#CElegans #Alzheimers #AlzheimersDisease #AD #Parkinsons #ParkinsonsDisease #PD #NeurologicalDisease
I'll be honest I do not know too much about Alex outside of the classroom. This is what I do know though: she is a good student-really thinks about things, she works hard, she is awesome with kids (evidenced by when she stepped up and watched my daughter for me when I was in a pickle) and is courageous (evidenced by joining a college sport team in a sport she never played before-lacrosse). She is kind and I imagine she would make a really great friend.
Advanced neurological diseases such as Alzheimer’s (AD) and Parkinson’s (PD) have no known cure for their victims. Alzheimer’s disease is a persistent disorder that slowly destroys brain tissue: permanently erasing memory, thinking skills, and years’ worth of knowledge. Parkinson’s disease gradually and permanently impairs both voluntary and involuntary movement. Patients suffering from these progressive neurological diseases are subjected to rounds of therapies and medications that are only capable of subsiding the life-altering symptoms they experience.
According to the Parkinson’s Foundation each year 60,000 Americans are diagnosed with PD and a staggering 500,000 Americans will be diagnosed with AD, as predicted by The Bright Foundation. The fate of these individuals is sealed after diagnosis. Dr. Alexander Videnovic advises that PD patient’s life expectancy drops to 10-20 years after diagnosis. Healthline estimates that those suffering from AD are expected to only live a short 3-10 years. What if these diseases could be prevented from ever manifesting? What if the grim fate of over 560,000 Americans could be reversed in a matter of one year?
A small, unassuming nematode may hold the solution to saving these 560,000 individuals. Caenorhabditis elegans experience an advanced aging process in its short 12-to18-year lifespan that parallels those seen in Homo sapiens. Graduate biology students at New York University found that with this advanced form of aging, C. elegans were also susceptible to a battery of progressive neurological disorders.
Additionally, C. elegans are capable of expressing human mutant genes that are responsible for causing the neuro-degenerative diseases. Notably, two disorders can be induced in the nematode using mutant human genes to become virtually identical to AD and PD. Upon injection, either mutant can be separately studied to track its manifestation in C. elegans.
Parkinson’s disease has been linked to death of the substantia nigra tissue within the brain. This disrupts the transmission of dopamine, a neurotransmitter primarily responsible for motor control, hence a PD patient’s chief complaint.
There are two ways one can develop PD- either by inheriting a mutant dopaminergic neuron degenerative gene, or by a variety of environmental factors. Because C. elegans lack the orthologous genes that interact with the human mutant, scientists focused on environmental factors that may subside dopaminergic neuron degeneration. When this disorder was induced to C. elegans, researchers noted a change in expression with implementing a caloric restrictive diet.
The infected nematodes that were deprived of food slowly were able to gain function over their once restricted movement. Though, those with large amounts of nutritional food were killed off quicker. They soon found out the connection between the two: sir-2.1. sir-2.1 is type of sirtuin, a metabolic regulation gene specific to phylum: Nematoda. It was determined that sir-2.1 modulates “calorie-restricted mediated” prevention of neurodegenerative PD in C. elegans. Biochemical and Biophysical Research Communications published that C.elegans, under a restricted diet, had a preventative effect on dopaminergic neurodegeneration.
Research is being conducted to identify a human gene that may modulate the effect of neurotoxic dopaminergic neuron degeneration, and whether this may or may not be influenced by a calorie capped diet.
Alzheimer’s disease is caused by an aggregation of Amyloid-beta plaques
in the brain. This causes degradation of connection areas within the brain. Amyloid-beta plaques are protein fragments that have been incorrectly snipped from a precursor protein. They then misfold and align themselves together and tend to stick in non-advantageous places. These plaques build-ups account for the massive losses of memory and knowledge associated with AD manifestation.
Largely, common practice has been focused on preventing the aggregation of these plaques, as opposed to stopping its manufacturing. Infected roundworms were given bouts of prospective treatments and were monitored for signs of progress. The Department of Molecular Biochemistry and Pharmacology of Milan discovered that after administration of various tetracyclines, a class of antibiotics used to kill susceptible microorganisms, the formation and collection of plaques dramatically decreased. The mechanism of how tetracyclines interact with the misshapen proteins is still largely unknown. Its use is known to mitigate the aggregation of Amyloid-beta plaques, ultimately increasing the lifespan of C. elegans that were once AD diagnosed.
This institute is now working on identifying the C. elegans mechanistic pathway of mitigating the aggregation of plaques, upon receiving medication. And next, predicting how these findings may translate when using human-like proteins.
Although an excellent model organism that has previously helped in understanding congenital heart disease, Automated Drug Screening, and practice treating obscure kidney disease has been in a sense re-discovered, work is still left to be done. C. elegans are able to express human genes allowing research to be conducted in a more appropriate test subject. Yet, C. elegans lack exact facilitator genes found in the human biological pathway. These biological pathways within the model must undergo major means of translation before remedies can be tailored for human use.
But think, we already found a suitable means to practice. We are now one step closer to finding a cure, sparing the lives of hundreds of thousands, and increasing valuable time spent with loved ones- all thanks to an unassuming parasite.
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