NEU 2080 - Exam 4 Review

Question-based flashcards pulled directly from the slideshows of Dr. Park's Introduction to Neuroscience course.

What cognitive changes are expected with natural aging?

Slower processing speed, reduced multitasking ability, mild memory decline.

What distinguishes normal aging from neurodegenerative disorders?

Normal aging is slow and mild; rapid or severe decline suggests a neurodegenerative disorder.

What biological changes contribute to cognitive decline in aging?

Reduced synapses, slower signaling, lower neurotransmitters, oxidative stress, DNA/protein damage, mitochondrial changes, reduced plasticity.

What is dementia?

A significant decline in memory and/or cognition that interferes with daily life, often including language, judgment, and problem-solving issues.

Why is early detection of dementia important?

Especially critical for identifying and managing neurodegenerative dementias early.

What are the first clinical steps when dementia is suspected?

Medical history, family history, and cognitive testing.

What follow-up tests are used if dementia is suspected?

Blood tests, MRI/CT scans, and CSF testing for biomarkers like amyloid beta.

Why is genetic testing important in Alzheimer's disease?

Because AD has a strong genetic component.

What is the difference between degenerative and non-degenerative dementia?

Degenerative involves neuron death; non-degenerative involves causes like vascular issues or substances.

What causes vascular dementia?

Stroke or small vessel disease.

What are key symptoms of vascular dementia?

Cognitive impairment plus movement problems, often after a stroke.

How is vascular dementia managed?

Medications targeting vascular health, such as antihypertensives.

What are symptoms of substance-related dementia?

Memory loss, poor attention, balance issues, eye tracking problems, and confabulation.

What is confabulation?

Fabricated memories used to fill gaps, believed to be true by the patient.

How is substance-related dementia treated?

Stop substance use, provide nutrition, and cognitive rehabilitation.

What is Alzheimer's disease (AD)?

A progressive neurodegenerative disorder causing gradual neuron loss.

What is the earliest symptom of AD?

Short-term memory loss (hippocampal damage).

What brain regions are affected later in AD?

Cortical regions, especially the prefrontal cortex.

What are the structural brain changes in AD?

Cortical shrinkage, enlarged ventricles, hippocampal atrophy, synapse loss.

What are the main pathological markers of AD?

Amyloid beta plaques and tau tangles.

What happens to the cholinergic system in AD?

Degeneration reduces acetylcholine levels, impairing memory and learning.

How is acetylcholine produced and broken down?

Produced via choline + acetyl-CoA (choline acetyltransferase); broken down by acetylcholinesterase.

How do AChE inhibitors work?

Prevent acetylcholine breakdown, increasing its availability.

Do AChE inhibitors cure AD?

No, AChE inhibitors only slow progression.

What is glutamate excitotoxicity?

Excess glutamate overstimulates receptors, causing neuron death.

What receptors are involved in glutamate toxicity?

AMPA and NMDA receptors.

How do NMDA antagonists help in AD?

Partially block receptors to reduce toxicity without stopping normal function.

What are major risk factors for AD?

Age (65+), female sex, genetics.

Why are women at higher risk for AD?

Estrogen decline and longer lifespan.

What is the role of APOE in AD?

Clears amyloid beta from the brain.

Which APOE variant increases AD risk?

APOE4.

Which APOE variant is protective?

APOE2.

How can APOE4 carriers reduce risk?

Exercise and stress reduction.

What genes are linked to familial early-onset AD?

APP, PSEN1, PSEN2.

What does APP normally do?

Produces soluble amyloid beta that supports synaptic plasticity.

What happens with APP mutations?

Increased production of toxic insoluble amyloid beta.

What do PSEN1 and PSEN2 mutations do?

Increase beta/gamma secretase activity, promoting plaque formation.

What are current treatments for AD?

AChE inhibitors, NMDA antagonists, psychiatric medications, supportive therapies.

How do anti-amyloid monoclonal antibodies work?

Bind amyloid plaques and promote microglial clearance.

Name examples of anti-amyloid drugs.

Aducanumab, Lecanemab, Donanemab.

Do anti-amyloid therapies reverse AD?

No, anti-amyloid therapies only slow progression.

What is a major challenge in studying AD in humans?

Brain tissue is mostly only available postmortem.

Why is it hard to study early-stage AD in humans?

Early-stage tissue is rarely accessible.

What is the 5xFAD mouse model?

A mouse with five human AD mutations (APP and PSEN1).

What pathology is seen in 5xFAD mice?

Amyloid plaques by 6 months, heavy clustering by 12 months.

What is the relationship between cancer and AD?

