Forgetting, Memory Disorders, and Neural Plasticity (6B) - MCAT Psychological and Social Foundations

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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