Forgetting, Memory Disorders, and Neural Plasticity (6B) - Psych & Soc

1. What is the decay theory of forgetting?

   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.

2. Which memory system is most impaired in patient H.M.-type cases?

   Declarative (explicit) long-term memory formation. Hippocampal damage prevents conscious memory formation.

3. What is motivated forgetting (repression) in psychodynamic theory?

   Unconscious blocking of anxiety-provoking memories from awareness. Freud's concept of defensive forgetting of traumatic content.

4. Identify the forgetting mechanism: old French vocabulary impairs learning Spanish words.

   Proactive interference. Old French knowledge interferes with new Spanish learning.

5. What are the two classic pathological findings in Alzheimer disease?

   Beta-amyloid plaques and neurofibrillary tangles (tau). Protein aggregates disrupt neural function and cause cell death.

6. What is proactive interference?

   Old information disrupts recall of newly learned information. Prior learning interferes forward in time with new material.

7. What is proactive interference in forgetting?

   Old learning disrupts recall of newly learned information. Earlier material interferes forward with later learning.

8. What is the encoding specificity principle?

   Retrieval improves when encoding and retrieval contexts match. Context similarity between learning and recall enhances memory.

9. What memory disorder is classically caused by thiamine (vitamin $B_1$) deficiency?

   Korsakoff syndrome. Chronic alcohol abuse depletes thiamine, damaging mammillary bodies.

10. What is motivated forgetting in psychoanalytic theory?

    Unconscious repression of distressing thoughts or memories. Defense mechanism pushes threatening content from awareness.

11. What is the misinformation effect in eyewitness memory?

    Post-event information distorts memory for the original event. Leading questions or false details contaminate original memory.

12. Which memory system is most impaired in patient H.M.-type anterograde amnesia?

    Explicit (declarative) long-term memory formation. Hippocampal damage impairs conscious fact/event memory.

13. What is the recency effect, and which memory store mainly explains it?

    Better recall for last items; primarily due to short-term memory. Recent items remain active in working memory buffer.

14. Which forgetting mechanism is described by the decay theory?

    Memory traces fade over time when not used. Decay theory proposes memories weaken through disuse over time.

15. Which two pathological findings are most associated with Alzheimer disease?

    Beta-amyloid plaques and neurofibrillary tangles (tau). Protein aggregates disrupt neural function and cause cell death.

16. What is the testing effect in learning and memory?

    Retrieval practice improves later recall more than restudying. Active recall strengthens memory pathways better than passive review.

17. What is long-term potentiation (LTP) in neural plasticity?

    Long-lasting increase in synaptic strength after repeated activation. Cellular mechanism underlying learning and memory formation.

18. What is the misinformation effect in eyewitness memory research?

    Post-event information distorts memory for the original event. Leading questions or false details contaminate original memory.

19. Identify the memory phenomenon: better recall when internal state at retrieval matches encoding.

    State-dependent memory. Mood or physiological state acts as retrieval cue.

20. What is the typical early cognitive symptom of Alzheimer disease?

    Progressive impairment in recent episodic memory. Difficulty forming new memories while older memories remain intact.

21. What is context-dependent memory?

    Recall improves when the retrieval environment matches the encoding context. Matching physical environments between encoding and retrieval enhances memory performance.

22. What is reconsolidation in memory?

    Reactivated memories become labile and are stored again with updates. Retrieved memories enter a malleable state before re-storage.

23. What cognitive mechanism best explains the recency effect?

    Last items remain in working (short-term) memory at recall. No interference from subsequent items when recall begins immediately.

24. What is mood-congruent memory?

    Mood biases recall toward memories with matching emotional valence. Current mood facilitates recall of similarly-valenced memories.

25. Identify the forgetting type: old phone number makes new number hard to recall.

    Proactive interference. Old information interferes forward with new learning.

26. What is the misinformation effect in eyewitness memory?

    Post-event information alters memory for the original event. Leading questions can implant false details that become part of memory.

27. What is Korsakoff syndrome and what is its classic cause?

    Amnestic disorder due to thiamine deficiency, often from alcoholism. Vitamin B1 deficiency damages memory circuits in chronic alcoholics.

