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Memory tricks for the brain & nervous system

From cranial nerves to neurotransmitters β€” neuroscience is full of lists that beg for mnemonics. These memory tricks lock in brain structures, action potentials, and nervous system divisions for your next exam.

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🧠 Neuroscience

Memory Tricks

Proven mnemonics — fast to learn, hard to forget.

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Cranial Nerves
Oh Oh Oh To Touch And Feel Very Good Velvet β€” AH! β€” Olfactory, Optic, Oculomotor, Trochlear, Trigeminal, Abducens, Facial, Vestibulocochlear, Glossopharyngeal, Vagus, Accessory, Hypoglossal
12 cranial nerves in order β€” one of the most tested lists in neuroscience
The 12 cranial nerves in order: I Olfactory (smell), II Optic (vision), III Oculomotor (eye movement), IV Trochlear (eye down/in), V Trigeminal (face sensation/chewing), VI Abducens (eye lateral), VII Facial (facial expression/taste), VIII Vestibulocochlear (hearing/balance), IX Glossopharyngeal (taste/swallowing), X Vagus (parasympathetic/organs), XI Accessory (neck/shoulder muscles), XII Hypoglossal (tongue).
πŸ“– Full Lesson β†’Difficulty: Intermediate
Sensory, Motor, or Both?
Some Say Marry Money But My Brother Says Big Brains Matter More. S=Sensory, M=Motor, B=Both. CN I,II,VIII = purely sensory. CN III,IV,VI,XI,XII = purely motor. CN V,VII,IX,X = both.
Most commonly tested nerves
Vagus (CN X): longest cranial nerve, parasympathetic to heart/lungs/gut. Trigeminal (CN V): largest cranial nerve, three branches (ophthalmic, maxillary, mandibular). Facial (CN VII): damaged in Bell's palsy β€” unilateral facial drooping.
Clinical connections
CN II damage β†’ blindness. CN III damage β†’ drooping eyelid (ptosis), dilated pupil. CN VI damage β†’ can't look laterally. CN VIII damage β†’ deafness or vertigo. CN X damage β†’ hoarse voice, difficulty swallowing.
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πŸƒ Cranial Nerves
Oh Oh Oh To Touch And Feel Very Good Velvet β€” AH!
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πŸƒ Answer
Oh Oh Oh To Touch And Feel Very Good Velvet β€” AH! β€” Olfactory, Optic, Oculomotor, Trochlear, Trigeminal, Abducens, Facial, Vestibulocochlear, Glossopharyngeal, Vagus, Accessory, Hypoglossal
Sensory, Motor, or Both? β€” Some Say Marry Money But My Brother Says Big Brains Matter More. S=Sensory, M=Motor, B=Both. CN I,II,VIII = purely sensory. CN III,IV,VI,XI,XII = purely motor. CN V,VII,IX,X = both.
Most commonly tested nerves β€” Vagus (CN X): longest cranial nerve, parasympathetic to heart/lungs/gut. Trigeminal (CN V): largest cranial nerve, three branches (ophthalmic, maxillary, mandibular). Facial (CN VII): damaged in Bell's palsy β€” unilateral facial drooping.
Clinical connections β€” CN II damage β†’ blindness. CN III damage β†’ drooping eyelid (ptosis), dilated pupil. CN VI damage β†’ can't look laterally. CN VIII damage β†’ deafness or vertigo. CN X damage β†’ hoarse voice, difficulty swallowing.
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Brain Lobes
FTOP β€” Frontal (executive), Temporal (hearing/memory), Occipital (vision), Parietal (sensation/spatial)
Four cerebral lobes and their primary functions
The cerebrum has four lobes: Frontal lobe β€” executive function, decision-making, motor control, Broca's area (speech production). Temporal lobe β€” auditory processing, memory (hippocampus), Wernicke's area (language comprehension). Occipital lobe β€” visual processing. Parietal lobe β€” somatosensory processing, spatial awareness, body position.
