1/59
Vocabulary flashcards for Huntington's Disease and Parkinson's Disease lecture.
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
Neurodegeneration
Progressive damage or death of neurons leading to a gradual deterioration of bodily functions controlled by the affected part of the nervous system.
Hypokinesia
A symptom of brain damage that involves lack of movement.
Hyperkinesia
A symptom of brain damage that involves involuntary excessive movements.
Huntington's Disease (HD)
Inherited neurodegenerative disorder affecting 5-10 people per 100,000, usually fatal after 20 years.
Chorea
Involuntary and irregular movements associated with Huntington's Disease.
Brain changes in HD
Profound, progressive destruction of the basal ganglia, especially the caudate nucleus and putamen, with massive neuronal loss of GABA output from the corpus striatum.
GABA (gamma-aminobutyric acid)
Inhibitory neurotransmitter contributing to motor control; decreased in Huntington's Disease.
Excitotoxicity
Abnormally high concentrations of glutamate leading to over excitation of nerve cells.
Huntingtin
Protein found in cytoplasm; defective form contains elongated stretch of glutamine in Huntington's Disease.
Caspase
'Killer enzyme', triggers apoptosis.
Transgenic mice
Mice with expanded CAG repeat introduced into Huntington's gene.
Synaptic plasticity
Underlies higher cognitive functions (learning, memory).
Brain-derived neurotrophic factor (BDNF)
Biological marker that may be impaired in transgenic mice.
Parkinson's Disease (PD)
2nd most common neurodegenerative disorder after Alzheimer's disease (AD).
Primary Motor Symptoms of PD
Tremor (pill rolling), rigidity, bradykinesia (slowness of movement), postural instability.
Bradykinesia
Slowness of movement.
PD pathology
Loss of dopaminergic cells in the substantia nigra that project to the striatum.
Lewy bodies
Aggregations of mis-folded α -synuclein forming the core.
Neuromelanin
Pigment found abundantly in the substantia nigra.
Dopamine
Inactivated by monoamine oxidase (MAO).
Synthetic L-DOPA
Crosses blood brain barrier (bbb).
Basal Ganglia
Groups of cerebral nuclei that play a role in the control and production of movement.
Dopamine and Basal Ganglia
Dopamine input from substantia nigra is excitatory via direct pathway (D1 receptors) and inhibitory via indirect pathway (D2 receptors).
Neurodegeneration
Progressive damage or death of neurons leading to a gradual deterioration of bodily functions controlled by the affected part of the nervous system.
Hypokinesia
A symptom of brain damage that involves lack of movement.
Hyperkinesia
A symptom of brain damage that involves involuntary excessive movements.
Huntington's Disease (HD)
Inherited neurodegenerative disorder affecting 5-10 people per 100,000, usually fatal after 20 years.
Chorea
Involuntary and irregular movements associated with Huntington's Disease.
Brain changes in HD
Profound, progressive destruction of the basal ganglia, especially the caudate nucleus and putamen, with massive neuronal loss of GABA output from the corpus striatum.
GABA (gamma-aminobutyric acid)
Inhibitory neurotransmitter contributing to motor control; decreased in Huntington's Disease.
Excitotoxicity
Abnormally high concentrations of glutamate leading to over excitation of nerve cells.
Huntingtin
Protein found in cytoplasm; defective form contains elongated stretch of glutamine in Huntington's Disease.
Caspase
'Killer enzyme', triggers apoptosis.
Transgenic mice
Mice with expanded CAG repeat introduced into Huntington's gene.
Synaptic plasticity
Underlies higher cognitive functions (learning, memory).
Brain-derived neurotrophic factor (BDNF)
Biological marker that may be impaired in transgenic mice.
Parkinson's Disease (PD)
2nd most common neurodegenerative disorder after Alzheimer's disease (AD).
Primary Motor Symptoms of PD
Tremor (pill rolling), rigidity, bradykinesia (slowness of movement), postural instability.
Bradykinesia
Slowness of movement.
PD pathology
Loss of dopaminergic cells in the substantia nigra that project to the striatum.
Lewy bodies
Aggregations of mis-folded α -synuclein forming the core.
Neuromelanin
Pigment found abundantly in the substantia nigra.
Dopamine
Inactivated by monoamine oxidase (MAO).
Synthetic L-DOPA
Crosses blood brain barrier (bbb).
Basal Ganglia
Groups of cerebral nuclei that play a role in the control and production of movement.
Dopamine and Basal Ganglia
Dopamine input from substantia nigra is excitatory via direct pathway (D1 receptors) and inhibitory via indirect pathway (D2 receptors).
Alzheimer's Disease (AD)
Results from a triad of increasing amyloid plaques, neurofibrillary tangles, and neuronal loss.
APP
β-amyloid precursor protein; the precursor to amyloid plaques.
γ-secretase
Secretase enzyme, when combined with β-secretase, cleaves APP to yield amyloid β plaques.
Presenilin
Mutations in presenilin genes increases γ-secretase activity.
ApoE4
Apolipoprotein; plays a role in cholesterol transport and strongly implicated in AD.
Neurofibrillary tangles
Fibrous inclusions in cytoplasm of neocortical neurons, correlate with cognitive deficits.
Tau
Main component of neurofibrillary tangles.
AD pathology
Loss of cholinergic neurons in basal forebrain.
AChE inhibitors
Blocks acetylcholinesterase (AChE) activity, increasing the availability of ACh at the synapse.
The neurochemical cause of parkinson's
A progressive loss of nigrostriatal dopamine neurons, causes a loss of motor control.
What are lewy bodies made of?
Alpha-synuclein, parkin, ubiquitin, and several other proteins.
Amyotrophic Lateral Sclerosis (ALS)
A selective and progressive degeneration of motor neurons in the brain and spinal cord.
What casuses ALS?
10% of patients have a genetic cause for this, which may involve mutations to superoxide dismutase.
What are some mechanisms involved in ALS?
Impaired glutamate transport, oxidative stress, protein aggregation, and mitochondrial dysfunction.