Alzheimers disease, also known as senile dementia is a neurodegenerative disorder that harms ones memory and other necessary mental functions. This neurodegenerative disease has become more prevalent in the elderly population. The biggest risk factor for cognitive decline has been aging, and researchers everywhere are looking to find ways to prevent this. Genetic reference panels have been one of the valuable ways to study these complex traits that give rise to this neurodegenerative disease. The problem arises in trying to identify the exact genetic modifiers and pathways of cognitive aging because there are many genes that play this role.
Genetic makeup functions as an important role in determining susceptibility and in determining how an individual ages, whether that is a successful trajectory with little cognitive decline, a more normal aging trajectory with some cognitive decline, or a more severe case which goes dementia, also known as a cognitive impairment which interferes with one's living abilities.
In the article, “Systems Genetics Identifies Hp1bp3 as a Novel Modulator of Cognitive Aging,” Catherine C. Kaczorowski et al. conducted a study in order to find ion channels and receptors in neurons that could be targets that either delay or stop cognitive deficits related to normal non pathological aging. They had discovered Hp1bp3 which is a heterochromatin binding protein as a genetic modifier of cognitive decline in normal non-pathological aging. In the study, researchers took two strains that get intermixed and randomly swap out parts of the genome that are coming from each of the parental strains. Once the strains have been mixed, they are able to mate for over 20 generations and are able to adjust and fix the genome. Researchers found that a part of chromosome 4 had been associated with contextual fear memory within middle aged mice. The areas of their genome are a different mosaic of the original founders, this is important when we begin genetic mapping to look for genes that influence cognitive decline. Advantage is we can control the environment and control the degree of genetic complexity, we are better able to identify genes that play a role in cognitive decline in studying a smaller population.
Similarly in recent studies, “Vulnerability and Resilience to Alzheimer’s Disease: Early Life Conditions Modulate Neuropathology and Determine Cognitive Reserve,” Sylvie L. Lesuis et al. focused on finding what other risk factors other than aging early on in life could lead to Alzheimer's disease in humans. In order to do this, researchers used transgenic models of rodents and placed them in either a ‘positive’ enriched environment or a ‘negative’ environment to display how environmental factors can affect one's brain function later on in life. Researchers found that those rodents who were placed in a positive environment resulted in a decrease of HPA axis reactivity, this results in lower CRH as well as lower glucocorticoid levels when exposed to a stressful event, that is how it will respond to the stressor. On the other hand, those rodents placed in a negative environment had shown that HPA axis reactivity had increased. Glucocorticoids as well as CRH are shown to be enhanced due to stressors early on in life. The idea is that increased levels of glucocorticoid can increase Aβ levels which plays an important role for these hormones in moderating AD neuropathology. Glucocorticoids are involved in the advancement of AD neuropathology.
Both researchers main purpose was to see what ways we can prevent cognitive deficits. It is important to note if we can identify the specific genes involved in
cognitive deficits, and we can also see what environmental factors results in
cognitive deficits then there could be a broader spectrum of treatments
we can find to stop this neurodegenerative disease that is harming specifically the elderly.
Although it may not stop the disease at once, now we know there are
some outside factors such as stress during an individuals early life that
could potentially lead to the disease.
References
Lesuis, Sylvie L., et al. “Vulnerability and Resilience to Alzheimer’s Disease: Early Life Conditions Modulate Neuropathology and Determine Cognitive Reserve.” Alzheimer's Research & Therapy, vol. 10, no. 1, 2018, doi:10.1186/s13195-018-0422-7.
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.
My husband was diagnosed with early onset Parkinson's disease at 57.his symptoms were shuffling of feet,slurred speech, low volume speech, degradation of hand writing, horrible driving skills, right arm held at 45 degree angle, things were tough for me, but now he finally free from the disease with the help of total cure ultimate health home, he now walks properly and all symptoms has reversed, he had trouble with balance especially at night, getting into the shower and exiting it is difficult,getting into bed is also another thing he finds impossible.we had to find a better solution for his condition which has really helped him a lot,the biggest helped we had was ultimatehealthhome they walked us through the proper steps,am highly recommended this ultimatehealthhome@gmail.com to anyone who needs help.
ReplyDelete