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Dementia involves impairments in functions of cognition that have a negative impact on daily life, and can involve memory impairments that exceed those which are prevalent in normal ageing (Kelley & Petersen, 2009). Other aspects of cognition should also be affected in dementia (for example attention, language, visuospatial skills and problem solving) and these impairments should exist in the absence of any conditions affecting perception (Kelley & Petersen, 2009). Different conditions can result in dementia, including Mild Cognitive Impairment, Alzheimer’s Disease, Frontotemporal Dementia and Vascular Dementia; each of these conditions can have implications on memory performance.

According to Heun et al. (2007), Mild Cognitive Impairment (MCI) can be recognised in people who have unaffected daily lives but a significant impairment in memory. MCI can also be identified as a decline in cognitive processes which is greater

than expected for normal ageing (Hämäläinen et al., 2007; Petersen et al., 2001). There is considerable debate over whether or not MCI is pre-requisite of Alzheimer’s Disease (AD). It has previously been stated that MCI is associated with the development of AD, that it is an early stage of the disease (Bennett et al., 2002; Heun et al., 2007), and that MCI ranks between normal elderly cognitive decline at one end of a scale and dementia at the other (Bröder, Herwig, Teipel, & Fast, 2008). MCI can be viewed as a high risk group for developing dementia but not all MCI patients progress to this stage (Chertkow et al., 2007; Pike, Rowe, Moss, & Savage, 2008).

Certain criteria must be present in experiments with MCI as participants. These include a presence of memory complaint, impaired performance in memory tasks which have been adjusted for age and education, general cognitive function remaining intact, absence of dementia, and daily living activities remaining normal (Belleville, Bherer, Lepage, Chertkow, & Gauthier, 2008; Meyer, Xu, Thornby, Chowdhury, & Quach, 2002). Wang and Zhou (2002) indicated that encoding in patients with MCI was very susceptible to impairment (Wang & Zhou, 2002), while other previous studies have indicated that retrieval and recollection of memories in MCI can be very impaired (Anderson et al., 2008; Bröder et al., 2008). If one considers the view that MCI is a pre-requisite to AD, then this is a good place to start when investigating pathological ageing.

Alzheimer’s Disease (AD) is one of the most common degenerative disorders affecting older adults which results in dementia (Ewers et al., 2012; Kelley & Petersen, 2009; Kidd, 2008), and impairments in memory are usually the first and earliest reported symptoms of AD (Bokde et al., 2010; Kidd, 2008). The disease was first observed by Aloysius Alzheimer in a patient with declining memory, confusion, disorientation, problems with expression and groundless suspicions (Kidd, 2008). After the patient’s death, an autopsy revealed atrophy of the brain (Kidd, 2008). The criteria

for diagnosing AD include the gradual progression of memory impairment along with cognitive impairments in one or more of the following: aphasia, apraxia, agnosia, dysexecutive function (see Table 1.1 below), and these impairments cannot be explained by other neurological or psychiatric disorders (Kelley & Petersen, 2009).

Memory impairments in AD have been reported in the domains of short- and long-term memory (MacDuffie, Atkins, Flegal, Clark, & Reuter-Lorenz, 2012), episodic memory (Salmon & Bondi, 2009), associative recognition memory (Hanaki et al., 2011) and spatial memory (Kessels, Feijen, & Postma, 2005). As the hippocampus and MTL have been implicated in the formation and storage of memory (Bayley & Squire, 2003;

L R Squire et al., 2004), it follows that atrophy of the MTL and hippocampus has been associated with AD (Jack et al., 1997). Jack and colleagues showed how the volume of the MTL and hippocampus was smaller in AD patients compared to healthy controls and that age was a factor in the decline of the volume of these structures (Jack et al., 1997). However, since this atrophy is apparent in the MTL and the hippocampus, these structures may then be used to predict the development of AD in MCI patients (Jack et al., 1999). Therefore atrophy to the hippocampus, which can be viewed with MRI, can be an indicator of subsequent AD.

Table 1.1: Diagnostic Criteria of the Alzheimer’s Type.

From “Alzheimer's disease and mild cognitive impairment,” by B. J. Kelley and R. C.

Petersen, 2009, Neurologic Clinics, 25, p. 29. Copyright [2009] by Elsevier. Reprinted with permission.

Frontotemporal Dementia (FTD) is a degenerative disorder which leads to deficits in behaviour, language and movement and can cause changes in personality, impulsiveness, overactivity or apathy (X. Wang, Shen, & Chen, 2013). After AD, it is the second most common cause of dementia (X. Wang et al., 2013). Pick (1892) first observed this type of dementia in a 71 year old man who was experiencing aphasia, dementia and behavioural problems. The autopsy revealed wasting of the temporal lobes (Goedert, Ghetti, & Spillantini, 2012). As such, degeneration of the frontal and temporal lobes along with other subcortical regions of the brain are associated with FTD (Goedert et al., 2012; Mackenzie et al., 2009).

Different pathologies have been associated with this disorder. These include a behavioural variant (semantic dementia) and progressive non-fluent aphasia (Hodges &

Miller, 2001; Mackenzie et al., 2009; Neary et al., 1998). With the behavioural variant, patients can become apathetic or they can exhibit socially improper behaviours (Baborie et al., 2012). Semantic dementia causes decrements in understanding meanings of words and identifying objects (Neary et al., 1998). Progressive non-fluent aphasia can cause problems with articulation, where speech is distorted but understanding words remains intact (Hodges & Miller, 2001). Until recently, it has been accepted that memory remains relatively intact in FTD. However, new evidence suggests that deficits in episodic memory (Hornberger & Piguet, 2012) and short-term and anterograde memory loss may be a factor in FTD (Baborie et al., 2012) with these types of memory declining in sufferers.

Vascular Dementia (VaD) is caused by hypoxia (loss of oxygen) or a haemorrhage (rupture of a blood vessel) in the brain, i.e. stroke (Battistin & Cagnin, 2010), with the consequence of dementia. VaD is used to refer to dementia under three different conditions: (1) multi-infarct dementia, where damage is caused by a series of

mini-strokes (Battistin & Cagnin, 2010); (2) a single ischemic lesion, resulting in atrophy due to a lack of oxygen (Sachdev et al., 2004); or (3) sub-cortical VaD, due to infarcts in small blood vessels within the cortex (Moretti et al., 2007; Price, Jefferson, Merino, Heilman, & Libon, 2005). VaD has been shown to cause disruptions and impairments across a range of cognitive domains, including attention, global memory, verbal memory, visual memory, execution function, abstract reasoning, working memory, language and speed of processing (Sachdev et al., 2004).

Leblanc, Meschia, Stuss and Hachinski (2006) have presented evidence for two types of genes involved in Vascular Dementia; one which increases susceptibility to VaD and another which influences the recovery of tissue following cerebrovascular disease. These genetic markers can allow for those at risk to be identified and a possible prophylactic treatment to be put in place (Leblanc et al., 2006). A set of diagnostic criteria have been developed for VaD: a cognitive decline must be present and this must include impairments in memory and deficits in at least two other cognitive domains; cerebrovascular disease must be identified (which can be carried out with neuroimaging); and finally, a clear relationship between the two above disorders must exist (Román et al., 1993), i.e. the impairments did not exist before the presence of cerebrovascular disease.

Four types of pathological ageing have been discussed here; MCI, AD, FTD and VaD, and these have shown to cause a large decrement in memory performance in adults with these conditions. While these decrements are considered to be attributed to disease, models of ageing can offer insight into the underlying processes regarding changes in cognitive performance in normal and pathological ageing.