Inverse correlation—having one reduces likelihood of the other.

What is the link between Down syndrome and AD?

Extra chromosome 21 increases APP → more amyloid beta → higher AD risk.

What is the function of the corpus callosum?

Connects the two hemispheres for communication.

What happens in split-brain syndrome?

Hemispheres cannot communicate.

How are visual fields processed in the brain?

Left visual field → right hemisphere; right visual field → left hemisphere.

Where are language centers typically located?

Left hemisphere (Broca's and Wernicke's areas).

Why can split-brain patients not name objects in the left visual field?

Information can't cross to the left hemisphere language centers.

Why CAN Split-brain patients name objects in the right visual field?

Information is already in the left hemisphere.

What is bimanual conflict?

Hands are still connected via hemispheres, during task that requires two independent actions, resulting in slower completion time and lack of accuracy.

Why can split-brain patients perform dual drawing tasks better?

Each hemisphere controls one hand independently.

What is the difference between normal aging and dementia?

Aging = mild decline, no major life impairment; Dementia = significant cognitive + functional impairment

What are key symptoms of dementia?

Memory loss + language + judgment + daily function impairment

What are the two types of dementia?

Nondegenerative (vascular, drugs) vs Degenerative (Alzheimer's, Parkinson's, Huntington's)

What are the hallmark symptoms of early Alzheimer's?

Short-term memory loss

What are the hallmark symptoms of late Alzheimer's?

Cognitive decline, behavior changes

What are the key brain changes in Alzheimer's disease?

Amyloid plaques + Tau tangles + brain atrophy

Where does Alzheimer's pathology start?

Hippocampus → spreads to cortex

What neurotransmitter is deficient in Alzheimer's disease?

Acetylcholine

Why is acetylcholine important?

Memory + learning

What do cholinesterase inhibitors do?

Prevent ACh breakdown → improve memory (temporary)

What is the mechanism of Memantine?

NMDA receptor antagonist → reduces glutamate toxicity

What is the strongest genetic risk factor for late Alzheimer's disease?

APOE ε4 allele

What genes are associated with early-onset Alzheimer's disease?

APP, PSEN1, PSEN2

What is the effect of an APP mutation?

↑ amyloid-beta production

How is Down syndrome linked to Alzheimer's disease?

Extra APP gene → ↑ amyloid → early AD

What is the relationship between cancer and Alzheimer's disease?

Inverse association (unclear mechanism)

What is the function of the corpus callosum?

Communication between hemispheres

How does the left vs right visual field process information?

Left field → right brain; Right field → left brain

What is intermanual conflict?

Hands act independently due to lack of hemispheric communication

What is the difference between survival and goal-motivated behavior?

Survival = homeostasis; Goal = reward/dopamine

What is the role of the hypothalamus?

Controls hormones, ANS, hunger, homeostasis

What is ghrelin?

"Hunger hormone" → increases appetite (before meals)

What is leptin?

"Fullness hormone" → decreases appetite (from fat cells)

What neurons does ghrelin target?

Activates NPY/AgRP → ↑ eating

What neurons does leptin target?

Activates POMC → α-MSH → MC4R → ↓ eating

What is the satiety pathway?

Leptin → POMC → α-MSH → MC4R → ↓ appetite

What happens in leptin deficiency?

No satiety → extreme obesity → treat with leptin

What is leptin resistance?

High leptin but brain ignores it → common obesity

What is insulin resistance?

Cells don't respond → high blood glucose

What does Semaglutide (GLP-1 agonist) do?

↓ appetite, ↑ insulin, slows digestion

What is Setmelanotide (Imcivree)?

MC4R agonist → works in POMC deficiency

What is the ob/ob mouse?

No leptin → responds to leptin treatment

What is the db/db mouse?

No leptin receptor → leptin resistance → no response to leptin

What is the POMC-null mouse?

No α-MSH → treat with MC4R agonist

What is the HFD mouse?

Diet-induced obesity → best human model

What is a circadian rhythm?

~24-hour internal biological clock

What are the 3 properties of circadian rhythms?

Self-sustained, entrainable, temperature compensated

Where is the SCN located?

Hypothalamus (above optic chiasm)

What is the function of the SCN?

Master clock controlling rhythms

How does light reset the clock?

Retinohypothalamic tract → SCN

What are core clock genes?

CLOCK + BMAL1 → ↑ PER + CRY → inhibit CLOCK/BMAL1 (negative feedback)

What is melatonin?

Released at night → sleep

What is cortisol?

Morning → wakefulness

Why does morning light matter?

Resets clock to 24h cycle

What does PER3 5R/5R indicate?

Morning person