28. What is confabulation in memory disorders?

    Unintentional fabrication of memories to fill recall gaps. Patient believes false memories are real; common in Korsakoff's.

29. What is decay theory of forgetting?

    Memory traces weaken over time when not accessed or rehearsed. Unused memories fade through biological degradation processes.

30. Which brain structure is most critical for forming new declarative memories?

    Hippocampus (medial temporal lobe). Damage here causes severe anterograde amnesia, as in patient H.M.

31. What is Korsakoff syndrome most classically caused by?

    Thiamine (vitamin $B_1$) deficiency, often due to alcoholism. Chronic alcohol depletes thiamine, damaging memory circuits.

32. What is Korsakoff syndrome most classically associated with?

    Thiamine ($\text{B}_1$) deficiency, often due to chronic alcoholism. Vitamin deficiency damages memory circuits in chronic drinkers.

33. What is long-term potentiation (LTP)?

    Persistent strengthening of synapses after repeated stimulation. Cellular basis of learning through enhanced synaptic transmission.

34. What is the key distinction between experience-expectant and experience-dependent plasticity?

    Expectant: universal input; Dependent: individual learning/experience. Species-typical vs individually-variable environmental inputs.

35. What is the recency effect?

    Enhanced recall for last items because they remain in working memory. Final items linger in short-term memory, allowing easier immediate retrieval.

36. Identify the memory phenomenon: better recall when retrieval context matches encoding context.

    Context-dependent memory. Environmental cues present during encoding aid retrieval.

37. What is the tip-of-the-tongue (TOT) phenomenon?

    Temporary inability to retrieve a known word or name. Feeling of knowing without successful retrieval access.

38. What is synaptic pruning in neural development and plasticity?

    Elimination of weak synapses to increase network efficiency. Refines neural circuits by removing unnecessary connections.

39. What is neural plasticity?

    The nervous system's capacity to change structure and function. Enables learning, memory, and recovery through synaptic reorganization.

40. What is proactive interference?

    Older information disrupts recall of newer information. Old learning interferes forward in time with new learning.

41. Identify the forgetting concept: memories become less accessible over time due to lack of rehearsal.

    Decay theory. Memories fade without use, like unused neural pathways weakening.

42. What is the recency effect attributed to in memory research?

    Last items remain in working memory at time of recall. Recent items still active in short-term/working memory.

43. What is the difference between repression and suppression?

    Repression is unconscious; suppression is conscious. Both block memories, but suppression involves conscious effort.

44. What is retroactive interference?

    New information interferes with recalling previously learned information. Recently learned information overwrites or blocks access to older memories.

45. What is repression in psychodynamic theory?

    Unconscious blocking of anxiety-provoking thoughts or memories. Defense mechanism prevents conscious access to threatening content.

46. What does the encoding specificity principle predict about retrieval?

    Recall improves when retrieval cues match conditions present at encoding. Memory is best when learning and testing contexts align.

47. Which brain structure is most associated with forming new explicit memories?

    Hippocampus (medial temporal lobe). Critical for consolidating short-term to long-term declarative memory.

48. What is repression in psychodynamic theory?

    Defense mechanism: unconscious blocking of anxiety-provoking content. Freudian concept of motivated forgetting of trauma.

49. What is long-term potentiation (LTP) in synaptic plasticity?

    Persistent strengthening of synapses after repeated activation. Cellular mechanism underlying learning and memory formation.

50. Identify the concept: a tip-of-the-tongue state with partial retrieval access.

    Tip-of-the-tongue phenomenon. This state involves temporary inability to fully access known information despite partial recall.

51. Identify the concept: after limb loss, the somatosensory cortex reorganizes its body map.

    Cortical remapping (experience-dependent neuroplasticity). Brain areas adapt function when input changes dramatically.

52. What is the tip-of-the-tongue phenomenon?

    Temporary inability to retrieve a known word or name. Partial activation without full retrieval access.

53. What is interference theory of forgetting?

    Forgetting due to competition between memories during retrieval. Other memories interfere with accessing the target memory.

54. What is confabulation in memory disorders?

    Unintentional fabrication of memories to fill gaps in recall. Brain creates false memories to maintain coherent narrative despite gaps.

55. What is retrieval failure as a cause of forgetting?

    Information is stored but cannot be accessed due to missing cues. Memory exists but lacks retrieval pathways or triggers.