πŸ“– Full Lesson β†’Difficulty: Beginner
Broca's vs Wernicke's
Broca's area (frontal lobe): speech production. Damage β†’ Broca's aphasia: can understand but can't speak fluently. Wernicke's area (temporal lobe): language comprehension. Damage β†’ Wernicke's aphasia: fluent but meaningless speech.
Motor and sensory cortex
Primary motor cortex: posterior frontal lobe, controls voluntary movement. Primary somatosensory cortex: anterior parietal lobe, receives touch/pain/temp signals. Homunculus: distorted body map on cortex β€” hands and lips have largest representation.
Limbic system
Includes hippocampus (memory formation), amygdala (fear/emotion), hypothalamus (homeostasis), cingulate gyrus (attention/emotion). H.M. case: bilateral hippocampus removal β†’ couldn't form new long-term memories.
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πŸƒ Brain Lobes
FTOP
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πŸƒ Answer
FTOP β€” Frontal (executive), Temporal (hearing/memory), Occipital (vision), Parietal (sensation/spatial)
Broca's vs Wernicke's β€” Broca's area (frontal lobe): speech production. Damage β†’ Broca's aphasia: can understand but can't speak fluently. Wernicke's area (temporal lobe): language comprehension. Damage β†’ Wernicke's aphasia: fluent but meaningless speech.
Motor and sensory cortex β€” Primary motor cortex: posterior frontal lobe, controls voluntary movement. Primary somatosensory cortex: anterior parietal lobe, receives touch/pain/temp signals. Homunculus: distorted body map on cortex β€” hands and lips have largest representation.
Limbic system β€” Includes hippocampus (memory formation), amygdala (fear/emotion), hypothalamus (homeostasis), cingulate gyrus (attention/emotion). H.M. case: bilateral hippocampus removal β†’ couldn't form new long-term memories.
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Action Potential
ReDePo β€” Resting, Depolarization, Repolarization β€” then Hyperpolarization (undershoot)
Resting β†’ stimulus β†’ Na⁺ in β†’ K⁺ out β†’ reset
Action potential steps: Resting potential (βˆ’70mV, Na⁺/K⁺ pump maintains). Depolarization β€” stimulus opens voltage-gated Na⁺ channels, Na⁺ rushes IN, membrane reaches +40mV. Repolarization β€” Na⁺ channels close, K⁺ channels open, K⁺ rushes OUT. Hyperpolarization β€” brief undershoot below βˆ’70mV (refractory period). Na⁺/K⁺ pump restores resting potential.
πŸ“– Full Lesson β†’Difficulty: Intermediate
All-or-nothing principle
Once threshold (βˆ’55mV) is reached, action potential fires at full strength every time β€” no partial action potentials. Stimulus strength coded by frequency of firing, not size of action potential.
Refractory period
Absolute refractory: Na⁺ channels inactivated β€” no action potential possible regardless of stimulus. Relative refractory: K⁺ channels still open β€” stronger stimulus can fire AP. Ensures one-way propagation.
Saltatory conduction
Myelinated neurons: action potential jumps node to node (nodes of Ranvier) β€” much faster than unmyelinated. Multiple sclerosis: myelin degradation β†’ slowed/blocked conduction β†’ neurological symptoms.
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πŸƒ Action Potential
Action potential β€” the phases?
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πŸƒ Answer
ReDePo β€” Resting, Depolarization, Repolarization β€” then Hyperpolarization (undershoot)
All-or-nothing principle β€” Once threshold (βˆ’55mV) is reached, action potential fires at full strength every time β€” no partial action potentials. Stimulus strength coded by frequency of firing, not size of action potential.
Refractory period β€” Absolute refractory: Na⁺ channels inactivated β€” no action potential possible regardless of stimulus. Relative refractory: K⁺ channels still open β€” stronger stimulus can fire AP. Ensures one-way propagation.
Saltatory conduction β€” Myelinated neurons: action potential jumps node to node (nodes of Ranvier) β€” much faster than unmyelinated. Multiple sclerosis: myelin degradation β†’ slowed/blocked conduction β†’ neurological symptoms.
