Save
Upgrade to remove ads
Busy. Please wait.
Log in with Clever
or
show password
Forgot Password?
Don't have an account?  Sign up 
Sign up using Clever
or
Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account. Your email address is only used to allow you to reset your password. See our Privacy Policy and Terms of Service.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
focusNode
Didn't know it?
click below
 
Knew it?
click below
Don't Know
Remaining cards (0)
Know
0:00
edit
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

Parkinson's disease

Uni of Notts, Neurobiology of disease, second year, topic 3

TermDefinition
Neurodegeneration Progressive loss of neurons via apoptosis, leading to impaired function such as motor, behavioural, or cognitive deficits
How neurodegenerative & psychiatric disorders differ No obvious neuron loss, involve some functional & structural changes. May include developmental defects but will always cause behavioural changes
Role of α-synuclein in Parkinson’s disease Misfolded α-synuclein aggregates into toxic fibrils forming Lewy bodies, contributing to neurodegeneration & neuroinflammation
Structure of α-synuclein *Example: no need to memorise* Small intrinsically disordered protein with amphipathic N-terminus, hydrophobic NAC region (aggregation-prone N-acetylcysteine), & acidic C-terminus
Disorder description of Parkinson's Progressive neurodegenerative involuntary movement disorder with increasing prevalence with age
Epidemiology of Parkinson’s Affects all races equally, ~50% more common in males, second most disabling condition in elderly after osteoarthritis
Main motor symptoms of Parkinson’s (remember at least 5) Bradykinesia, rigidity (akinesia), tremor at rest, postural abnormalities, reduced facial expression, speech disorders, & asymmetrical motor
later-stage symptoms of Parkinson’s Depression, dementia, endocrine dysfunction
Primary neurochemical cause of Parkinson’s Loss of dopamine in the caudal nigrostriatal pathway affecting basal ganglia function
How neurotransmitter loss progresses in Parkinson’s Dopamine is lost in mesolimbic pathways, then hypothalamic, then cortical noradrenaline & ACh systems. Finally neuropeptides are lost from spinal & interneurons in the striatum
Neuromelanin & its purpose in diagnosing Parkinson's Pigment in dopaminergic neurons giving dark colour; its loss reflects degeneration of these neurons
How Parkinson's is detected using imagery PET imaging with DAT ligands shows reduced presynaptic dopamine transporters, but not post-synaptic D2-like receptors
Lewy bodies Intracellular aggregate cores of α-synuclein fibrils disrupting neuronal function & causing dementia in 50% of patients
How α-synuclein affects synaptic function Disrupts vesicle trafficking, inhibits dopamine synthesis enzymes (TH, AADC),& inhibits VMAT then facilitates synaptic vesicle recycling
How dopamine accumulation causes neuronal damage Cytosolic dopamine auto-oxidises to form ROS & redox-positive DA quinones, causing oxidative stress & toxicity
Genetic causes of Parkinson's Rare mutations from familial relations with Parkinson's (e.g. SNCA, LRRK2) lead to protein aggregation or mitochondrial dysfunction
Drug-related environmental factors MPTP from contaminated opioids is converted to MPP+ by MAO-B leading to mitochondrial toxicity. Herbicides like paraquat cause oxidative stress to dopaminergic neurones
How L-DOPA is used to treat Parkinson's Crosses BBB & converted to dopamine in the brain (DA can't cross the BBB) to restore signalling
Carbidopa Administered with DOPA to inhibit peripheral AADC, preventing dopamine formation outside the brain leading to peripheral effects like nausea, anorexia or low blood pressure
Side effects of L-DOPA treament Can still have unwanted side effects like rapid fluctuations between Parkinson's phenotype & peripheral side effects. Side effects worsen progressively if used longterm
Alternative treatments used in Parkinson’s D2-like agonists (e.g. ropinirole), MAO-B/COMT inhibitors (administered with DOPA), & newer adenosine/muscarinic drugs. Potentially neurodegeneration reversing treatments
4 types of movement disorder Upper motor-neuron: Weakness, spasticity, hyperflexia Lower motor-neuron: Weakness, atrophy, hypoflexia Involuntary movement: Uncontrolled movements Cerebellar: poor coordination, ataxia, balance deficits
Created by: Denny12
Popular Neuroscience sets

 

 



Voices

Use these flashcards to help memorize information. Look at the large card and try to recall what is on the other side. Then click the card to flip it. If you knew the answer, click the green Know box. Otherwise, click the red Don't know box.

When you've placed seven or more cards in the Don't know box, click "retry" to try those cards again.

If you've accidentally put the card in the wrong box, just click on the card to take it out of the box.

You can also use your keyboard to move the cards as follows:

If you are logged in to your account, this website will remember which cards you know and don't know so that they are in the same box the next time you log in.

When you need a break, try one of the other activities listed below the flashcards like Matching, Snowman, or Hungry Bug. Although it may feel like you're playing a game, your brain is still making more connections with the information to help you out.

To see how well you know the information, try the Quiz or Test activity.

Pass complete!
"Know" box contains:
Time elapsed:
Retries:
restart all cards