Thursday, March 4, 2021

The Wisest People in America Need Our Help

     In the United States alone, a whopping 15% of the population consists of older people (>65). And by 2030, this number is expected to increase to 20%. As more of these elderly people exist in the population,  diseases and illnesses become more prevalent due to aging. The true reality starts to sink in for the elderly, and many look for hope through medical care. One of the most important things that the elderly are at risk of losing is their cognitive processing. Cognitive processing starts to decline as people get older. Processing speeds, memory, and even simple reasoning abilities start to diminish. Dementia, Alzheimer's, Parkinson's, frontotemporal degeneration are all consequences of cognitive aging. It is a sad reality that the people with over twice the life experience we have, the wisest heads on Earth, are losing it due to age. Cognitive decline is a huge problem right now and will be an even bigger problem in the future as there will be more elderly people in the future. We must find a cure and help the elderly not only because we can learn from them, but also we owe it to them because they are the ones who allowed us to have life. When we were babies, they nurtured us and made us healthy men and women; We simply owe it to them. We must strive hard for a cure, and through research, there is hope.

    In the paper titled Systems genetics identifies Hp1bp3 as a novel modulator of cognitive aging written by main author Sarah M. Neuner, a gene was identified called Hp1bp3 that codes for a protein. This protein is diminished in elderly people with cognitive impairments. The paper urges that this is only one of many proteins involved in cognitive aging, and also calls for identifying more genes that can impact cognitive decline which will aid in the prevention and treatment of these cognitive illnesses. Specifically, In the actual experiment, mice were given foot shocks to assess fear conditioning. Fear responses were assessed by measuring freezing behavior in each mice. The mice with less protein forgot how to freeze properly. The researchers found that much of the variance in freezing behavior is attributed to genetic factors, and when they probed deeper they found the variation had to do specifically with differences in the gene Hp1bp3. The researchers confirmed the role of the Hp1bp3 gene in cognitive aging when they did another experiment with wild-type (WT) and a knockout (KO) mice for Hp1bp3; the KO mice forgot the conditioned fear response and demonstrated cognitive aging. This experiment provides clear evidence that the Hp1bp3 gene is an important regulator to prevent cognitive aging. This is one paper that provides evidence for a novel gene that directly influences cognitive deficits. However, we must continue to identify these types of genes to develop a sound treatment that targets all types of genes rather than this one alone.

In another article, researchers found 5 different genes that are involved in Dementia, Parkinson's, and Alzheimer's; three major cognitive diseases that result from old age. Unlike the previous paper, these genes are involved in the onset and causation of cognitive diseases. These genes are SCNA, APOE, GBA, BIN1, and TMEM175. Specifically, The SCNA gene makes the protein alpha-synuclein, an important protein in Lewy bodies; a characteristic of dementia. While the APOE gene makes the protein apoenzymes; a key role in Alzheimer's. It is important to note that in this research article, the presence of these genes causes cognitive disease, while in the previous article, the absence of the Hp1bp3 gene determined cognitive decline. Nonetheless, this research article introduces 5 new genes that are responsible directly for cognitive aging, however, there is much more work to do. In addition, many times a gene can be mutated and it is not always so clear as to which genes we need more of and which genes we need less of. However, we are on the right track and we must continue to identify other genes that play a role in cognitive aging and disease.

Without a doubt, the more genes we identify, the better chance we have at treating these cognitive diseases. It also develops awareness of the different types of genes that are involved. However, we must continue to strive for a cure; the identification of the types of genes involved is only the first step to developing a precision treatment plan that targets these genes. We need to decide whether to overexpress some genes while we suppress others while taking into account the genes that have been mutated. For these reasons, we must continue striving hard to develop a cure and realize that we have only scratched the surface. If we are to develop a cure for these cognitive diseases, we must continue to identify related genes and experiment with them to see which combination or a mix of genes can produce the best cure. It is also not as easy as it sounds, genome sequencing is a tedious process and there are many struggles involved. However, the effort is worth it to develop a cure for these awful cognitive deficits that impede the lifestyle of the elderly. 

References


Chia, R., Sabir, M.S., Bandres-Ciga, S. et al. Genome sequencing analysis identifies new loci associated with Lewy body dementia and provides insights into its genetic architecture. Nat Genet (2021). https://doi.org/10.1038/s41588-021-00785-3


Neuner, Sarah M., et al. “Systems Genetics Identifies Hp1bp3 as a Novel Modulator of Cognitive Aging.” Neurobiology of Aging, vol. 46, 2016, pp. 58–67., doi:10.1016/j.neurobiolaging.2016.06.008.


1 comment:

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