56. Which option best defines encoding specificity principle?

    Recall improves when retrieval context matches encoding context. Environmental cues from learning enhance memory retrieval.

57. What is confabulation?

    Unintentional fabrication of memories to fill in memory gaps. Brain creates false memories to maintain coherent narrative despite gaps.

58. What is neurogenesis and where does it occur most notably in adults?

    Creation of new neurons; notably in the hippocampal dentate gyrus. Adult brain generates new cells for learning and memory.

59. What is retrograde amnesia?

    Loss of previously formed memories, especially near the causal event. Memories prior to the amnesia-inducing event are lost, with recent ones most affected.

60. What is retroactive interference?

    Newer information disrupts recall of older information. New learning interferes backward in time with old memories.

61. What is retrieval-induced forgetting?

    Practicing recall of some items suppresses related competing items. Selective practice creates competition between related memories.

62. What is motivated forgetting (repression) in psychodynamic theory?

    Unconscious blocking of anxiety-provoking memories. Defense mechanism protecting ego from traumatic content.

63. What is retroactive interference in memory?

    New information disrupts recall of previously learned information. Like trying to remember old phone numbers after learning new ones.

64. What is Alzheimer disease characterized by at the neural level?

    Amyloid-$\beta$ plaques and neurofibrillary tangles (tau). Protein aggregates disrupt neural function and cause cell death.

65. What is the primacy effect attributed to in the serial position curve?

    More rehearsal leads to better encoding into long-term memory. Early items get more rehearsal time before capacity limits.

66. What is proactive interference?

    Old information interferes with learning or recalling new information. Prior knowledge disrupts the acquisition or recall of newer, similar material.

67. What is confabulation in the context of memory disorders?

    Unconscious fabrication of memories to fill gaps in recall. False memories are created unintentionally to compensate for genuine recall deficits.

68. What brain structure is classically implicated in anterograde amnesia?

    Hippocampus (medial temporal lobe). Critical for consolidating short-term to long-term memories.

69. What is Alzheimer disease most characteristically associated with at the neural level?

    Amyloid-$\beta$ plaques and neurofibrillary tangles (tau). Protein deposits disrupt neural function and cause dementia.

70. What is Alzheimer disease characterized by at the neural level?

    Beta-amyloid plaques and neurofibrillary tangles (tau). Plaques disrupt neural communication; tangles kill neurons.

71. What is confabulation as seen in Korsakoff syndrome?

    Unintentional fabrication of memories to fill gaps in recall. Patients create false memories without intent to deceive.

72. Identify the memory distortion: incorporating misleading post-event information into recall.

    Misinformation effect. False details from others contaminate original memory traces.

73. Which brain structure is most associated with anterograde amnesia when damaged?

    Hippocampus (medial temporal lobe). Critical for consolidating new explicit memories into cortical storage.

74. What is Alzheimer disease, in terms of primary cognitive impairment?

    Progressive neurodegeneration with prominent episodic memory loss. Neurodegenerative disease starting with hippocampal damage affecting recent memories.

75. What is retroactive interference?

    New information disrupts recall of previously learned information. Recent learning interferes backward in time with older material.

76. What is the primacy effect, and which memory system mainly supports it?

    Better recall for early items; mainly long-term memory encoding. Early items get more rehearsal time for LTM consolidation.

77. What is confabulation in memory disorders?

    Unintentional fabrication of memories to fill recall gaps. Brain creates false memories without awareness of inaccuracy.

78. What is decay theory of forgetting?

    Memory traces fade over time when not used or rehearsed. Biological degradation of memory engrams without rehearsal.

79. What is the decay theory of forgetting?

    Memory traces fade over time when not actively used. Based on the idea that unused neural connections weaken.

80. What is a flashbulb memory?

    Vivid, high-confidence memory for an emotional event (not always accurate). Emotional arousal enhances encoding but doesn't guarantee accuracy.

81. What is the serial position effect?

    Better recall for early (primacy) and late (recency) list items. Middle items lack the rehearsal advantage of first or recency of last.

82. What is proactive interference in memory?

    Old information disrupts learning or recall of new information. Prior learning interferes forward with subsequent learning.

