Exam 3

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Parkinson’s Disease (PD) is the

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second most common age-related neurodegenerative disorder.

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Approximately (%?) of Parkinson's patients are diagnosed before the age of (): this is called:

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5-10% are diagnosed before the age of 50: this is called early-onset PD.

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Symptoms vary from patient to patient and:

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not everyone is affected by all of them. Rate of disease progression also varies

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The first most common primary symptom of Parkinson's disease is

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Tremors. In the early stages of the disease, 70% of patients experience a slight tremor in the hand, foot or less commonly in the jaw, or face. While body part moves, tremor lost.

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There are secondary symptoms of Parkinson's disease including:

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Pain and loss of energy which is ranked as some of the most debilitating in a survey of PD patients

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The suspected causes of PD include both:

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genetic and environmental factors

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Genetics: about (%?) of Parkinson's patients have (what/who) with Parkinson's.

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about 15-25% of Parkinson's patients have a relative with Parkinson's.

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Researchers have found several genes that are

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risk factors for PD.

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These genes are two of the best characterized known risk factors for PD:

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Parkin and Pink

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SNCA encodes for the protein ( ), which helps create “ ” in the brain, specifically the

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SNCA encodes for the protein alpha-synuclein, which helps create “Lewy bodies” in the brain, specifically the substantia nigra.

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Lewy bodies are

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clumps of alpha synuclein strands bound together.

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In healthy neurons, alpha-synuclein helps

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with synaptic transmission.

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The Parkin gene codes for a protein that transports other ( ) around and helps mark molecules for..., which is called?

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The Parkin gene codes for a protein that transports other molecules around and helps mark molecules for disposal inside the neuron.

- Cellular trafficking

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One proposed mechanism for how Parkin may contribute to PD is this damages the cell’s ability to

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to clear out excess waste proteins leading to the Lewy bodies

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The gene Pink seems to increase free radical production, leading to damage of

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substantia nigra neurons.

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The nigra neurons are especially

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susceptible to damage by Pink.

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The nigra neurons make and secrete ( ) in a pathway to the ( ) in the brain.

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dopamine, the basal ganglia

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This pathway is called the

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nigrostriatal pathway, based on where it begins and ends.

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No symptoms of PD are visible until

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most of the dopamine neurons are gone, up to 70%

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Damage begins

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5-7 years before symptoms appear.

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Most cases of PD do not appear

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to have genetic origins (95% are sporadic)

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Some scientists have suggested that Parkinson's disease may occur when a (...) dopaminergic neurons.

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when a toxin selectivity destroys dopaminergic neurons.

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Has been known for a number of years that several: (...) that can cause Parkinson's-like symptoms, such as ( )

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Has been known for a number of years that several: toxins that can cause Parkinson's-like symptoms, such as MPTP

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MPTP discovered as contaminant in home-made fentanyl

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a drug used illicitly

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treatments

Levodopa is a dopamine ( ), a substance that is converted into dopamine by an ( ).

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Precursor, an enzyme in the substantia nigra neurons.

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Alleviates symptoms for a

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limited amount of time

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Lesioning procedures that provide relief from Parkinson's symptoms are:

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pallidotomy and thalamotomy.

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Pallidotomy can alleviate

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rigidity and bradykinesia symptoms

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thalamotomy helps to

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control tremors

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Deep brain stimulation (DBS) appears to be a

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safer and more effective surgery

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Deep brain stimulation (DBS) generally preferred surgical option because it has the same:

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if not better results than pallidotomy and thalamotomy.

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DBS an electrode implanted in brain, usually on single side:

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into either the thalamus or subthalamic nucleus

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AD numbers Americans:

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Fifteen years ago: roughly 500 thousand Americans had AD

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Current AD numbers for Americans:

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5.8 million Americans currently have AD, 1% 60 yrs old, doubles every 5 yrs of age

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AD numbers estimate:

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by 2050 could be 15 million in the US

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AD numbers worldwide:

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estimated that more than 35 million people currently have AD

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Genetic studies for AD show:

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Two main types of AD: Early-onset AD is rare, affecting people 30 to 64 years old. Late-onset AD more common. It affects people over age 65.

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AD and the brain:

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First neural changes in hippocampus & cholinergic basal forebrain

Affected areas shrink as neurons die, are the tangles which are inside the cells

Plaques across neocortex at first

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Changes begin decades before symptoms

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20% of 35 yr old's had some tangles and plaques (Braak scale)

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Mild AD can include

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confusion, poor judgment & mood changes

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Moderate AD can include

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problems recognizing people, language and thought difficulty, and wandering

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Insevere AD

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extreme shrinkage occurs in the brain.

