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Aging and dementia (Three theories of aging memory (1. Frontal lobe…

- - - - Crystallised intelligence refers to knowledge that is invariant and is typified by measures of language ability such as the Mill Hill Vocabulary Test (Raven 1982) and the National Adult Reading Test.
      - Fluid intelligence represents the ability to think flexibility and is best characterised and fluid intelligence dissociate with age. Vocab remains either invariant with age or actually shows an improvements ( Sathouse et al. 1996). In contrast, fluid intelligence declines with age.
      - Some researchers have proposed that there is a link between fluid intelligence and afe0related memory losee - the argument being that memory is an activity which requires cognitive flexibility both at encoding and retrieval. As a results, any loss of cognitive flexibility would be sure to affect memory. A number of studies have supported this idea. Holland and Rabbitt (1990) showed that the specificity of autobiographical recall in older subjects was predicted by problem solving tasks (which demonstrated fluidity).
  - - - The decrease in processing resources with aging has been related to the so-called cognitive primitives, i.e. working memory, inhibition, and processing speed, which can be considered as variables that influence the cognitive system (e.g., Verhaeghen, et al. 2003). These general constructs have, indeed, become a central feature in explaining age-related differences in older adults in many cognitive domains.
        
        In the case of working memory, intended as the amount of cognitive resources available to store information while at the same time processing incoming or recently accessed information for use in other cognitive tasks (Baddeley, 1986), a large number of studies have clearly shown a poorer working memory performance in older adults in comparison to younger adults (e.g., De Beni and Palladino, 2004
  - - - It is striking that general mental slowing appears to account for almost all of the aging effect on memory. The account suggests that an older person given sufficient time would behave just like
        a younger person, and that training designed to improve processing speed should improve memory too.
- - - - Similarly, using the latest structural MRI techniques to measure cortical thickness, Bakkour et al. (2013) catalogued a network of brain areas, particularly involving prefrontal cortex, susceptible to age-related decline.
      - Tisserand et al. (2004) studied individuals with a mean age of 72 and gave them 2 MRI scans separated by 3 years.
        They also administered a battery of cognitive tests (including memory tests) and the results of these allowed Tisserand et
        al. to divide participants into ‘decliners’ and ‘non-decliners’. In the former (compared to the latter), brain density was
        lower not only in the hippocampus but also the frontal pole, prefrontal cortex, inferior temporal gyrus, and parietal
        cortex.
      - BUT these results could be the result or the cause of cognitive decline!
        
        Amiera et al. (2014)- brains of well educated and poorly educated adults were scanned at repeated intervals, as well as cognitive measures being taken. In well educated individuals, the first signs of decline were seen in the brain approximated 7 years before any decline was seen in cognitive measures. Less educated group: onset of brain decline and decline in cognition were more tightly coupled in time. This suggests taht some level of compensation amy occur in the brain of more well-educated individuals. Therefore in individuals that maintain faster processing, memory may be maintained at a higher level for longer despite underslying brain degeneration.
      - Raz et al. (2004), for example, conducted a pair of MRI scans on the brains of individuals across a 5 year interval and used these to estimate the volume of the hippocampus and entorhinal cortex (the remaining temporal lobe tissue). They found that the shrinkage of the hippocampus increased with age: 1.2% per annum for those over 50 compared with 0.5% per annum in those under 50. Nevertheless, aging has effects that are widespread across the brain.
  - - - Cohen et al. (2001) have found, by comparing MRI brain scans across a 2-year interval in 50-60 year-olds either positive or negative for the APOE gene, that hippocampal volume loss is greater in those with the gene even when no cognitive signs of AD are detectable.
      - The effects of AD on the brain are very widespread. In Bakkour et al.’s (2013) study, described above, MRI scans from AD patients (mean age 77) were compared with those of age-matched healthy older (mean age 78) and younger (mean age 22) controls. Group differences were detectable across much of the brain. Nevertheless, loss was greatest in the left hemisphere and in the temporal and parietal cortices. The reduction in cortical thickness was 18% in some regions for the AD vs. young comparison, compared to only 5% for the healthy old vs. young comparison. Moreover, the overall profile was very different between healthy aging and AD: AD is not simply a continuation of the normal aging trajectory, but appears to be qualitatively different at a neural level.
      - Price et al. (2002) One prominent hypothesis is that amyloid deposits (plaques) and soluble forms of amyloid lead to neuronal dysfunction and cell death. Pathology, in particular neurofibrillary tangles, is prominent in the medial temporal lobe early in the disease and spreads outward to association cortex over time
- - - - Hall et al, (2007) gave repeated memory tests to patients with dementia. Each year a person was in eduction was associated with a delay in memory decline
        
        Lenehon et al, (2015): this is not due to the education itself its related to maintatining a high level of cognitive functioning in old age