Caused by damage, disease, psychological trauma or by the use of certain drugs.
Sufferers can not remember large parts of their life, or are unable to make new memories.
Explanation of Amnesia (1)
Schacter (1987): forgetting is caused by impaired explicit memory (Knowledge we try to access when we are trying to rememeber something) as explicit memory is often retain.
Amnesiac's have normal proceduaral memory (Motor skills and memory we access unconsciously)
Have a loss of declarative memory (explicit).
Explanation of Amnesia (2)
Anterograde Amnesia (an inability to form new long term memories) and Retrograde Amnesia (loss of memory for past events) are associated with the hippocampus.
The hippocampus is responsible for consolidation of memory.
Patients with Anterograde Amnesia are unable to consolidate their memories, and so cannot create new ones.
Patients with Retrograde Amnesia can consolidate older memories better than newer ones.
Neurological process that involves gradually converting information from short term memory into long term memory.
Involves synapses between neurons and the creation of signals between two neurons which will eventually become sensitized with eachother if the process is rehearsed or recalled.
Suffered from Amnesia.
Orignially given surgery to remove the part of the brain causing him to have fits.
Instead, the front half of the hippocampus and the amygdala were removed.
HM was unable to form long term memories.
He was important as it showed where memory is located in the brain.
Remondes and Schman (2004)
lesioned the hippocampus of rats.
found that with damage to the hippocampus rats could learn a maze but forget it easily
i.e, they could not consolidate memory.
Suggests the hippocampus plays a key role in memory
Reed and Squire (1998)
Performed MRI scans.
Found that all 4 of his patients with amnesia had damage to their hippocampus and those with more servere symptoms had lesions on their temporal lobe.
Characterised by B-amyloid plaques forming on the brain.
This is difficult to diagnose until after the patients death.
Sufferers may experience language difficulties, impaired memory etc...
Explanation of Alzheimer's Disease (1)
B-amyloid plagues (harmful molecules of protein) build up in the spaces between neurons causing the cerebral cortex to shrink and interfers with neuro transmitters.
Explanation of Alzheimer's Disease (2)
Buld up of tau protein (tangles) causing the cell body of neurons to degenerate.
Explanation of Alzheimer's Disease (3)
Alzherimers Disease has been genetically linked to Down's Syndrome.
People with Down's Syndrome have an extra chromosome (21) and this gene is related to producing an excess of B-amyloid proteins.
Problem with this explanation: 50% of Down's Syndrome patients get Alzheimers, but 50% don't and so the link is not definate.
Murphy and Levini (2010)
Link between B-amyloid deposits and cognitive problems is weak.
Murphy and Levini: B-amyloid triggers a chain of events which is continuous, regardless of B-amyloid levels.
Been suggested that the formation of tangles is an important effect of the chain.
Suggests that the development of the plagues is unstopable, and that tangles can make the condition worse.
St George- Hyslop (2000)
Half of Alzheimers patients have relatives who are (or were) sufferers suggesting some relation between genes and Alzheimers.
Hock et al
Triggered an immune response to B-amyloid protein in Alzheimers patients for an experiement.
Those with the strongest immune responses (genetically ditermined) destroyed most of the B-amyloid and stopped deteriorating in their memory.
Suggests that we don't really know much about te link between genes and B-amyloid