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This deck focuses on 6b Forgetting Memory Disorders Plasticity, giving you a quick way to review the definitions, rules, and examples that matter most for MCAT Psychological Social Foundations.
Study 6b Forgetting Memory Disorders Plasticity in MCAT Psychological Social Foundations with focused flashcards that help you recognize the idea, recall the key rule, and apply it in practice-style prompts.
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What is the decay theory of forgetting?
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Forgetting occurs as memory traces fade with time without use. This theory posits that unused memories naturally weaken and fade over time without interference or retrieval issues.
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This deck focuses on 6b Forgetting Memory Disorders Plasticity, giving you a quick way to review the definitions, rules, and examples that matter most for MCAT Psychological Social Foundations.
Work through these flashcards in short sessions. Try to answer each prompt before flipping the card, then revisit any cards you miss until the explanation feels automatic.
Answer: Forgetting occurs as memory traces fade with time without use. This theory posits that unused memories naturally weaken and fade over time without interference or retrieval issues.
Answer: Declarative (explicit) long-term memory formation. Hippocampal damage prevents conscious memory formation.
Answer: Unconscious blocking of anxiety-provoking memories from awareness. Freud's concept of defensive forgetting of traumatic content.
Answer: Proactive interference. Old French knowledge interferes with new Spanish learning.
Answer: Beta-amyloid plaques and neurofibrillary tangles (tau). Protein aggregates disrupt neural function and cause cell death.
Answer: Old information disrupts recall of newly learned information. Prior learning interferes forward in time with new material.
Answer: Old learning disrupts recall of newly learned information. Earlier material interferes forward with later learning.
Answer: Retrieval improves when encoding and retrieval contexts match. Context similarity between learning and recall enhances memory.
Answer: Korsakoff syndrome. Chronic alcohol abuse depletes thiamine, damaging mammillary bodies.
Answer: Unconscious repression of distressing thoughts or memories. Defense mechanism pushes threatening content from awareness.
Answer: Post-event information distorts memory for the original event. Leading questions or false details contaminate original memory.
Answer: Explicit (declarative) long-term memory formation. Hippocampal damage impairs conscious fact/event memory.
Answer: Better recall for last items; primarily due to short-term memory. Recent items remain active in working memory buffer.
Answer: Memory traces fade over time when not used. Decay theory proposes memories weaken through disuse over time.
Answer: Beta-amyloid plaques and neurofibrillary tangles (tau). Protein aggregates disrupt neural function and cause cell death.
Answer: Retrieval practice improves later recall more than restudying. Active recall strengthens memory pathways better than passive review.
Answer: Long-lasting increase in synaptic strength after repeated activation. Cellular mechanism underlying learning and memory formation.
Answer: Post-event information distorts memory for the original event. Leading questions or false details contaminate original memory.
Answer: State-dependent memory. Mood or physiological state acts as retrieval cue.
Answer: Progressive impairment in recent episodic memory. Difficulty forming new memories while older memories remain intact.
Answer: Recall improves when the retrieval environment matches the encoding context. Matching physical environments between encoding and retrieval enhances memory performance.
Answer: Reactivated memories become labile and are stored again with updates. Retrieved memories enter a malleable state before re-storage.
Answer: Last items remain in working (short-term) memory at recall. No interference from subsequent items when recall begins immediately.
Answer: Mood biases recall toward memories with matching emotional valence. Current mood facilitates recall of similarly-valenced memories.
Answer: Proactive interference. Old information interferes forward with new learning.
Answer: Post-event information alters memory for the original event. Leading questions can implant false details that become part of memory.
Answer: Amnestic disorder due to thiamine deficiency, often from alcoholism. Vitamin B1 deficiency damages memory circuits in chronic alcoholics.
Answer: Unintentional fabrication of memories to fill recall gaps. Patient believes false memories are real; common in Korsakoff's.
Answer: Memory traces weaken over time when not accessed or rehearsed. Unused memories fade through biological degradation processes.