83. What is neurogenesis and where is it most associated in adults?

    Formation of new neurons; classically in the hippocampal dentate gyrus. Continues throughout life, supporting learning and memory.

84. What is cue-dependent forgetting?

    Failure to retrieve due to absence of cues present during encoding. Retrieval fails when cues from the original learning context are absent.

85. Which memory system declines earliest in Alzheimer disease: episodic or procedural?

    Episodic (explicit) memory declines earlier than procedural memory. Declarative recall of personal events is impaired first, with skills affected later.

86. What is source monitoring error?

    Misattributing the origin of a memory (where or how it was learned). Confusing whether you read something or someone told you about it.

87. What is Alzheimer disease characterized by at the neural level?

    Amyloid-$\beta$ plaques and neurofibrillary tangles (hyperphosphorylated tau). Protein aggregates disrupt neural function and cause cell death.

88. Which brain structure is most classically linked to anterograde amnesia?

    Hippocampus (medial temporal lobe). Critical for transferring short-term to long-term memory.

89. What is the defining cognitive feature of Alzheimer disease?

    Progressive decline in memory and other cognitive functions. Neurodegeneration causes memory loss before other symptoms.

90. What is retroactive interference in memory?

    New information disrupts recall of older information. Recent learning interferes backward with previously learned material.

91. What is motivated forgetting in psychoanalytic theory?

    Unconscious repression of anxiety-provoking memories. Defense mechanism pushes threatening content from consciousness.

92. What is Korsakoff syndrome most classically associated with?

    Thiamine (vitamin $B_1$) deficiency, often due to alcoholism. Chronic alcohol use depletes thiamine, damaging memory circuits.

93. What is anterograde amnesia?

    Inability to form new long-term memories after the causal event. Post-event brain damage prevents consolidation of new experiences into long-term storage.

94. What is the recency effect in list recall?

    Enhanced recall of late items still held in working memory. Recent items remain active in short-term storage.

95. Which brain structure is most associated with forming new declarative memories?

    Hippocampus (medial temporal lobe). Critical for consolidating short-term into long-term memories.

96. Which memory system is typically most impaired early in Alzheimer disease?

    Episodic (declarative) memory for recent events. Hippocampal damage first affects new episodic memory formation.

97. What is the recency effect?

    Enhanced recall for last items because they remain in working memory. Last items are still active in STM during immediate recall.

98. What is source monitoring error?

    Misattributing the origin of a memory (source confusion). Forgetting where, when, or how information was learned.

99. What is the primacy effect attributed to?

    Greater rehearsal leads to better encoding into long-term memory. First items get more rehearsal time before new items arrive.

100. What is motivated forgetting in psychoanalytic theory?

     Unconscious repression of distressing memories. Defense mechanism pushing traumatic memories from consciousness.

101. What is decay theory of forgetting?

     Memory traces fade over time when not accessed or rehearsed. Synaptic connections weaken without reinforcement.

102. Which brain structure is most associated with anterograde amnesia when damaged?

     Hippocampus (medial temporal lobe). Critical for consolidating new explicit memories into LTM.

103. What is the primacy effect attributed to in memory research?

     Early items receive more rehearsal and enter long-term memory. More rehearsal time transfers items to long-term storage.

104. What brain structure damage is most associated with anterograde amnesia?

     Hippocampus (medial temporal lobe) damage. Hippocampus consolidates new declarative memories into cortex.

105. What is neural plasticity?

     The nervous system's capacity to change structure or function with experience. Brain adaptability enables reorganization in response to learning or injury.

106. What is repression in psychodynamic theory?

     Unconscious exclusion of anxiety-provoking memories from awareness. Defense mechanism blocks traumatic memories from consciousness.

107. What is long-term potentiation (LTP) in neural plasticity?

     Persistent strengthening of synapses after repeated activation. Molecular basis of learning; increases synaptic transmission efficiency.

108. What is encoding failure as a cause of forgetting?

     Information never entered long-term memory due to poor encoding. Insufficient attention or processing prevents memory formation.

109. What is synaptic pruning?

     Elimination of weaker synapses to increase efficiency of neural networks. Developmental refinement removes inefficient connections to optimize brain function.

