alzheimer’s [Internet]. Chicago: Alzheimer’s association; 2017. [cited 31 Aug 2017]. Available from: https://www.alz.org/alzheimers_disease_stages_of_alzheimers.asp#stage3 (5) Alzheimer’s association. Younger/Early Onset Alzheimer’s & Dementia [Internet] Chicago: Alzheimer’s association; 2017. [cited 31 Aug 2017]. Available from: https://www.alz.org/alzheimers_disease_early_onset.asp (6) BrightFocus Foundation. Amyloid Plaques and Neurofibrillary Tangles [Internet]. Clarksburg: BrightFocus Foundation; 2017. [cited 31 Aug 2017]. Available from: https://www.brightfocus.org/alzheimers/infographic/amyloid-plaques-and-neurofibrillary-tangles (7) Svenskt Demenscentrum. Fakta| Om ärftlig alzheimer [Internet]. Stockholm: Svenskt Demenscentrum; 2009. [cited 11 Sep 2017] Available from: http://www.demenscentrum.se/Fakta-om-demens/Demenssjukdomarna/Alzheimers-sjukdom/Nar-alzheimer-gar-i-slakten/Fakta--Om-arftlig-alzheimer/