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Neurotransmitters
GASSED β€” GABA, Acetylcholine, Serotonin, Substance P, Endorphins, Dopamine
6 major neurotransmitters and their primary roles
Key neurotransmitters: GABA (inhibitory β€” reduces neuronal excitability, anxiety relief). Acetylcholine (neuromuscular junction, learning, parasympathetic). Serotonin (mood, sleep, appetite β€” low levels linked to depression). Substance P (pain transmission). Endorphins (natural pain relief, euphoria). Dopamine (reward, motivation, motor control β€” low in Parkinson's, dysregulated in schizophrenia).
πŸ“– Full Lesson β†’Difficulty: Intermediate
Excitatory vs Inhibitory
Excitatory (increase chance of action potential): glutamate (most common excitatory), acetylcholine, dopamine, norepinephrine. Inhibitory (decrease chance): GABA (most common inhibitory), glycine. Effect depends on receptor, not just neurotransmitter.
Clinical connections
Depression: low serotonin/norepinephrine β†’ SSRIs block reuptake. Parkinson's: low dopamine (substantia nigra) β†’ tremors, rigidity. Alzheimer's: low acetylcholine. Anxiety: low GABA β†’ benzodiazepines enhance GABA. Schizophrenia: excess dopamine hypothesis.
Synapse mechanics
AP arrives at terminal β†’ Ca²⁺ channels open β†’ vesicles fuse β†’ neurotransmitter released into synaptic cleft β†’ binds postsynaptic receptors β†’ reuptake or enzymatic degradation. Cocaine blocks dopamine reuptake β€” excess dopamine in cleft.
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πŸƒ Neurotransmitters
GASSED
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πŸƒ Answer
GASSED β€” GABA, Acetylcholine, Serotonin, Substance P, Endorphins, Dopamine
Excitatory vs Inhibitory β€” Excitatory (increase chance of action potential): glutamate (most common excitatory), acetylcholine, dopamine, norepinephrine. Inhibitory (decrease chance): GABA (most common inhibitory), glycine. Effect depends on receptor, not just neurotransmitter.
Clinical connections β€” Depression: low serotonin/norepinephrine β†’ SSRIs block reuptake. Parkinson's: low dopamine (substantia nigra) β†’ tremors, rigidity. Alzheimer's: low acetylcholine. Anxiety: low GABA β†’ benzodiazepines enhance GABA. Schizophrenia: excess dopamine hypothesis.
Synapse mechanics β€” AP arrives at terminal β†’ Ca²⁺ channels open β†’ vesicles fuse β†’ neurotransmitter released into synaptic cleft β†’ binds postsynaptic receptors β†’ reuptake or enzymatic degradation. Cocaine blocks dopamine reuptake β€” excess dopamine in cleft.
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CNS vs PNS
CNS = Brain + Spinal Cord Β· PNS = Everything else (Somatic + Autonomic)
Somatic (voluntary) Β· Autonomic: Sympathetic (fight-or-flight) vs Parasympathetic (rest-and-digest)
CNS: brain + spinal cord β€” integration and command center. PNS: all nerves outside CNS. Somatic PNS: voluntary control of skeletal muscles. Autonomic PNS: involuntary β€” smooth muscle, cardiac muscle, glands. Sympathetic: fight-or-flight (↑heart rate, dilate pupils, ↓digestion). Parasympathetic: rest-and-digest (↓heart rate, constrict pupils, ↑digestion).
πŸ“– Full Lesson β†’Difficulty: Beginner
Sympathetic specifics
Thoracolumbar (T1-L2). Preganglionic: short, releases ACh. Postganglionic: long, releases norepinephrine (except sweat glands β€” ACh). Effects: ↑heart rate, bronchodilation, glycogenolysis, vasoconstriction, pupil dilation, ↓GI motility.