Answer: Hippocampus (medial temporal lobe). Damage here causes severe anterograde amnesia, as in patient H.M.
Answer: Thiamine (vitamin B1) deficiency, often due to alcoholism. Chronic alcohol depletes thiamine, damaging memory circuits.
Answer: Thiamine (extB1) deficiency, often due to chronic alcoholism. Vitamin deficiency damages memory circuits in chronic drinkers.
Answer: Persistent strengthening of synapses after repeated stimulation. Cellular basis of learning through enhanced synaptic transmission.
Answer: Expectant: universal input; Dependent: individual learning/experience. Species-typical vs individually-variable environmental inputs.
Answer: Enhanced recall for last items because they remain in working memory. Final items linger in short-term memory, allowing easier immediate retrieval.
Answer: Context-dependent memory. Environmental cues present during encoding aid retrieval.
Answer: Temporary inability to retrieve a known word or name. Feeling of knowing without successful retrieval access.
Answer: Elimination of weak synapses to increase network efficiency. Refines neural circuits by removing unnecessary connections.
Answer: The nervous system's capacity to change structure and function. Enables learning, memory, and recovery through synaptic reorganization.
Answer: Older information disrupts recall of newer information. Old learning interferes forward in time with new learning.
Answer: Decay theory. Memories fade without use, like unused neural pathways weakening.
Answer: Last items remain in working memory at time of recall. Recent items still active in short-term/working memory.
Answer: Repression is unconscious; suppression is conscious. Both block memories, but suppression involves conscious effort.
Answer: New information interferes with recalling previously learned information. Recently learned information overwrites or blocks access to older memories.
Answer: Unconscious blocking of anxiety-provoking thoughts or memories. Defense mechanism prevents conscious access to threatening content.
Answer: Recall improves when retrieval cues match conditions present at encoding. Memory is best when learning and testing contexts align.
Answer: Hippocampus (medial temporal lobe). Critical for consolidating short-term to long-term declarative memory.
Answer: Defense mechanism: unconscious blocking of anxiety-provoking content. Freudian concept of motivated forgetting of trauma.
Answer: Persistent strengthening of synapses after repeated activation. Cellular mechanism underlying learning and memory formation.
Answer: Tip-of-the-tongue phenomenon. This state involves temporary inability to fully access known information despite partial recall.
Answer: Cortical remapping (experience-dependent neuroplasticity). Brain areas adapt function when input changes dramatically.
Answer: Temporary inability to retrieve a known word or name. Partial activation without full retrieval access.
Answer: Forgetting due to competition between memories during retrieval. Other memories interfere with accessing the target memory.
Answer: Unintentional fabrication of memories to fill gaps in recall. Brain creates false memories to maintain coherent narrative despite gaps.
Answer: Information is stored but cannot be accessed due to missing cues. Memory exists but lacks retrieval pathways or triggers.
Answer: Recall improves when retrieval context matches encoding context. Environmental cues from learning enhance memory retrieval.
Answer: Unintentional fabrication of memories to fill in memory gaps. Brain creates false memories to maintain coherent narrative despite gaps.
Answer: Creation of new neurons; notably in the hippocampal dentate gyrus. Adult brain generates new cells for learning and memory.
Answer: Loss of previously formed memories, especially near the causal event. Memories prior to the amnesia-inducing event are lost, with recent ones most affected.
Answer: Newer information disrupts recall of older information. New learning interferes backward in time with old memories.
Answer: Practicing recall of some items suppresses related competing items. Selective practice creates competition between related memories.
Answer: Unconscious blocking of anxiety-provoking memories. Defense mechanism protecting ego from traumatic content.
Answer: New information disrupts recall of previously learned information. Like trying to remember old phone numbers after learning new ones.
Answer: Amyloid-β plaques and neurofibrillary tangles (tau). Protein aggregates disrupt neural function and cause cell death.
Answer: More rehearsal leads to better encoding into long-term memory. Early items get more rehearsal time before capacity limits.
