Mighty Mitochondria and Neurodegenerative Diseases – Science in the News

While sitting in your elementary school classroom or making some amorphous jelly shape studded with jellify beans, you may have heard the phrase “ mighty mitochondria ” from your studies on the cell structures. More than just a catchy alliteration, this phrase accurately describes one of the most fundamental components of the cells that make up our bodies. Mitochondria, often referred to as the “ powerhouses of the cellular telephone ”, were beginning discovered in 1857 by physiologist Albert von Kolliker, and by and by coined “ bioblasts ” ( life germs ) by Richard Altman in 1886. The organelles were then renamed “ mitochondria ” by Carl Benda twelve years former. It wasn ’ deoxythymidine monophosphate until more than half a century had passed since their discovery that the function of mitochondria began to be unravel [ 1 ] .
today, “ mighty mitochondrion ” are known to play a critical character in providing energy to the cell, maintaining cellular metabolism, deoxyadenosine monophosphate well as regulating cell survival and death. These organelles are responsible for converting food molecules and oxygen into adenosine triphosphate ( ATP ). ATP can then be used to provide energy for the cell [ 2 ]. not surprisingly, because of their central role in the cell, dysfunctions in mitochondria have been linked to numerous diseases. Most recently, defects in mitochondria have been linked to the process of neurodegeneration – the liberal death or personnel casualty in function of neurons, the cells that make up our brains and nervous organization. such damage to distinct subsets of neurons is the root causal agent of diseases such as Alzheimer ’ sulfur, Parkinson ’ south, Huntington ’ second, and Amyotrophic Lateral Sclerosis ( ALS, or Lou Gherig ’ randomness disease ). Whether mitochondrial disability causes neurodegeneration in these diseases or is merely a consequence of it remains indecipherable. however, the testify that these organelles play a hard character in neurodegeneration is growing [ 3 ] .

Alzheimer’s, Aggregation, and Mitochondrial Damage

Alzheimer ’ south disease, the 6th lead cause of death in the United States, is equitable one model of a neurodegenerative disease being linked to mitochondrial dysfunction. Alzheimer ’ randomness is characterized by progressive degeneration of neurons in the lens cortex and hippocampus, the mind regions known for intellectual capacity and memory repositing, respectively. This degeneration results in a range of symptoms including dementia, difficulty in trouble resolution, and climate disturbances .
originally, it was believed that abnormal collection, or clumping, of a protein called amyloid beta ( Aβ ) was the campaign of Alzheimer ’ mho disease, as brains of Alzheimer ’ randomness patients are riddled with price caused by these accumulate proteins. however, recent studies have shown that symptoms of Alzheimer ’ s occur well before this price is visible. Aβ, which is a protein that is normally found in healthy cells, only becomes toxic when it becomes misfolded or abnormal in the cell. It is now thought that these rid pre-aggregated abnormal pieces of Aβ protein are the disease trigger ; that even before the protein clumps together, the disease has started.

A study done by Dr. ShiDu Yan at Columbia University Medical Center found that these abnormal Aβ molecules could cause price to the mitochondrion and inhibit their transport within the cell – something that ’ s particularly authoritative in neurons. The structure of the nerve cell is identical alone as they have long projections, called axons, which form connections with early neurons in order to communicate information. These axons can be american samoa long as one meter ( from your brain to the tips of your fingers, for model ! ), so the transport of mitochondrion to the end of the axon is essential to providing energy to maintain healthy neural connections, or synapses [ 5 ]. Without the ability to maintain synaptic connections, these neurons finally die off, resulting in disease .

The Role of Reactive Oxygen Species

Another connection between mitochondrial dysfunction and neurodegenerative diseases is the overproduction of damaging molecules called reactive oxygen species ( ROS ). ROS are highly active oxygen derivatives that can cause extreme wound and stress to cell structures, ultimately leading to cell death. While ROS are normally created by mitochondria during ATP production, the cell has protective enzymes to convert ROS to less harmful forms, thereby preventing extensive damage. In cases of high ROS output, however, the cell is unable to defend itself and accumulates these toxic species over time. overproduction of ROS in neurons is frequently observed in patients with Parkinson ’ south and Huntington ’ s disease, a well as ALS. additionally, mutations in ROS-converting enzymes are normally found in patients with familial ALS [ 3 ] .
Besides being the “ cell powerhouses ”, mitochondrion are even more “ mighty ” as they are the lone structure in the cell other than the nucleus that contains DNA. Mitochondrial DNA is relatively humble, encoding only 37 genes compared to the approximately 25,000 genes in the deoxyribonucleic acid of the nucleus. however, fundamental genes that encode proteins for producing ATP are found in this minor group. Mitochondrial DNA mutations and deletions have been found in both patients and shiner models of neurodegenerative diseases such as Alzheimer ’ mho and Parkinson ’ mho disease, normally as a resultant role of damage by ROS [ 6 ] .
Findings such as these in the past 10-15 years have provoked a bowel movement in neurodegenerative disease inquiry towards understanding the function of mitochondria in cell metamorphosis, energy, and death in hopes of identifying electric potential targets for therapeutics. It has become increasingly more apparent that the common connect among all neurodegenerative diseases is the dysfunction in mitochondria and their attendant inability to provide energy and assert cell health. much research is being devoted to determining the demand mechanisms by which the mitochondrion are damaged and induce further destruction. even calm, I think we can all appreciate that mitochondria are army for the liberation of rwanda more mighty and critical to our wellbeing than we ever understood them to be in elementary school.

Kelsey Taylor is a PhD scholar in the Biological and Biomedical Sciences program at Harvard Medical School .


[ 1 ] Allen, Anna. “ Who Discovered Mitochondria ” Who Discovered It. hypertext transfer protocol : //www.whodiscoveredit.com/who-discovered-mitochondria.html
[ 2 ] hypertext transfer protocol : //en.wikipedia.org/wiki/Mitochondrion
[ 3 ] Petrozzi, L., Ricci, G., Giglioli, N.J., Siciliano, G., Mancuso, M. 2007. Mitochondria and Neurodegeneration. Bioscience Reports 27, 87-104.

[ 4 ] 2011 Alzheimer ’ s Disease Facts and Figures. Alzheimer ’ s Association. 2011. hypertext transfer protocol : //www.alz.org/downloads/Facts_Figures_2011.pdf
[ 5 ] Columbia University Medical Center. “ early role of mitochondria in Alzheimer ’ s Disease may help explain limitations to current beta starchlike hypothesis. ” ScienceDaily, 13 Oct. 2010. hypertext transfer protocol : //www.sciencedaily.com/releases/2010/10/101013122557.htm
[ 6 ] Yang, J., Weissman, L., Bohr, V., Mattson, M. 2009. Mitochondrial DNA Damage and Repair in Neurodegenerative Disorders. DNA Repair 7, 1110-1120. hypertext transfer protocol : //www.ncbi.nlm.nih.gov/pmc/articles/PMC2442166/

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