Presbycusis Research Paper

Mitochondria, dubbed the ‘powerhouse of the cell’, are a type of organelle present in most human cells. Their primary function is to generate Adenosine Triphosphate (ATP), the cell’s principal source of chemical energy. Unlike most other organelles, mitochondria store their own set of genetic material, distinct from the DNA situated in a cell’s nucleus. Although this ‘mitochondrial genome’ represents only 0.1% of a cell’s genetic information, it often plays a significant role in development.

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There are hundreds of neurodegenerative diseases (NDD) and the etiology for most of the random conditions remain a universal mystery (Nieoullon 2011). A deterioration of specific functions of the neuron cells of the central nervous system is the most common characteristic of NDD. Neurons are responsible for transmitting essential information to other nerve, muscle and glandular cells (Przedborksi, Jackson-Lewis 2003). Emerging research has recently identified mitochondrial dysfunction as a recurrent elemental link in numerous neurodegenerative disorders (Ghano,

On the other hand fusion is associated with optimization of mitochondrial functions and is regulated by three major proteins i.e. mitofusin 1(Mfn1), mitofusin 2(Mfn2) and optic atrophy protein1(OPA1). Mfn1 and Mfn2 are mitochondrial transmembrane proteins localized to the outer membrane. During mitochondrial fusion Mfn 1 and Mfn 2 form hetero-oligomeric and homo-oligomeric complexes that join outer membranes of mitochondria. Inner mitochondrial membrane fusion is mediated by OPA1 and Mfn 1. Mounting evidence implicate that the expression level of mitochondrial dynamin proteins i.e. Drp 1, Opa 1, Mfn-1, Mfn-2 is decreased in the pathogenesis of complex neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and Huntington's disease while Fis-1 levels are increased which results in abnormal mitochondrial distribution in neurons of AD patients as compared to age-matched controls. These changes in mitochondrial dynamics significantly impact almost all aspects of mitochondrial functions including energy metabolism, calcium buffering, reactive oxygen species(ROS) generation and apoptosis

Central Auditory Processing Disorder is a broad term for several disorders in which the affects the way the brain processes

Many seniors suffer from hearing loss. Sadly, many more are suffering from the effects of hearing loss and do not even know it. They face physical and emotional issues that are frustrating, angering, and depressing, but they can't put their finger on what is wrong. Often, the issues can be traced back to a loss of hearing, but first they need to consider that this might be an issue and pursue the treatments that could correct their hearing-related issues.

Peripheral hearing loss, in addition to other types of hearing loss, is very common among the elderly. For those who develop permanent, peripheral hearing loss in older age, there are two main etiologies. Exposure to severe acoustic trauma can cause hearing loss at any age. However, a life-time exposure of lower level environmental noise can also lead to hearing loss due to noise. In addition, the phenomenon of presbycusis, age related hearing loss, also occurs in a large number of elderly people. This paper seeks to untangle the connections and interactions between noise induced hearing loss and presbycusis in older adults.

One piece of knowledge that I have applied to my life outside the classroom is the material from chapter 9: Deafness and hearing loss. I have regular interactions with two students from another classroom who are deaf and communicated with an interpreter. Reading the tips for communicating with someone who is deaf helped out immeasurably with the class and made the interaction easy and lead to a good dynamic creating the opportunity for excellent conversations.

The mitochondrion is known as the powerhouse of the cell. It is similar to the engine in a car. This organelle is known for giving the cell energy to function properly. The mitochondrion is the place where cellular respiration and many other processes, including protein translation, autophagy and oxidative phosphorylation occur. The damage of this vital organ would be distressing to the body. When the mitochondrion fails to produce enough energy or ATP (andesine triphosphate) to support the cell’s functions, this phenomenon is known as mitochondrial disease. Due to failure of critical physiological processes, a person inflicted with mitochondrial disease will have loose muscles, coordination issues, involuntary movement of the eyes, and the inability to exercise. Additionally, the individual will have poor growth and even neurological problems. Though quite rare, the disease is extremely dangerous.

