Release date: 2015-11-30
Remember Charles in "Rise of the Orbs"? He is the father of scientist Will and a dementia patient. Will researched a drug for the treatment of human neurotrophic diseases in orangutans. In fact, he is also working hard to treat his father, Charles. By chance, Will put his own medicine into his father's body, and found that his father's illness was good in a short time, and the IQ was soaring... However, in reality, there is no such life-saving and long-brained medicine.
Alzheimer's disease (Alzheimer disease, AD), the main manifestation is memory loss, forgetting in the blink of an eye, gradually develop into cognitive impairment, become an old child. In order to eliminate the discrimination that may be caused by Alzheimer's disease, there has been a voice calling for a change of name, and a large representative called for a change to the name "Old Age Amnesia". AD has plagued countless families in the world, and even became the most terrible disease except cancer. We have no good way to take AD, and we don't even know its cause. We can only blame it on genetic factors and environmental factors. Epidemiological investigations suggest that normal aging is the most important risk factor for AD, but who can we not be old?
At present, the treatment of AD is mainly to control the symptoms, so that it deteriorates slowly. However, it will slowly become more serious. We have no good way to completely prevent the development of the lesion, even if Will gives his father a fight. The drug eventually produced resistance and had serious complications.
The sooner we discover AD, the sooner we can start treatment and slow down its development. At present, we must find that AD must wait until the symptoms of memory loss occur. However, the brain lesions of AD can only appear for 10 to 15 years. If it can be found before the symptoms appear, even when the brain just begins to have lesions. Discovering it will undoubtedly increase a major advantage of AD prevention. So, can we discover the signs of AD earlier?
Scientific research has found that some changes in brain imaging may lead to the development of early AD lesions before symptoms appear.
We know that AD is a disease of central nervous system degeneration, yes! It is "the brain is broken," so scientists analyze the image of the brain.
In a scientific study, Dr. Stephen's research team at the Cleveland Clinic in the United States divided 45 subjects into two groups, one with high AD genetic risk (ApoEε4, the main genetic risk factor for carrying AD). Subjects, they are more likely to have Alzheimer's disease (you can simply and rudely understand that they will get AD in minutes); the other group is subjects with low genetic risk. Before the study began, the two groups of subjects were normal and had no symptoms of AD.
These subjects do a functional magnetic resonance imaging (fMRI) examination of the brain every 5 years. During the fMRI, they have to do memory tests at the same time, and work their brains during their recall. The blood signal images of their brains were recorded by fMRI.
The researchers found that at the beginning of the study, subjects in the high-risk group were more active in brain tests during memory testing, and their brains worked hard to compensate for functional impairment caused by AD lesions. However, with the development of AD lesions, their brain activity is reduced, and it is no longer able to compensate for the functional damage caused by the lesion, so the symptoms of AD begin to appear - memory loss.
In the low-risk group, the brain activity was relatively low at the beginning of the study, and the work was not so hard. But as they age, brain activity slowly increases. At this time, the brain works hard to compensate for the deterioration of brain memory caused by aging, so they have no serious memory loss, because the human body has a normal compensatory reserve.
(The figure above shows the fMRI map of brain activity in the low-risk and high-risk groups at the beginning of the study, at 18 months and 57 months. The colored part of the graph indicates brain activity. You can see: a. The brain of the low-risk group Activities increased with age; b. Brain activity in the high-risk group was strong at the beginning of the study and then decreased. The original image was derived from the reference.)
It can be simply summed up as a thing that normal people can recall with only general brain power. People with AD brain lesions need to spend a lot of brain power to recall. That is to say, for normal people, the memories are very easy; for those with AD brain lesions, the memories are very laborious, and later they become more and more powerless.
The significance of this study is that brain fMRI can help detect early brain lesions in AD, and early treatment to delay the disease (secondary prevention of the disease: early detection, early diagnosis, early treatment); in addition, can also be used to assess early treatment The effect is to guide patients to use effective treatments.
Studies have shown that early treatment is effective, can prevent the development of AD lesions more effectively, and can even completely prevent the appearance of AD symptoms. The evaluation of the efficacy of early treatment is also necessary. “If treatment begins before symptoms of AD appear, it is more likely to successfully delay the progression of the lesion,†Stephen said.
If brain fMRI (or other higher-end imaging tests, such as PET) can be used for early diagnosis of AD, then we can span 10 to 15 years of long-term disease development, and AD is found before symptoms appear. Taking a picture of the brain, you can find Alzheimer's disease 10 years in advance, this is not a fantasy.
references:
1.Rao SM, Bonner-Jackson A, Nielson KA, et al. Genetic risk for Alzheimer's disease alters the five
-year trajectory of semantic memory activation in cognitively intact elders. NeuroImage 2015; 111: 136-46.
2.Reiman EM, Langbaum JB, Tariot PN, et al. CAP—advancing the evaluation of preclinical Alzheimer
Disease treatments. Nature Reviews Neurology 2015. doi:10.1038/nrneurol.2015.177.
Source: Medical Pulse
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