Neurodegeneration: Difference between revisions
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'''Neurodegeneration''' describes the loss of structure or function to nervous tissue<ref>Merriam-Webster. (n.d.). Medical Dictionary. Available: http://www.merriam-webster.com/medlineplus/neurodegeneration. Last accessed 09/11/2014.</ref>. Neurodegenerative diseases include [ | '''Neurodegeneration''' describes the loss of structure or function to nervous tissue<ref>Merriam-Webster. (n.d.). Medical Dictionary. Available: http://www.merriam-webster.com/medlineplus/neurodegeneration. Last accessed 09/11/2014.</ref>. Neurodegenerative diseases include [[Alzheimer's disease|Alzheimer’s]], [[ALS|ALS]], [[Huntington’s disease|Huntington’s]] and [[Parkinson’s|Parkinson’s]]<ref>Bredeson, D. (2006). Cell death in the nervous system. Nature, 796-802.</ref>. All of these diseases manifest with different symptoms. For example Parkinson's affects the basal ganglia of the [[brain|brain]], which result from degenerative loss of [[dopamine|dopamine]]<ref>Garrett E. Alexander, Department of Neurology, Emory University School of Medicine, Atlanta, Ga, USA. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181806/</ref>. This causes symptoms of rigid muscles, impaired posture and balance, tremor and many more. Huntingtons disease is caused by a [[mutation|mutation]] in either of an individual's two copies of a [[genes|gene]] called Huntingtin<ref>Department of Medical Genetics, Wellcome Trust Centre for the Study of Molecular Mechanisms in Disease, Cambridge Institute of Medical Research, Addenbrooke's Hospital.</ref>.This results in the lack of muscle coordination and a decline in mental and behavoural symptoms<ref>"Huntington's DiseaseHope Through Research", NINDS, Publication date April 19, 2015. http://www.ninds.nih.gov/disorders/huntington/detail_huntington.htm</ref> | ||
<span style="line-height: 1.5em;">Most of the physiological mechanisms whereby neurodegenerative diseases develop and progress share the common feature where [ | <span style="line-height: 1.5em;">Most of the physiological mechanisms whereby neurodegenerative diseases develop and progress share the common feature where [[Proteins aggregate|proteins aggregate]] – that is, the accumulation of misfolded proteins which clump together either intra or extracellularly<ref>Aguzzi, A., and O'Connor, T. (2010). Protein aggregation diseases: pathogenicity and therapeutic perspectives. Nature, 237-248.</ref>. This feature suggests a commonality of the pathological processes of neurodegenerative diseases; this might allow for neuroprotective medicine to be developed to counter protein accumulation<ref>Nieoullon, A. (2011). Neurodegenerative diseases and neuroprotection: current views and prospects. Journal of Applied Biomedicine, 173-183.</ref>.</span> | ||
< | Oxidative stress has been suggested to play an important role in neurodegeneration, that is, the stress associated with the increased production of oxidizing species (such as free radicals) or the decrease in the efficacy of antioxidant defence. Severe oxidative stress can lead to cell death.<ref>Lennon SV, Martin SJ, Cotter TG (1991). "Dose-dependent induction of apoptosis in human tumour cell lines by widely diverging stimuli". Cell Prolif. 24 (2): 203–14</ref> | ||
=== References === | |||
<span style="line-height: 1.5em;"><references /></span><br> | <span style="line-height: 1.5em;"><references /></span><br> | ||
Latest revision as of 17:17, 3 December 2015
Neurodegeneration describes the loss of structure or function to nervous tissue[1]. Neurodegenerative diseases include Alzheimer’s, ALS, Huntington’s and Parkinson’s[2]. All of these diseases manifest with different symptoms. For example Parkinson's affects the basal ganglia of the brain, which result from degenerative loss of dopamine[3]. This causes symptoms of rigid muscles, impaired posture and balance, tremor and many more. Huntingtons disease is caused by a mutation in either of an individual's two copies of a gene called Huntingtin[4].This results in the lack of muscle coordination and a decline in mental and behavoural symptoms[5]
Most of the physiological mechanisms whereby neurodegenerative diseases develop and progress share the common feature where proteins aggregate – that is, the accumulation of misfolded proteins which clump together either intra or extracellularly[6]. This feature suggests a commonality of the pathological processes of neurodegenerative diseases; this might allow for neuroprotective medicine to be developed to counter protein accumulation[7].
Oxidative stress has been suggested to play an important role in neurodegeneration, that is, the stress associated with the increased production of oxidizing species (such as free radicals) or the decrease in the efficacy of antioxidant defence. Severe oxidative stress can lead to cell death.[8]
References
- ↑ Merriam-Webster. (n.d.). Medical Dictionary. Available: http://www.merriam-webster.com/medlineplus/neurodegeneration. Last accessed 09/11/2014.
- ↑ Bredeson, D. (2006). Cell death in the nervous system. Nature, 796-802.
- ↑ Garrett E. Alexander, Department of Neurology, Emory University School of Medicine, Atlanta, Ga, USA. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181806/
- ↑ Department of Medical Genetics, Wellcome Trust Centre for the Study of Molecular Mechanisms in Disease, Cambridge Institute of Medical Research, Addenbrooke's Hospital.
- ↑ "Huntington's DiseaseHope Through Research", NINDS, Publication date April 19, 2015. http://www.ninds.nih.gov/disorders/huntington/detail_huntington.htm
- ↑ Aguzzi, A., and O'Connor, T. (2010). Protein aggregation diseases: pathogenicity and therapeutic perspectives. Nature, 237-248.
- ↑ Nieoullon, A. (2011). Neurodegenerative diseases and neuroprotection: current views and prospects. Journal of Applied Biomedicine, 173-183.
- ↑ Lennon SV, Martin SJ, Cotter TG (1991). "Dose-dependent induction of apoptosis in human tumour cell lines by widely diverging stimuli". Cell Prolif. 24 (2): 203–14