Parasympathetic specifics
Craniosacral (CN III, VII, IX, X + S2-S4). Preganglionic: long, releases ACh. Postganglionic: short, releases ACh. Effects: ↓heart rate, bronchoconstriction, ↑GI motility, pupil constriction, bladder contraction.
Enteric nervous system
Sometimes called the "second brain" β€” intrinsic nervous system of GI (gastrointestinal) tract with 500 million neurons. Can function independently of CNS. Contains as many neurons as spinal cord. Communicates with CNS (central nervous system) via vagus nerve.
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πŸƒ CNS vs PNS
CNS vs PNS β€” what's in each?
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πŸƒ Answer
CNS = Brain + Spinal Cord Β· PNS = Everything else (Somatic + Autonomic)
Sympathetic specifics β€” Thoracolumbar (T1-L2). Preganglionic: short, releases ACh. Postganglionic: long, releases norepinephrine (except sweat glands β€” ACh). Effects: ↑heart rate, bronchodilation, glycogenolysis, vasoconstriction, pupil dilation, ↓GI motility.
Parasympathetic specifics β€” Craniosacral (CN III, VII, IX, X + S2-S4). Preganglionic: long, releases ACh. Postganglionic: short, releases ACh. Effects: ↓heart rate, bronchoconstriction, ↑GI motility, pupil constriction, bladder contraction.
Enteric nervous system β€” Sometimes called the "second brain" β€” intrinsic nervous system of GI (gastrointestinal) tract with 500 million neurons. Can function independently of CNS. Contains as many neurons as spinal cord. Communicates with CNS (central nervous system) via vagus nerve.
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Sleep Stages
1-2-3-REM, repeat β€” "Non-REM climbs down then REM dreams"
N1 (light) β†’ N2 (sleep spindles) β†’ N3 (deep/slow-wave) β†’ REM (dreaming) β€” cycle repeats ~90 min
Sleep cycles through 4 stages repeating ~every 90 minutes. N1: lightest sleep, easily awakened, hypnic jerks. N2: sleep spindles and K-complexes, ~50% of sleep. N3: slow-wave/deep sleep, hardest to wake, memory consolidation, growth hormone release. REM (Rapid Eye Movement): dreaming, muscle atonia, memory consolidation, brain nearly as active as waking.
πŸ“– Full Lesson β†’Difficulty: Beginner
REM details
REM sleep: rapid eye movements, vivid dreams, muscle paralysis (atonia β€” prevents acting out dreams). REM behavior disorder: atonia fails β†’ physically acts out dreams. REM increases across night β€” most REM in last third of sleep. Sleep deprivation β†’ REM rebound.
Sleep disorders
Insomnia: difficulty falling/staying asleep. Sleep apnea: breathing stops repeatedly (OSA most common). Narcolepsy: sudden sleep attacks, cataplexy (muscle tone loss triggered by emotion) β€” hypocretin deficiency. Sleepwalking occurs in N3 (not REM).
Circadian rhythm
~24-hour biological clock controlled by suprachiasmatic nucleus (SCN (suprachiasmatic nucleus)) of hypothalamus. Light β†’ retina β†’ SCN β†’ suppresses melatonin (pineal gland). Melatonin rises at night β†’ promotes sleep. Jet lag/shift work disrupts circadian alignment.
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πŸƒ Sleep Stages
Sleep stages β€” the cycle?
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πŸƒ Answer
1-2-3-REM, repeat β€” "Non-REM climbs down then REM dreams"
REM details β€” REM sleep: rapid eye movements, vivid dreams, muscle paralysis (atonia β€” prevents acting out dreams). REM behavior disorder: atonia fails β†’ physically acts out dreams. REM increases across night β€” most REM in last third of sleep. Sleep deprivation β†’ REM rebound.
Sleep disorders β€” Insomnia: difficulty falling/staying asleep. Sleep apnea: breathing stops repeatedly (OSA most common). Narcolepsy: sudden sleep attacks, cataplexy (muscle tone loss triggered by emotion) β€” hypocretin deficiency. Sleepwalking occurs in N3 (not REM).
