CLOA - Explain how biological factors affect a cognitive process Flashcards
Alzheimer’s Disease
- a serious degenerative brain disease
- symptoms include memory impairment, difficulty speaking, attention problems, altered personality
what causes Alzheimer’s?
- abnormal protein fragments that kill brain cells
- begins at the hippocampus
- amyloid plaques
- neurofibrillary tangles
- reduced metabolism in the hippocampus (Mosconi, 2005)
amyloid plaques
- caused by sticky deposits of amyloid-ß proteins that accumulate in the brain
- they damage axon and dendrite membranes
- plaques are formed from the degenerating axons and dendrites
neurofibrillary tangles
- accumulation of an abnormal form of tau protein
- structural support of neurons collapses
- tangles occur in the microtubules
tau protein
a component of the support structure of neurons
how does AD impair cognitive functions?
- degradation of the neurons in the brain
- leading to widespread atrophy (shrinking)
episodic memory
memory for events/personal experiences
semantic memory
general knowledge about the world, concepts, language
procedural memory
memory for the performance of particular actions
effect of AD on various types of memory
- Salthouse and Becker (1998): analyzed data from 180 AD patients and over 1000 normal elderly individuals, and found that AD primarily impaired episodic memory
- Hodges et al. (1994) measured semantic memory in AD patients with tasks (e.g. naming pictures of objects or animals) and found a steady decline in semantic
memory - procedural memory is also affected but to a lesser extent
Mosconi (2005) - Aim
To investigate early detection of Alzheimer’s
role of hippocampus
encoding and transferral of STM to LTM
Mosconi (2005) - Process
- Longitudinal study following a sample of 53 normal and healthy participants between 9 years and 24 years
- PET scans were used together with a computer program to measure hippocampus metabolism
Mosconi (2005) - Findings
participants showing early signs of reduced metabolism in the hippocampus associated with later development of AD
Mosconi (2005) - Conclusion
The hippocampus is a central part of memory processes and reduced metabolism may be a sign of AD
lesions
damage to brain tissue
how do lesions affect memory?
- manifests as memory loss
- demonstrates that different memories are stored in different areas of the brain
Main study: Scoville and Milner (1957)
Scoville and Milner (1957)
case study on Henry Molaison
- epileptic who had parts of his brain (including the hippocampus) removed
- his epilepsy was cured but he developed severe anterograde amnesia and partial retrograde amnesia
- intact STM but couldn’t transfer semantic or episodic memories to the LTM
- his ability to store procedural memory in the LTM remains intact
- his memory prior to the surgery appears largely intact
- he has some capacity for working memory (could maintain short conversations)
what can be learned from HM’s case?
- memory systems are highly specialized and complex
- hippocampus plays a critical role in transferral between STM and LTM
- however the hippocampus doesn’t appear to be the site of permanent storage itself
- the fact that HM has deficits in some types of memories but not in other suggests that the brain has multiple memory systems located in different regions
relationship between HM’s brain damage and his memory deficits
Corkin (1997)
- scanned HM’s brain using MRI
- parts of the temporal lobes (including the hippocampus) was missing
- these parts are theorized to play an important role in the transferral of memories from STM to LTM
- as they are involved in specific neurotransmitter pathways (e.g. acetylcholine, which is associated with semantic and episodic memory)
what to write when asked: “Explain how 1 biological factor may affect 1 cognitive process”
- biological factor: Alzheimer’s Disease; cognitive process: memory
- describe functions of the hippocampus
- explain hippocampus’ role in memory formation and recall
- describe symptoms and effects of AD
- explain the causes of neurofibrillary tangles and amyloid plaques and their biological effects
- refer to Salthouse and Becker (1988) and Hodges et al (1994) for cognitive effects of AD