110. What is the misinformation effect?

     Post-event information alters memory for the original event. Leading questions or false details contaminate original memories.

111. What cognitive mechanism best explains the primacy effect?

     More rehearsal transfers early items into long-term memory. First items get extra processing time before new items arrive.

112. What is Korsakoff syndrome and its most common cause?

     Amnestic syndrome from thiamine deficiency, often due to alcoholism. Damages mammillary bodies and dorsomedial thalamus.

113. What is Korsakoff syndrome most strongly associated with?

     Thiamine (vitamin $B_1$) deficiency, often due to chronic alcoholism. Damages mammillary bodies and thalamus, causing severe amnesia.

114. What is Korsakoff syndrome and what is its key nutritional cause?

     Amnestic syndrome from thiamine (vitamin $B_1$) deficiency. Common in chronic alcoholism; causes severe memory deficits.

115. What is the cue-dependent theory of forgetting?

     Forgetting due to insufficient retrieval cues, not lost storage. Memory exists but cannot be accessed without proper environmental triggers.

116. What is decay theory of forgetting?

     Memory traces fade over time when not accessed or used. Neural connections weaken without rehearsal, like unused paths becoming overgrown.

117. What is the difference between retrograde amnesia and anterograde amnesia?

     Retrograde: loss of past memories; anterograde: cannot form new memories. Retrograde affects past memories before injury; anterograde affects memory formation after injury.

118. What is retroactive interference in forgetting?

     New learning disrupts recall of previously learned information. Later material interferes backward with earlier learning.

119. What is the serial position effect in free recall?

     Better recall for early (primacy) and late (recency) list items. Middle items lack the rehearsal and recency advantages.

120. What is the recency effect, and which memory system mainly supports it?

     Better recall for late items; mainly short-term/working memory. Recent items remain in STM/working memory for immediate recall.

121. Which memory system primarily explains the recency effect?

     Short-term or working memory (items still active). Last items remain in immediate memory, not yet displaced by new information.

122. What is the defining cognitive deficit in Alzheimer disease?

     Progressive impairment of episodic memory and other cognition. Recent memories fade first while procedural and semantic memory persist longer.

123. What brain structure is most associated with forming new explicit memories?

     Hippocampus (medial temporal lobe). Critical for consolidating declarative memories.

124. What is anterograde amnesia?

     Inability to form new long-term explicit memories after onset. Can't transfer new experiences from STM to LTM.

125. What is the definition of forgetting in cognitive psychology?

     Failure to retrieve previously encoded and stored information. Distinguishes from encoding or storage failures - the memory exists but can't be accessed.

126. What is confabulation (commonly seen in Korsakoff syndrome)?

     Unintentional fabrication of memories to fill gaps in recall. Patient believes false memories are real, not intentional lying.

127. What is Alzheimer disease characterized by at the neural level?

     Beta-amyloid plaques and neurofibrillary tangles (tau). Protein deposits disrupt neural communication and kill brain cells.

128. Identify the forgetting mechanism: failure to recall due to missing retrieval cues.

     Cue-dependent forgetting (retrieval failure). Information remains stored but inaccessible without proper retrieval context.

129. What is confabulation in the context of memory disorders?

     Unintentional fabrication of memories to fill gaps in recall. Brain creates false memories to maintain coherent narrative.

130. What is Korsakoff syndrome most classically associated with?

     Thiamine (vitamin $B_1$) deficiency, often due to alcoholism. Chronic alcohol depletes thiamine, damaging mammillary bodies.

131. What is the tip-of-the-tongue phenomenon?

     Temporary retrieval failure with a feeling a memory is accessible. Partial activation occurs but full retrieval threshold isn't reached.

132. What is the misinformation effect?

     Post-event information alters memory for the original event. New information contaminates and distorts original memory traces.

133. What is synaptic pruning in neural development and plasticity?

     Elimination of weaker synapses to strengthen frequently used pathways. Brain optimizes connections by removing unused synapses.

134. Which brain structure is classically required for forming new explicit memories?

     Hippocampus (medial temporal lobe). This structure consolidates declarative memories for long-term storage.

135. What is retrograde amnesia?

     Loss of explicit memories formed before the onset of amnesia. Past memories are lost while new memory formation remains intact.