Circadian rhythm β€” ~24-hour biological clock controlled by suprachiasmatic nucleus (SCN (suprachiasmatic nucleus)) of hypothalamus. Light β†’ retina β†’ SCN β†’ suppresses melatonin (pineal gland). Melatonin rises at night β†’ promotes sleep. Jet lag/shift work disrupts circadian alignment.
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Neuron Structure
DABS β€” Dendrites (receive), Axon (transmit), Body (soma), Synapse (communicate)
Signals flow: dendrites β†’ soma β†’ axon β†’ axon terminal β†’ synapse
Neuron anatomy: Dendrites β€” tree-like extensions that receive signals from other neurons. Cell body (soma) β€” contains nucleus, integrates signals. Axon hillock β€” where action potential is initiated if threshold is met. Axon β€” transmits electrical signal. Myelin sheath (from Schwann cells in PNS, oligodendrocytes in CNS) β€” speeds conduction. Axon terminals β€” release neurotransmitters into synapse.
πŸ“– Full Lesson β†’Difficulty: Beginner
Neuron types
Sensory (afferent): carry signals from body to CNS. Motor (efferent): carry signals from CNS to muscles/glands. Interneurons: connect neurons within CNS β€” most numerous type. Unipolar (one process), bipolar (two), multipolar (many dendrites β€” most motor neurons).
Glial cells
Astrocytes: BBB (Blood-Brain Barrier) maintenance, nutrient support. Oligodendrocytes: myelin in CNS. Schwann cells: myelin in PNS. Microglia: immune defense of CNS. Ependymal cells: line ventricles, produce CSF (cerebrospinal fluid). Outnumber neurons ~10:1.
Neuroplasticity
Brain's ability to reorganize by forming new neural connections. Hebbian learning: "neurons that fire together, wire together." LTP (Long-Term Potentiation β€” the strengthening of synapses with repeated use) = cellular basis of memory. Occurs throughout life but greatest in childhood.
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πŸƒ Neuron Structure
DABS
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πŸƒ Answer
DABS β€” Dendrites (receive), Axon (transmit), Body (soma), Synapse (communicate)
Neuron types β€” Sensory (afferent): carry signals from body to CNS. Motor (efferent): carry signals from CNS to muscles/glands. Interneurons: connect neurons within CNS β€” most numerous type. Unipolar (one process), bipolar (two), multipolar (many dendrites β€” most motor neurons).
Glial cells β€” Astrocytes: BBB (Blood-Brain Barrier) maintenance, nutrient support. Oligodendrocytes: myelin in CNS. Schwann cells: myelin in PNS. Microglia: immune defense of CNS. Ependymal cells: line ventricles, produce CSF (cerebrospinal fluid). Outnumber neurons ~10:1.
Neuroplasticity β€” Brain's ability to reorganize by forming new neural connections. Hebbian learning: "neurons that fire together, wire together." LTP (Long-Term Potentiation β€” the strengthening of synapses with repeated use) = cellular basis of memory. Occurs throughout life but greatest in childhood.
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Brainstem
MMP β€” Midbrain, Medulla, Pons β€” "Must Monitor Pulse"
Midbrain (reflexes) Β· Pons (breathing/sleep) Β· Medulla (vital functions)
The brainstem connects the brain to the spinal cord with 3 parts: Midbrain β€” visual/auditory reflexes, dopamine production (substantia nigra). Pons β€” breathing rhythm, sleep, relays signals between cerebrum and cerebellum. Medulla oblongata β€” vital functions: heart rate, blood pressure, breathing, vomiting, swallowing. Brainstem death = no spontaneous breathing or reflexes.
πŸ“– Full Lesson β†’Difficulty: Intermediate
Cerebellum
Not part of brainstem but sits behind it. "Little brain" β€” coordinates movement, balance, fine motor control. Damage β†’ ataxia (uncoordinated movement), dysmetria (misjudging distances), intention tremor. Receives input from motor cortex and sensory systems.
