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Flashcards

Theories of cognitive ageing: decline, speed and dementia

Becca Sidley Inglês 48 flashcards

Flashcards do conjunto (48)

  1. 1Theories of Cognitive Decline in Ageing (4)General theories: Make the assumption that cognitive ageing is due to a single cause
    * Common cause theory
    * Lack of inhibition theory
    * Reduced processing resources theory
    * Processing speed theory
  2. 2Common Cause TheoryCame from looking at empirical evidence; deterioration of core biological processes responsible for both cognitive and physiological decline.
  3. 3Common cause theory: Li & Lindenberg sensory deficit theory.Strong correlations have been found between cognitive performance, auditory and visual sensitivity and grip strength in the elderly.
    - Idea that cognitive decline is much like sensory decline; so they may rely on a single neurological factor.
    - Supported by the fact that much age variance shared by sensory performance (i.e by how well elderly do can be predicted by how well the can hear or see etc)
  4. 4Common cause theory: Similarities to De-differentiation theory- D.D theory argued that with increased ageing everything becomes strongly disconnected.
    - CC is another expression of this lack of specificty/specialaisation
    (e.g argument about reasons for bi-lateral activations)
    -This lack of specificity has been interpreted by some as a direct consequences of cognitive ageing.
    *However other theories have argued for a compensatory explanation for these lack of specificity correlations (Cabezza et al; Ro et al)
  5. 5Criticism of Common Cause theory: X- Criticized as it doesn't provide a clear causal mechanism: it doesn't allow us to understand how this 'common factor' actually operates.
    **some have argued this function that explains loss could be dopamine but there is not yet a definite answer**
  6. 6Cognitive ageing as an inhibition/selective attention problem Hasher & Zacks- Idea that lack of inhibition of unwanted info is related to the cognitive deficits found.
  7. 7What type of theory is this? What is this theory related to?It is related to WM and selective attention: it is an attention theory.
    -Idea that older people find it harder to filter out irreverent information and struggle to focus just on the relevant info.
    *this has been argued to possibly overload the working memory and effect new learning (espcially on timed tasks).
  8. 83) Cognitive ageing as a processing resource problem Craik & Byrd.Deficits in the elderly due to reduce attention capacity of reduced processing resources
    -working memory has a small number of available resources, and sometimes we need to do things simultaneously.
  9. 9Evidence for cognitive resource theory:According to this theory if the load increases we will see further cognitive deficits...
    1) Concurrent dual tasks in older people have greater impact on performance than in young (stroop task complex?).
  10. 10How is this theory linked to possible LTM deficits?- This can in turn explain deifict in LTM - as it will rely on W.M combing different elements/sources - inability to do this will effect formation of LTM.
  11. 11CriticismsX evideence of older people not performing as well under divided attention conidtions is not reliable proof - doesnt determine the cause its just a possible explanation
    x criticsed for being ainly descirptive: used technology to explain what people have found but doesnt actually provide a reliable mechanism to be identiifed as a cause.
  12. 124) cognitive ageing as a reduction in processing speed SALTHOUSE.- most influential and well sited theory
    - Cogntiive decline is caused by a general flowing of processing speed.
  13. 13Proccesing speed and attentional WM tasks?Processing speed has been argued to be the main problem in poor performance of elderly in attention and working memory tasks.
    - by accounting for processing speed differences between young and old it removed a lot of the differences found between ages on cogntiive tasks.
    *if you use measurment of processing speed as a factor it accaounted for most age related variance*
  14. 14Positives of processing speed:** Statistically it has good explanatory power as if you remove reaction times there are few cognitive deficit differences found
    **compatible with neuroantomical evidence (synaptic density and white matter degradation).
    **proccessing speed is a mjaor component of congitive ageing and has clear links with changes in the brain.
  15. 152 mechanisms argued to underlie the relationship between processing speed and cognition1) limited time mechanism
    2) silumatinously mechanism.
    **they can apply to complex tasks not just simple.
  16. 16Limited time mechanism- cognitive operations need to be completed in a specified time and slow processing speed affects successful completion
    E.G assembly line factor; if early operations are too slow later operations will also be effected.
    - the machine cannot stop so it is slowed down (by ageing) cognitive processes therefore can come out diminished as they don't have the speed to perform the required operation in time.
