Parkinson’s-Disease.ppt

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1、Parkinsons DiseaseAn Overview of Conventional and Experimental TreatmentsBackground Parkinsons disease is a disorder that affects nerve cells in the part of the brain controlling muscle movement Disease is progressive signs/symptoms worsen over time Eventually is disabling, but progresses gradually

2、Believed to be caused by genetics, environmental factors or a combination of the twoParkinsons Disease Stats First desribed by James Parkinson in 1817 Affects 1 million in the U.S. Onset typically between 50-60 years of age, and slowly progresses with age Average onset is 62.4 years of ageNeurologic

3、al Basis “Neurodegenerative Disease” : caused by degeneration (dysfunction and death) of neurons within the brain (nigrastriatal pathway of the basal ganglia) NORMAL BRAIN FUNCTION Basal Ganglia Cells in substantia nigra produce/release dopamine Dopamine released by SN neurons lands on neurons of ot

4、her brain centers, controlling their firing Main targets are caudate nucleus and putamen (striatum) This basal ganglia pathway is involved in regulation of movementNeurological Basis PARKINSONS BRAIN FUNCTIONBasal Ganglia Cells of substantia nigra degenerate These cells can no longer produce adequat

5、e amounts of dopamine Neurons of striatum, etc. are no longer well regulated, thus do not behave in normal manner Results in loss of control of movements leads to symptoms characteristic of Parkinsons diseaseCharacteristic Symptoms MOTOR tremor bradykinesia rigidity/freezing in place lack of facial

6、expression postural instability stooped, shuffling gait NONMOTOR diminished sense of smell low voice volume foot cramps sleep disturbance depression constipation droolingConventional Treatments: Medication LEVODOPA (L-DOPA) precursor to dopamine, converted to dopamine by nerve cells in the brain Tre

7、atment with dopamine not possible, because dopamine cant cross blood-brain barrier Generally combined with carbidopa (Sinemet) helps levodopa get to the brain + reduces some side effects Extended use often produces dyskinesias uncontrolled movements (writhing, twitching, shaking) among other minor s

8、ide effectsConventional Treatments: Medication DOPAMINE AGONISTS not changed into dopamine, but rather act LIKE dopamine at brain synapses where dopamine is usually present (nigrostriatal pathways in Parkinsons patients) Used both as adjuncts to L-Dopa therapy and in younger Parkinsons disease patie

9、nts Side effects similar to levodopa, but less likely to develop involuntary movements, more likely to cause hallucinationsConventional Treatments: Medication MAO Inhibitors (Selegiline) COMT Inhibitors AnticholinergicsConventional Treatments: Surgery Thalamotomy Involves destruction of small amount

10、s of tissue in the thalamusmajor center for relaying messages/transmitting sensations Can cause slurred speech and lack of coordination Pallidotomy electric current used to destroy small amount of tissue in the pallidum (globus pallidus) May improve tremors, rigidity by interrupting pathway between

11、globus pallidus and thalamus Conventional Treatments: Surgery Deep Brain Stimulation implant device, pacemaker-like unit transmits impulses to electrodes placed in subthalamic nucleus Produces same effects of lesion surgeries, but can be turned on and offExperimental Treatment: Surgery Fetal Cell Tr

12、ansplant Therapy stem cells obtained via aborted fetus, grown in culture, transplanted into Parkinsons patient at nigrostriatal pathway New cells establish connections and “replace” cells originally lost, these cells function normally and even produce dopamine Autologous “Self” Transplant analagous

13、to fetal cell transplant, except that precursor nerve cells are taken from patient and coaxed to produce dopamine, then implanted back into original patient Reduces threat of autoimmune response and reduced “controversial baggage” associated with FCT therapyExperimental Treatment: Surgery Retinal Pi

14、gmented Epithelial Cell Transplant Dopamine-producing cells taken from pigmented retinal epithelium Mechanism of transplant analagous to fetal cell transplant therapy If loss of contact from substrate, these cells die Consequently, lower risk of aberrant integrationpossible cause of dyskinesias seen

15、 in some FCT patientsSourcesAminoff, M. (2003). Parkinson Primer: Overview of Parkinsons Disease. Retrieved November 16, 2005, from . This source provided me with the most of the background information necessary in explaining the foundation of the disease. This source was especially helpful in deter

16、mining the characteristic symptoms of the disorder as well as statistics. Freed, C.R., Green, P.E., Breeze, R.E., Tsai, W., DuMouchel, W., Kao, R., Dillon, S., et al. (1994). Transplantation of Embryonic Dopamine Neurons for Severe Parkinsons Disease. New England Journal of Medicine, 344, (7), 710-7

17、19.This source played a large part in writing the actual paper. In this article was information on the background of stem cells, implications in stem cell research, and most beneficial, the actual experimental procedure itself. Lieberman, A. (2004). What is Parkinsons Disease? Retrieved November 14, 2005, from .This source didnt help much background information on the disease, but did help in providing an comprehendable version of the substantia nigra and its role in development of Parkinsons disease. Also beneficial were the figures associated with this source.