Reticular formation
Network throughout brainstem β€” regulates arousal, sleep-wake cycle, attention. RAS (reticular activating system β€” the network that keeps the brain alert) β€” keeps brain alert. Damage β†’ coma. Anesthetics suppress RAS. Caffeine β†’ blocks adenosine (sleep signal) β†’ increased RAS activity.
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πŸƒ Brainstem
MMP
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πŸƒ Answer
MMP β€” Midbrain, Medulla, Pons β€” "Must Monitor Pulse"
Cerebellum β€” Not part of brainstem but sits behind it. "Little brain" β€” coordinates movement, balance, fine motor control. Damage β†’ ataxia (uncoordinated movement), dysmetria (misjudging distances), intention tremor. Receives input from motor cortex and sensory systems.
Reticular formation β€” Network throughout brainstem β€” regulates arousal, sleep-wake cycle, attention. RAS (reticular activating system β€” the network that keeps the brain alert) β€” keeps brain alert. Damage β†’ coma. Anesthetics suppress RAS. Caffeine β†’ blocks adenosine (sleep signal) β†’ increased RAS activity.
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Memory Types
EELS β€” Explicit (Episodic + Semantic), Implicit (Skills + Priming)
Explicit = conscious recall Β· Implicit = unconscious, automatic
Memory types: Explicit (declarative) β€” requires conscious recall. Episodic: personal events ("my graduation"). Semantic: facts/knowledge ("Paris is in France"). Implicit (non-declarative) β€” unconscious. Procedural: motor skills (riding a bike). Priming: prior exposure influences later response. Classical conditioning. Explicit memory requires hippocampus; implicit does not β€” explains why amnesiacs can still learn skills.
πŸ“– Full Lesson β†’Difficulty: Intermediate
Memory stages
Encoding β†’ Storage β†’ Retrieval. Sensory memory: fraction of a second (iconic, echoic). Short-term/working memory: 7Β±2 items, ~20 seconds without rehearsal. Long-term memory: potentially unlimited, indefinite duration. Rehearsal and emotion strengthen long-term storage.
LTP and memory
Long-term potentiation: repeated stimulation strengthens synaptic connections. NMDA (N-methyl-D-aspartate) receptors: require simultaneous pre- and postsynaptic activity ("coincidence detectors"). AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor insertion β†’ stronger synapse. Blocked by alcohol (explains blackouts).
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πŸƒ Memory Types
Memory types β€” explicit vs implicit?
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πŸƒ Answer
EELS β€” Explicit (Episodic + Semantic), Implicit (Skills + Priming)
Memory stages β€” Encoding β†’ Storage β†’ Retrieval. Sensory memory: fraction of a second (iconic, echoic). Short-term/working memory: 7Β±2 items, ~20 seconds without rehearsal. Long-term memory: potentially unlimited, indefinite duration. Rehearsal and emotion strengthen long-term storage.
LTP and memory β€” Long-term potentiation: repeated stimulation strengthens synaptic connections. NMDA (N-methyl-D-aspartate) receptors: require simultaneous pre- and postsynaptic activity ("coincidence detectors"). AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor insertion β†’ stronger synapse. Blocked by alcohol (explains blackouts).
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Hypothalamus Functions
The 4 Fs β€” Feeding, Fighting, Fleeing, mating (the Four F's of survival)
Hunger Β· Aggression Β· Fear response Β· Reproduction β€” plus temperature and homeostasis
The hypothalamus is the master regulator of homeostasis. Controls: body temperature (thermostat of the body), hunger and thirst, sleep-wake cycles (circadian rhythm via SCN), autonomic nervous system, hormone release via pituitary (releasing/inhibiting hormones), emotion and stress responses. Also controls the "4 Fs" β€” feeding, fighting, fleeing, and reproduction.