Deletions can occur to a single base or several thousands of bases, anywhere on the molecule. MtDNA point mutations are mostly found in genes that code proteins as well as in tRNAs and rRNAs. When mitochondria fail, cells become damaged or even die. Eventually, entire systems can fail when enough cells injure or die. Mitochondrial diseases can either be inherited or spontaneous. These diseases are more present in children; however, adult onset is occurring more often. Common diseases and symptoms associated with mtDNA mutations include Kearns-Sayre syndrome, Pearson’s marrow-pancreas syndrome, diabetes, epilepsy, deafness, Alzheimer’s disease, and, in some rare cases, Parkinson’s disease. Genotype and phenotype association is complex with mtDNA mutations because a certain mutation can cause variable phenotypes, and one phenotype can result from many mutations working together. Factors may include tissue distribution, nuclear background, and varying dependence of organs on oxidative phosphorylation for

Otitis media is the infection of the middle ear. Two common types of ear infection are Acute Otitis Media (AOM) and Otitis Media with Effusion (OME). Signs that point to AOM include pain, inflammation, fever, and hearing loss. Usually, AOM is a bacterial infection which frequently develops after the blockage of Eustachian tubes associated with a respiratory tract infections. OME is a middle ear effusion without acute inflammation and minimal symptoms, where fluid remains in the ear after the respiratory infection has resolved. This is a Quality Assessment/Quality Improvement project designed to determine of the rate of adherence to Otitis Media practice guidelines in the UMHS Pediatrics clinics. The charts of all pediatric patients seen the

Several mitochondrial diseases such as chronic progressive external ophthalmoplegia (CPEO), Kearns- Sayre syndrome (KSS), the syndrome of neurogenic muscle weakness, ataxia and retinitis pigmentosa (NARP), as well as LS, LHON, MERRF, and MELAS manifest in childhood and have limited therapeutic options. Mitochondrial protein dysfunction has also been linked with varying degrees of evidence to Parkinson’s disease (PD), Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS) (Lin and Beal, 2006; Trushina and McMurray, 2007), schizophrenia, and autism (Manji et al., 2012; Rossignol and Frye, 2012). Acquired mitochondrial disorders are represented in certain cancers (Wallace, 2012) and metabolic disorders (Nasrallah and Horvath, 2014). For example, mutations in the mitochondrial form of superoxide dismutase SOD1, which functions to protect mitochondria from superoxide damage, is linked to the progression of ALS; (Vehvilainen et al., 2014) NADH dehydrogenase 4 to LHON; (Kornmann, 2013) PARKIN to the familial form of PD;(Schmidt et al., 2010) and TCA cycle enzymes to oncogenesis (Schaefer et al.,

Mitochondria are responsible for producing over 90% of the energy needed to susutain life. When mitochondria fail, less and less energy is generated within our cells, this is mitochondrial disease. This disease can be attributed to mitochondrial mutations. It is estimated that between 10-15 people I every 100,000 people are affected – (these figures have been taken from berg biochemistry).

Accumulation of DNA damage occurs with increasing age, causing cells to deteriorate and malfunction. While DNA damages incur constantly in cells of living organisms, most of the damages are repaired in healthy individuals. However, some DNA damage accumulate as the DNA polymerases and other repair mechanisms cannot correct defects at a rapid enough pace as the rate of damage. In particular, damage to mitochondrial DNA may lead to mitochondrial dysfunction. Maintenance of metabolic homeostasis along with appropriate stress responses absolutely requires proper mitochondrial function. Mitochondrial dysfunction is known to play a critical role in aging and as well as other numerous human diseases, for example cancer and neurodegenerative disorders

Deafness is like a deepening frost, it damages your life little by little. I have been deaf for about 3 days once, due to my ears having an infection. Have you ever had a very bad day? Well, I will first try to explain what it feels like. Strikes of thunder, unwanted party crashes, people yelling through your mind, shaking your head trying to get your hearing back. If you used to be able to hear, theres nothing as cruel as memory. Its not even possible to escape into sadness. You feel like you aren't even who you are anymore. Isn't it funny to lose your self just by losing one sense? little pieces