136. What is confabulation in memory disorders?

     Unintentional fabrication of memories to fill gaps in recall. Brain injury causes false memories without intent to deceive.

137. Identify the key distinction between recall and recognition.

     Recall retrieves without cues; recognition identifies with cues. Recall generates answers; recognition selects from options.

138. What is the misinformation effect?

     Post-event information alters memory for an original event. Leading questions or suggestions contaminate original memory traces.

139. Which option best describes the misinformation effect?

     Post-event information distorts memory for the original event. Leading questions or false details alter original memory traces.

140. What is mood-congruent memory?

     Better recall of information consistent with current mood. Happy people recall positive events more easily than negative ones.

141. What is the tip-of-the-tongue phenomenon?

     Temporary inability to retrieve a known word, with partial access. Demonstrates partial activation without full retrieval.

142. What is decay theory of forgetting?

     Memory traces weaken over time when not accessed or rehearsed. Unused neural connections gradually fade without reinforcement.

143. What is reconsolidation in the context of memory updating?

     Reactivated memories become labile and can be modified then restabilized. Retrieved memories enter unstable state allowing modification.

144. Identify the forgetting pattern: a rapid initial drop in recall that later levels off.

     Ebbinghaus forgetting curve. Shows exponential decay: most forgetting occurs immediately.

145. What is state-dependent memory?

     Recall improves when internal state matches the state at encoding. Mood or physiological state acts as a retrieval cue.

146. What is neurogenesis and where is it classically observed in adults?

     Formation of new neurons; classically in the hippocampus. Adult brain creates new neurons, especially in memory regions.

147. What memory type is typically spared in anterograde amnesia: explicit or implicit?

     Implicit (procedural) memory is relatively spared. While explicit memory formation is impaired, non-declarative skills can still be acquired.

148. What is Korsakoff syndrome, and what is its most common cause?

     Amnestic syndrome from thiamine deficiency, usually due to alcoholism. Chronic alcohol depletes thiamine (B1), damaging mammillary bodies.

149. What is retroactive interference in memory?

     New information disrupts recall of previously learned information. Recent learning interferes with older memory retrieval.

150. What is motivated forgetting in psychodynamic theory?

     Repression of anxiety-provoking memories from conscious awareness. Unconscious defense mechanism blocks traumatic memories.

151. What is proactive interference in memory?

     Old information disrupts recall of newly learned information. Past learning interferes with new learning, like old phone numbers blocking new ones.

152. Which memory system primarily explains the recency effect?

     Short-term (working) memory availability. Recent items remain active in STM during immediate recall.

153. Which memory system primarily explains the primacy effect?

     Long-term memory (items rehearsed and encoded). First items get more rehearsal time, transferring to long-term storage.

154. What is the spacing effect in long-term memory formation?

     Distributed practice improves long-term retention vs cramming. Multiple study sessions beat massed practice for retention.

155. What is Korsakoff syndrome most commonly caused by?

     Thiamine (vitamin B$1$) deficiency, often due to chronic alcoholism. Alcohol impairs thiamine absorption, damaging mammillary bodies.

156. Identify the forgetting concept: a tip-of-the-tongue state during recall.

     Retrieval failure (temporary access problem, not loss of storage). Memory trace exists but activation threshold isn't quite reached.

157. What is the primary finding of Ebbinghaus's forgetting curve?

     Forgetting is rapid soon after learning, then levels off. Shows exponential decay: most forgetting occurs within hours/days.

158. What is the typical early cognitive symptom of Alzheimer disease?

     Progressive impairment in episodic memory (recent events). Difficulty forming new memories while older memories remain intact.

159. What is the hallmark memory deficit in Alzheimer disease?

     Progressive impairment of explicit (episodic) memory, early on. Recent personal experiences are forgotten while procedural memory persists.

160. What is the key memory deficit in Korsakoff syndrome?

     Prominent anterograde amnesia with confabulation. Severe difficulty forming new memories, often with false memory creation.

161. What is the key memory deficit in Alzheimer disease early in the course?

     Impaired formation of new explicit (episodic) memories. Hippocampal damage affects recent memory consolidation first.

162. What is the primacy effect?

     Enhanced recall for early items due to greater rehearsal into LTM. Initial list items benefit from more rehearsal, transferring them to long-term memory.