πŸ“– Full Lesson β†’Difficulty: Intermediate
Hypothalamus-pituitary axis
Hypothalamus releases releasing hormones (CRH (corticotropin-releasing hormone), TRH, GnRH, GHRH) into portal blood β†’ anterior pituitary releases tropic hormones (ACTH, TSH, LH/FSH, GH) β†’ target glands respond. Negative feedback closes the loop. Posterior pituitary stores/releases ADH and oxytocin (made in hypothalamus).
Thermoregulation
Anterior hypothalamus: responds to overheating β€” triggers sweating, vasodilation. Posterior hypothalamus: responds to cold β€” triggers shivering, vasoconstriction. Fever: pyrogens raise hypothalamic set point β†’ body temperature rises to fight infection.
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πŸƒ Hypothalamus Functions
Hypothalamus β€” the 4 Fs?
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πŸƒ Answer
The 4 Fs β€” Feeding, Fighting, Fleeing, mating (the Four F's of survival)
Hypothalamus-pituitary axis β€” Hypothalamus releases releasing hormones (CRH (corticotropin-releasing hormone), TRH, GnRH, GHRH) into portal blood β†’ anterior pituitary releases tropic hormones (ACTH, TSH, LH/FSH, GH) β†’ target glands respond. Negative feedback closes the loop. Posterior pituitary stores/releases ADH and oxytocin (made in hypothalamus).
Thermoregulation β€” Anterior hypothalamus: responds to overheating β€” triggers sweating, vasodilation. Posterior hypothalamus: responds to cold β€” triggers shivering, vasoconstriction. Fever: pyrogens raise hypothalamic set point β†’ body temperature rises to fight infection.
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Neurological Disorders
PASS β€” Parkinson's (dopamine↓), Alzheimer's (ACh↓/plaques), Schizophrenia (dopamine↑), Stroke (FAST)
FAST for stroke: Face drooping, Arm weakness, Speech difficulty, Time to call 911
Major neurological disorders: Parkinson's disease β€” loss of dopamine neurons in substantia nigra β†’ tremor, rigidity, bradykinesia. Alzheimer's β€” amyloid plaques, neurofibrillary tangles, loss of ACh β†’ progressive memory loss. Schizophrenia β€” excess dopamine hypothesis β†’ hallucinations, delusions. Stroke β€” blocked (ischemic) or burst (hemorrhagic) blood vessel β†’ FAST symptoms. Multiple sclerosis β€” myelin destruction β†’ varied neurological deficits.
πŸ“– Full Lesson β†’Difficulty: Advanced
Parkinson's treatment
L-DOPA (crosses blood-brain barrier, converted to dopamine). Dopamine agonists. Deep brain stimulation. Cannot give dopamine directly β€” does not cross BBB. MPTP (toxin) destroys substantia nigra β†’ acute Parkinson's β€” led to discovery of dopamine's role.
Alzheimer's pathology
Amyloid-Ξ² plaques (extracellular) β€” from APP (amyloid precursor protein) cleavage by beta and gamma secretase. Tau tangles (intracellular) β€” hyperphosphorylated tau disrupts microtubules. ApoE4 allele = major genetic risk. Cholinesterase inhibitors (donepezil) slow ACh breakdown β€” symptomatic treatment only.
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πŸƒ Neurological Disorders
PASS
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πŸƒ Answer
PASS β€” Parkinson's (dopamine↓), Alzheimer's (ACh↓/plaques), Schizophrenia (dopamine↑), Stroke (FAST)
Parkinson's treatment β€” L-DOPA (crosses blood-brain barrier, converted to dopamine). Dopamine agonists. Deep brain stimulation. Cannot give dopamine directly β€” does not cross BBB. MPTP (toxin) destroys substantia nigra β†’ acute Parkinson's β€” led to discovery of dopamine's role.
Alzheimer's pathology β€” Amyloid-Ξ² plaques (extracellular) β€” from APP (amyloid precursor protein) cleavage by beta and gamma secretase. Tau tangles (intracellular) β€” hyperphosphorylated tau disrupts microtubules. ApoE4 allele = major genetic risk. Cholinesterase inhibitors (donepezil) slow ACh breakdown β€” symptomatic treatment only.
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