  17. 17Simultaneity Mechanism.- higher congitive operations involve simulatnoues or near siumlatnous processing.
    - Simulationly can be compromised if early operations are lost (delayed) because later operations take too long or if operations tha require simulatnious exection become un-synchronised due to delays in execution.
    - This means wont be able to perform tasks at the same time to the same quality; particularly in tasks where you need to retain in mind the output from one task in order to complete the other.
    = clear processing speed can potentially account for attention and memory differences.
  18. 18Links to episodic impairment as an associative memory deficit.- Very specific theory to memory
    -episodic deficit seen as an impairment in creating novel associations between seperate items
    E.g can remember the object but not the color of it
    = problem in retrieving associations - but could be linked to processing speed or processing resources deficits - as the deficit is greater when encoding is more effortfull .
  19. 19INDIVIUDAL DIFFERENCES IN COGNTIIVE AGEING:- compared to younger people there is much greater variability in older people
    - older people of similar ages can have very different congitive performance - variability increases as we age.
  20. 20Individual differences in cognitive ageing: Heritability and IQ;- Also great variability in peoples IQ - which has been argued to be partly due to our genetic make up.
    - MZ twins have high IQ concordance; therefore its plausible that some cognitive abilities are also heritable.
    - IQ has been suggested not only as a result of the mechanism that can cause ageing, but also a factor that by itself can determine how well we will age
    e.g life choices, diet, risk taking.
  21. 21Individual differences in cognitive ageing Cardiovascular Disease- need good circulation to perform well in cognitive and psychical tasks - with age and lifestyles choices circulation can become impaired which can lead to impaired cognitive functioning.
  22. 22STROKES (2)disrupt the blood supply to the brain and can result in cell death.
    *risk of stroke increases considerably with age (2/3 over age of 65).
    Ischemic stroke; damage due to blockage that disrupts blood oxygen getting to cell; this will lead to neuronal death.
    Hemorrhagic: weak area in a blood vessel caused the an anuerism which it can trust and result un-hemorrhaging in or around the brain.
  23. 23Effects of strokes1) stroke can have either very specific effects on cognitive or motor functioning.
    i.e specific in the area where the oxygen is deprived but also many additional problems with general cognitive performance
  24. 24Heart diseases/failures.-Coronary heart disease and congestive heart failure have been linked to cog impairments and both are more frequent in older adults .
    - General problems with blood supply. which can impact on cognitive functioning.
    Risk factors include high blood pressure, high levels of blood cholesterol, diabetes, smoking, heavy alcohol consumption, drug use, unhealthy diet; all have big impact on cognitive functioning and can contribute to individual variability.
  25. 25Cognitive ageing and lifestyle. Can we slow down/reverse ageing without drugs?Does physical exercise improve cognitive functioning;
    is there is a link to cardiovascular health it has been argued that if we implemented a fitness program it could see improvements.
  26. 26Colcombe & Kramer (2003)- meta analysis examined effects of physical exercise (aerobic or aerobic+strength exercises).
    = found exercise improve congitive function more than the control group.
    = executive tasks most affected, may relatre to an accumaltive effect, as execxutivetasks rely on many simpler congitive proccesses cobmined.
    **combined exercise had better results than just aerobic and both short and long training was effective (although longer programmes were most effective).
    *only 30+ showed significant improvement**
  27. 27Park et al (2013) 2 types of engagement.Looked specifically at cognitive training and enrichment needed to improve cognitive abilities
    2 types of engagement:
    Productive
    &
    Receptive
  28. 28Productive engagement:- active learning and sustained activation of working memory, long term memory and other executive processes
    e.g digital photography & photo editing
  29. 29Receptive Engagement- passive observation, activation of existing knowledge, familiy activities.
    e.g social interaction activ iites, puzzles, listening to music.
  30. 30Findings == productive engagement groups showed greater improvement in episodic memory than receptive engagement groups.
    *effect was mainly down to the digital photography.
  31. 31Reasons why effect on episodic memory?= episodic memory benefited because productive activities improved strategic organisation behaviors.
    = unclear why this occurred, may be because people become better at learning/understanding things/organisation information better.
  32. 32DEMENTIA: Broad Definition.- affects all aspects of mind and brain.