163. What does the Ebbinghaus forgetting curve describe?

     Forgetting is rapid soon after learning, then levels off. Shows exponential decay pattern: most forgetting occurs early.

164. What is mood-congruent memory?

     Recall is biased toward memories that match one's current mood. Current emotional states selectively facilitate recall of emotionally consistent memories.

165. What is Korsakoff syndrome most strongly associated with?

     Thiamine (vitamin $B_1$) deficiency, often due to chronic alcoholism. Nutritional deficiency from alcohol abuse damages brain areas involved in memory.

166. What is neurogenesis, and where is it classically observed in adults?

     New neuron formation; classically in the hippocampus (dentate gyrus). Adult brains can generate new neurons, especially for memory.

167. What is encoding failure as a cause of forgetting?

     Information never enters long-term memory due to poor encoding. Insufficient attention or processing prevents transfer from STM to LTM.

168. What is confabulation in memory disorders?

     Unintentional fabrication of details to fill memory gaps. Brain unconsciously creates plausible stories to explain memory gaps.

169. What is the key memory feature of Korsakoff syndrome?

     Severe anterograde amnesia with confabulation. Thiamine deficiency causes memory loss with false memories.

170. What is decay theory of forgetting?

     Memories weaken over time when not accessed or rehearsed. Suggests memory traces physically deteriorate without use.

171. Which brain structure is most classically linked to anterograde amnesia when damaged?

     Hippocampus (medial temporal lobe). Critical for consolidating new explicit memories.

172. Which option best describes the serial position effect in free recall?

     Better recall for early (primacy) and late (recency) list items. Middle items show poorest recall due to less rehearsal and displacement.

173. What is Alzheimer disease characterized by at the neural level?

     Beta-amyloid plaques and neurofibrillary tangles (tau protein). Protein deposits disrupt neural function and connectivity.

174. What is the spacing effect in memory and forgetting?

     Distributed practice produces better long-term retention than cramming. Spaced repetition strengthens memory consolidation over time.

175. What is Korsakoff syndrome, and which deficiency most commonly causes it?

     Amnestic disorder from thiamine ($B_1$) deficiency, often in alcoholism. Chronic alcohol depletes thiamine, damaging memory circuits.

176. What is proactive interference in memory?

     Old information disrupts recall of newly learned information. Past learning interferes with new memory formation.

177. What is decay theory of forgetting?

     Memories fade over time because memory traces weaken with disuse. Based on the idea that neural connections weaken without use.

178. What is the recency effect attributed to in the serial position curve?

     Recent items remain available in working (short-term) memory. Last items haven't been displaced from STM buffer yet.

179. What is repression in the context of forgetting?

     Motivated forgetting of anxiety-provoking material (psychodynamic). Unconscious blocking of traumatic memories to reduce psychological distress.

180. Which receptor is classically required to induce LTP in many hippocampal synapses?

     NMDA receptor (glutamate receptor; calcium-permeable when unblocked). Calcium influx triggers cascades that strengthen synaptic connections.

181. What is the difference between experience-expectant and experience-dependent plasticity?

     Expectant: universal inputs; dependent: individual learning-specific changes. Expectant uses species-typical inputs; dependent uses unique individual experiences.

182. Which memory system is typically spared in classic anterograde amnesia: explicit or implicit?

     Implicit (procedural) memory is relatively preserved. Motor skills and habits remain intact despite declarative loss.

183. What is interference theory of forgetting?

     Forgetting occurs because other memories disrupt encoding or retrieval. Competing memories hinder the encoding or retrieval of target information, leading to forgetting.

184. What is repression in the psychodynamic view of forgetting?

     Unconscious blocking of anxiety-provoking memories from awareness. Defense mechanism that protects ego from threatening content.

185. What is the primacy effect in list recall?

     Enhanced recall of early items due to increased rehearsal into LTM. More rehearsal time transfers early items to long-term storage.

186. What is Alzheimer disease characterized by at the neural pathology level?

     Beta-amyloid plaques and neurofibrillary tangles (tau) with cortical atrophy. Protein deposits disrupt neural function and cause cell death.

187. What is confabulation in a memory disorder?

     Unintentional fabrication of memories to fill memory gaps. Brain fills gaps with false memories without conscious lying.