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AD Symptoms include many:

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weight loss, much memory loss, bladder and bowel control loss and others

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AD, the underlying mechanism

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Tauists vs. BAPtists, most important underlying "cause" of AD debated: Tau tangles inside neurons vs B-APP (Beta-amyloid precursor protein) extra-cellular

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Dr.Tanzi found early AD risk genes:

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BAPtist proponent, Amyloid precursor protein (APP)

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Dr. Allen Roses discovered the risk factor of having a gene type that codes for:

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APOE, a cholesterol carrying protein is a "Tauist" Epsilon 4 allele = higher risk, thought this may be involved with clearing out excess Beta-amyloid

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AD Diagnosis to death

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about 7 years

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Amyloid precursor protein (APP)

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Associated with synaptic function, Beta-amyloid plaques which interfere with synapses

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Tangles are

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inside neurons

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Acetylcholine

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is responsible for muscular contracts

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Memory acetylcholine is important

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in the brain for learning and forming new memories

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It is important to determine whether:

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plaques or tangles are the primary causal factors, or potentially other factors

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Another brain change has been observed in AD:

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a decrease in acetylcholine neurons in the basal forebrain

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Four of the five drugs currently approved to treat AD:

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enhance acetylcholine neurotransmission, they slow breakdown of acetylcholine

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Acetylcholine staining in the brain correlates well with:

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memory performance

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Isaacson has proposed that acetylcholine enhances the production of:

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the "good" amyloid

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Lack of acetylcholine increases:

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the "bad" amyloid

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Nerve growth factor (NGF) and Brain-Derived Neurotrophic Factor (BDNF) both stimulate

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acetylcholine synthesis, improve memory in aged animals

- Trophic factors for brain cells

- Specific to certain subset of neurons, cholinergic neurons

- NGF in Aging/AD

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The Protected Brain

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Neurotrophins are nutrients for the brain

Protected by the skull, meninges

Immune system separate

Protected from substances in circulation by the blood-brain-barrier

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Neural activity Long-term potentiation (LTP):

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using neurons, cognition

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Rita Levi-Montalcini:

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discovered NGF

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Once NGF is increased

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its effects seem to last for long term

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What increases endogenous NGF/BDNF?

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(Nerve growth factor, Brain-derived neurotrophic factor) - Physical exercise

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Stroke symptoms the public should know:

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1. Severe headaches 2. change in vision 3. Change in speech 4. lateralized weakness or numbness 5. Generally, sudden change in behavior

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F.A.S.T.:

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Facedrooping, arms not being able, speech, time to call

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80% of strokes are:

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ischemic infarcts

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Ischemia:

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reduction of blood flow, leading to infarction

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20% of strokes are:

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hemorrhagic: bleeding

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Primary pathogenic feature is

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disruption of supply of nutrients (oxygen and glucose) to the brain, resulting from disrupted blood flow

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Thrombus

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blood clot that forms inside a blood vessel - building up fat deposits

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Middle cerebralartery (MCA)

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Site for 2/3 of strokes

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Broca’s aphasia

Nonfluent language output

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• reducedin phrase length & complexity

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Broca’s aphasia

Agrammatism:

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• poorsentence structure – no articles, modifiers, complex verb forms.

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Broca’s aphasia

Language comprehension

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• adequate,but rarely normal – can respond to simple commands

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Wernicke’s aphasia •

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• Language output: fluent – normal phrase length, using all grammatical elements

• Content may be paraphasic or empty.

• Phonemic paraphasia: “smoon” for “spoon”

• Semantic paraphasia: “cup” for “spoon” • Neologism: “snopel”

• Empty speech: like, thing, stuff, you know • Language comprehension: poor

• Naming: poor

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Right hemisphere damage:

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Neglect

• Most often due to damaged posterior parietal lobe.

• Inability to respond to or acknowledge stimuli present in left hemispace.

• Attentional neglect – failure to attend to stimuli in left hemispace

• Even in absence of neglect, when shown stimuli in both visual fields, patients will “extinguish” stimuli in left visual field.

• Representational neglect – loss of internal mental representation of space opposite side of lesion (e.g., Milan square, baseball diamond, Golden Gate Bridge).

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Intentional – reduced/delayed movements to contra-lesional side

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lack of response to stimuli on left side.

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Other effects of right-hemisphere stroke

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• Visuospatial impairment

• Motor impersistence – inability to maintain a posture.

• Aprosody of language – inability to produce intonation required for adequate speech.

• Anosognosia – unawareness or denial of a deficit

• Patients with RH lesions have poorer outcomes than LH patients.

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Hemorrhagic strokes

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• Can be within brain itself (Intracerebral) or beneath coverings of brain (subdural or subarachnoid).

• Rupture of arteries.

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Most common cause is hypertension (~80% of cases)

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high pressure causes wear & tear.

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• Other causes:

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• Anti-coagulation drugs or diseases that impair coagulation.

• Closed head injuries.

• Arteriovenous malformation – congenital, tangled bundle of arteries & veins.

• Aneurysms

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Most commonly occurs in

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• deep, small arteries of brain – not in MCA, ACA, or PCA areas.

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Most commonly rupture age

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• 40-70

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Most commonly occurs on

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anterior communicating artery (ACoA), in the Circle of Willis.

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ACoA supplies the basal forebrain, but also

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• important for memory function.

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The second primary symptom of Parkinson’s disease it

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Rigidity: stiffness or inflexibility of muscles.

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The third primary symptom of Parkinson’s disease is

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Bradykinesia: is slowing of voluntary movement, especially from resting position

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The fourth primary symptom of Parkinson’s disease is

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postural problems: maintaining standing posture difficult

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Substaniainomnota:

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the nonnamed substance

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The cerebral cortex for AD

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limbicsystem shrinks