Answer: Old information interferes with learning or recalling new information. Prior knowledge disrupts the acquisition or recall of newer, similar material.
Answer: Unconscious fabrication of memories to fill gaps in recall. False memories are created unintentionally to compensate for genuine recall deficits.
Answer: Hippocampus (medial temporal lobe). Critical for consolidating short-term to long-term memories.
Answer: Amyloid-β plaques and neurofibrillary tangles (tau). Protein deposits disrupt neural function and cause dementia.
Answer: Beta-amyloid plaques and neurofibrillary tangles (tau). Plaques disrupt neural communication; tangles kill neurons.
Answer: Unintentional fabrication of memories to fill gaps in recall. Patients create false memories without intent to deceive.
Answer: Misinformation effect. False details from others contaminate original memory traces.
Answer: Hippocampus (medial temporal lobe). Critical for consolidating new explicit memories into cortical storage.
Answer: Progressive neurodegeneration with prominent episodic memory loss. Neurodegenerative disease starting with hippocampal damage affecting recent memories.
Answer: New information disrupts recall of previously learned information. Recent learning interferes backward in time with older material.
Answer: Better recall for early items; mainly long-term memory encoding. Early items get more rehearsal time for LTM consolidation.
Answer: Unintentional fabrication of memories to fill recall gaps. Brain creates false memories without awareness of inaccuracy.
Answer: Memory traces fade over time when not used or rehearsed. Biological degradation of memory engrams without rehearsal.
Answer: Memory traces fade over time when not actively used. Based on the idea that unused neural connections weaken.
Answer: Vivid, high-confidence memory for an emotional event (not always accurate). Emotional arousal enhances encoding but doesn't guarantee accuracy.
Answer: Better recall for early (primacy) and late (recency) list items. Middle items lack the rehearsal advantage of first or recency of last.
Answer: Old information disrupts learning or recall of new information. Prior learning interferes forward with subsequent learning.
Answer: Formation of new neurons; classically in the hippocampal dentate gyrus. Continues throughout life, supporting learning and memory.
Answer: Failure to retrieve due to absence of cues present during encoding. Retrieval fails when cues from the original learning context are absent.
Answer: Episodic (explicit) memory declines earlier than procedural memory. Declarative recall of personal events is impaired first, with skills affected later.
Answer: Misattributing the origin of a memory (where or how it was learned). Confusing whether you read something or someone told you about it.
Answer: Amyloid-β plaques and neurofibrillary tangles (hyperphosphorylated tau). Protein aggregates disrupt neural function and cause cell death.
Answer: Hippocampus (medial temporal lobe). Critical for transferring short-term to long-term memory.
Answer: Progressive decline in memory and other cognitive functions. Neurodegeneration causes memory loss before other symptoms.
Answer: New information disrupts recall of older information. Recent learning interferes backward with previously learned material.
Answer: Unconscious repression of anxiety-provoking memories. Defense mechanism pushes threatening content from consciousness.
Answer: Thiamine (vitamin B1) deficiency, often due to alcoholism. Chronic alcohol use depletes thiamine, damaging memory circuits.
Answer: Inability to form new long-term memories after the causal event. Post-event brain damage prevents consolidation of new experiences into long-term storage.
Answer: Enhanced recall of late items still held in working memory. Recent items remain active in short-term storage.
Answer: Hippocampus (medial temporal lobe). Critical for consolidating short-term into long-term memories.
Answer: Episodic (declarative) memory for recent events. Hippocampal damage first affects new episodic memory formation.
Answer: Enhanced recall for last items because they remain in working memory. Last items are still active in STM during immediate recall.
Answer: Misattributing the origin of a memory (source confusion). Forgetting where, when, or how information was learned.
Answer: Greater rehearsal leads to better encoding into long-term memory. First items get more rehearsal time before new items arrive.
Answer: Unconscious repression of distressing memories. Defense mechanism pushing traumatic memories from consciousness.