188. What is repression in psychodynamic theory?

     Unconscious blocking of anxiety-provoking thoughts from awareness. In Freudian theory, distressing memories are unconsciously suppressed to alleviate psychological discomfort.

189. What is source monitoring error in memory?

     Misattributing the origin of a memory (source confusion). Forgetting where, when, or how information was acquired.

190. Identify the key difference between anterograde and retrograde amnesia.

     Anterograde: cannot form new memories; retrograde: cannot recall old. Anterograde affects future memory formation; retrograde affects past.

191. What is the recency effect attributed to?

     Recent items remain in short-term/working memory at recall. Last items are still active in working memory during recall.

192. What is proactive interference in memory?

     Old information disrupts learning or recall of new information. Previous learning interferes with acquiring new material.

193. Which memory system primarily explains the primacy effect?

     Long-term memory encoding via rehearsal. Early items get more rehearsal time for LTM consolidation.

194. What is motivated forgetting in psychodynamic theory?

     Unconscious blocking of anxiety-provoking memories (repression). Defense mechanism pushes threatening memories from consciousness.

195. Which option best describes the Ebbinghaus forgetting curve?

     Rapid initial forgetting followed by a slower rate of decline. Shows exponential decay: most forgetting occurs immediately.

196. What is retroactive interference in memory?

     New information disrupts recall of previously learned information. Recent learning interferes with past memories, like new passwords overriding old ones.

197. What is the primacy effect, and which memory store mainly explains it?

     Better recall for early items; primarily due to long-term memory. Early items get more rehearsal time, entering LTM.

198. What is Korsakoff syndrome most classically caused by?

     Thiamine (vitamin $B_1$) deficiency, often due to chronic alcoholism. Damages mammillary bodies and dorsomedial thalamus.

199. Identify the forgetting mechanism: new phone number makes old number hard to recall.

     Retroactive interference. New number overwrites or blocks access to old number.

200. What is cue-dependent forgetting?

     Failure to recall due to absence of cues present at encoding. Environmental or internal cues needed for retrieval are missing.

201. What is long-term potentiation (LTP)?

     Persistent increase in synaptic strength after high-frequency stimulation. Repeated activation strengthens connections, serving as a basis for learning.

202. What is context-dependent memory?

     Recall improves when external environment matches encoding context. Physical location serves as a powerful retrieval cue.

203. What is neurogenesis, and where does it notably occur in adults?

     Formation of new neurons; notably in the hippocampal dentate gyrus. Continues throughout life, supporting learning and memory.

204. What is synaptic pruning in neural development?

     Elimination of weak synapses to increase network efficiency. Refines neural circuits by removing unnecessary connections.

205. What is the primacy effect?

     Enhanced recall for early items due to greater rehearsal into LTM. First items get more rehearsal time, strengthening LTM encoding.

206. What is neurogenesis and where is it classically observed in adults?

     Formation of new neurons; classically in the hippocampal dentate gyrus. Adult brain retains capacity to generate new neurons for learning.

207. What is retrieval failure (cue-dependent forgetting)?

     Inability to access stored memory due to insufficient retrieval cues. Memory exists but can't be accessed without proper contextual triggers.

208. What is Alzheimer disease characterized by at the cellular level?

     Beta-amyloid plaques and neurofibrillary tangles (tau). Tau tangles inside neurons; plaques between neurons.

209. Which option best describes decay theory of forgetting?

     Memory traces fade over time when not used or reactivated. Memories weaken without rehearsal, like unused paths becoming overgrown.

210. Which neurotransmitter system is notably reduced in Alzheimer disease?

     Cholinergic signaling (acetylcholine). Loss of ACh neurons impairs memory and cognitive function.

211. What is synaptic pruning in neural development and plasticity?

     Elimination of weak synapses to increase efficiency of networks. Brain optimizes by removing unused neural connections.

212. What is Alzheimer disease characterized by at the neural level?

     Amyloid-$\beta$ plaques and neurofibrillary tangles (tau). Protein accumulations disrupt neuronal function and contribute to cognitive decline.

213. What is the serial position effect?

     Better recall for early (primacy) and late (recency) list items. Position in sequence affects memorability of items.

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