By Harriet Milligan
Life expectancy in humans has steadily increased over the last 50 years, and due to this our bodies are not adapted to live the additional 10 to 20 years. Increasing lifespans has drawn attention to a number of disease impacting the elderly population. One of the most prominent diseases in this category is Alzheimer’s disease. This neurodegenerative disease is characterized by a loss of memory and other cognitive deficits. In the United States, Alzheimer’s is the 6th leading cause of death.
The symptoms and physiological changes associated with Alzheimer’s are well-documented, but the underlying cause of why this damage happens as well as indicators for Alzheimer’s are still relatively unknown. Previous studies have shown that the accumulation of amyloid-β occurs before the onset of the symptoms and it is considered the first physiological signs for Alzheimer’s. Up until a recent study the location of these initial amyloid-β accumulation has not been studies largely due to the difficulty of studying this mechanism with the lag between changes in the brain and signs of symptoms. Using PET and MRI scans, researchers were able to locate areas where amyloid-β accumulate before Alzheimer’s symptoms were observed.
In a recent study, a cohort of 473 individuals were divided into three groups based on their initial amyloid-β levels in both the cerebrospinal fluid (the fluid that surrounds the brain and spinal cord) and in the brain itself. Each group was studied longitudinally, by accumulation of amyloid-β was measured as well as the location of this accumulation. The groups are summarized in table 1.
Table 1 The groups used for this study are based on the initial amyloid-β levels. The accumulation of amyloid-β plaques in the brain was measured using a PET scan.
The results of this study showed significant accumulation of amyloid-β in early-accumulators compared to non-accumulators. The brain areas that were most prominently influenced were the orbitofrontal cortex, precuneus, insula and the posterior/isthmus cingulate cortex. Collectively these areas make up the default mode network.
The default mode network (DMN) is a recently defined area in neuroscience. It is often described as the network involved in “wakeful rest”. This means that it is not activated when tasks are done, but instead most active when daydreaming, activating certain memories or other internal activities. This is where the brain thinks about others and the self. The accumulation of amyloid-β in this area is an indicator of Alzheimer’s which can lead to atrophy (neuron death) in these areas.
Damage to the DMN can lead to ethical questions regarding one’s sense of self. If this area is compromised, say in a case of Alzheimer’s, what happens to self identity? Along with losing one’s memory, if the ability to think about the self and others is lost, is one still living? Aging and Alzheimer’s can bring about questions regarding the grey area between physical and mental living. If scientists can find a drug to prevent Alzheimer’s will it cure both the physical and psychological symptoms? If not is it really a cure?
References
Palmqvist, S., Schöll, M., Strandberg, O., Mattsson, N., Stomrud, E., Zetterberg, H., …
Hansson, O. (n.d.). Earliest accumulation of β-amyloid occurs within the default-mode
network and concurrently affects brain connectivity. https://doi.org/10.1038/s41467
017-01150-x
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