Parkinson's Disease Notes
BLOCK A – PARKINSONS
2012 Class Test
Discuss, with examples, the basis for the use of current and emerging therapeutic strategies to treat Parkinson’s disease.
2011 Class Test
Discuss the role of the ubiquitin-proteasome system and mitochondria in Parkinson’s disease.
2009 Class Test
Discuss, with examples, current and emerging therapeutic strategies used in the treatment of Parkinson’s disease.
2010/11 Exam
Discuss, with examples, the rationale for the use of current and emerging therapeutic strategies in the treatment of Parkinson’s disease.
GENERAL STUFF TO MENTION
What is it?
Neurodegenerative disorder. Occurs due to death of dopamine neurons in the substantia nigra.
Syptoms: Rigidity, pill-rolling, slowness of movement, abnormal gait. Later behavioural and mental problems occur.
Pathology: Lewy bodies (a-synuclein inclusions) and reduced dopamine activity.
No cure.
Who gets it?
Over 50s, usually.
Why do they get it?
Idiopathic disease (no known cause). Mostly genetic, sometimes environmental.
Considerted non-genetic, but small proportion have first degree relative also effected. a-synuclein (SNCA), parkin (PRKN), leaucine-rich repeat kinase 2 (LRRK2), PTEN-induced putative kinase 1 (PINK 1) gene mutations implicated in disease.
SNCA mutations found in familial PD cases.
LRRK2 mutations found in familial and sporadic cases.
Pesticide exposure and head injuries are possible causes.
Drug addicts in California trying to make MPPP, ending up with MPTP imperfections developed PD symptoms within 3 days of taking drug.
Chlorpyrifos and organochloride insecticides are implicated. Rotenone and paraquat pesticides implicated.
Other cool facts to wow marker.
Caffeine consumption and tobacco smoke appear to be neuroprotective against PD.
Treatments
What are they? How do they work? Anything else cool?
DOPA decarboxylase inhibitors (carbidopa; co-careldopa, benserazide; co-beneldopa) – prevent the conversion of levodopa
2012 Class Test
Discuss, with examples, the basis for the use of current and emerging therapeutic strategies to treat Parkinson’s disease.
2011 Class Test
Discuss the role of the ubiquitin-proteasome system and mitochondria in Parkinson’s disease.
2009 Class Test
Discuss, with examples, current and emerging therapeutic strategies used in the treatment of Parkinson’s disease.
2010/11 Exam
Discuss, with examples, the rationale for the use of current and emerging therapeutic strategies in the treatment of Parkinson’s disease.
GENERAL STUFF TO MENTION
What is it?
Neurodegenerative disorder. Occurs due to death of dopamine neurons in the substantia nigra.
Syptoms: Rigidity, pill-rolling, slowness of movement, abnormal gait. Later behavioural and mental problems occur.
Pathology: Lewy bodies (a-synuclein inclusions) and reduced dopamine activity.
No cure.
Who gets it?
Over 50s, usually.
Why do they get it?
Idiopathic disease (no known cause). Mostly genetic, sometimes environmental.
Considerted non-genetic, but small proportion have first degree relative also effected. a-synuclein (SNCA), parkin (PRKN), leaucine-rich repeat kinase 2 (LRRK2), PTEN-induced putative kinase 1 (PINK 1) gene mutations implicated in disease.
SNCA mutations found in familial PD cases.
LRRK2 mutations found in familial and sporadic cases.
Pesticide exposure and head injuries are possible causes.
Drug addicts in California trying to make MPPP, ending up with MPTP imperfections developed PD symptoms within 3 days of taking drug.
Chlorpyrifos and organochloride insecticides are implicated. Rotenone and paraquat pesticides implicated.
Other cool facts to wow marker.
Caffeine consumption and tobacco smoke appear to be neuroprotective against PD.
Treatments
What are they? How do they work? Anything else cool?
DOPA decarboxylase inhibitors (carbidopa; co-careldopa, benserazide; co-beneldopa) – prevent the conversion of levodopa