    -Organic symtomes that cause behavioural, cogntive and emotional deficits.
    -usually degenerative (progressive decline).
    - Incurable and irreversible.
    -in most cases etiology also remains unknown.
  33. 33Prevalence and future estimates. Prince et alEpidemic of dementia because life expectancy has increased age is a high risk factor (much more common in developing countries)
    = however a recent study has shown that we may need to revise estimates downwards - as new estimates from a study saw small reduction in the rates of increase
    *could be down to more health life style choices which may delay the appearance of some forms of dementia.
  34. 34Prevelance of different forms of dementia:- Frontotemporal
    Lewy Body
    Vascular
    Alzheimers
    **Alzheimer is the most common.
    ** often vascular and AZ share some symptoms; shown at later stages of vascular dementia.
  35. 35ALZHEIMERS DISEASE: Brain Structure-Gross atrophy, especially at later stages of the disease.
    -Vast shrinkage, particularly in the hippo campus and internal cortex.
    (responsible for episodic memory deficits)
    - As it progresses these effects on the brain become more widespread and less specified.
  36. 36ALZHEIMER'S DISEASE Brain Function..- there are changes in activity not just structure - much less activity in AD patients.
  37. 37ALZHEIMER'S DISEASE Pathological featuresSpecific types of pathology are associated with AZ.
    Amyloid plaques: insoluble proteins based structures which form on the outside of neurons.
    - these plaques impair communication between cells and use of nutrients e.g glucose.
    2) Neurofibrillary tangles
    - changes in protein called Tau effect the skeleton by disintegrating the cells microtubles.
    -Tau protein threads form tangles inside the cell - which impair movement of nutrients within the cell
    *this in turn can activate cell destruction.
  38. 38Problems with the pathological features identified?X are not deifntive charecteistics as their presence has been found in the brain of many normal functioning older adults.
    **also present a long time before onset of any cognttiive symtoms.
  39. 39The 5 key stages of AZ:- it can be an asymptomatic disorder; present for decades before e see any symtoms
    1) preclinical AD
    2)Mild cognitive ipairment
    3) MILD AD
    4) MODERATE AD
    5) SEVERE AD.
  40. 401) pre clinical- dementia related changes in the brain can appear many years before any actual cogntiive symtoms but can still be detected in functional scans and in some cases by genetic tests
  41. 412) Mild cognitive impairments- more memory problems than just due to normal ageing process, so many thing its just absent mindedness and goes undetected.
    - But doesn't yet fit the criteria for dementia diagnosis.
  42. 423) MILD AD- Diagnosis likely-
    - detreriotion of memory problems
    - Addtional cognitive/information processing erors (e.g poor problem solving and judgement).
    - impaired thinking and expression
    - small mood and persoanility changes e.g irritable or withdrawn.
  43. 434) MODERATE AD- further deterioiation of memory problems also extending to autobiographical memories.
    - Confusion,poor judgement, disoreitnation.
    - loss of indepence - can need assitance in every day functions.
    - significant emotional and persoanlity changes (develop fears, become suspicous of family friends, sometimes hallucinate too)
  44. 445) SEVERE AD- PRE-fatal stage
    - loose ability to communicate coherently.
    - constant assistance needed
    - decline in physical ability too.
  45. 45AZ & Working memory- Clear drop in W.M performance in AZ' much bigger than in normal ageing.
    -Study that used AD and matched eldelrey normal controls tested on task designs to examine the central executive.
    = impaired performance for AD deteriorating across sessions
    - the elderly controls however showed smaller impairments and no deterioration across sessions.
  46. 46AZ & Long term memory Fleishman et al- AD affects new explicit learning i.e anterograde amnesia) and ability to learn new things.
    -This effects both recollection and familiarity.
    *some findings have suggest that MCI patients familiarity is persevered suggesting a possible progression of the disease from recollection to familiairty.
    *these findings are consistant with wide spready neuropathology (especially in later stages).
  47. 47AZ & forgetting from LTM Christiansen et al (1998) o AD patients forget information abnormally fast?- tested different materials and types of test after matching performance at earlier delay (as AD patients were already impaired).
    = found evidence for greater impairment in recollection compared to familiarity in A.D patients.
    X SMALL NUMBERS OF AD PATIENTS
    X STUDIES DIFFICULT TO CONDUCT WITH PATIENTS WHO HAVE SUCH POOR MEMORY.
  48. 48AZ & THE IMPLICIT MEMORY: RELIGIOUS ORDER STUDY.IJ

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FlashCards sobre Sem título, criado por Becca Sidley em 13-05-2016.
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