Printer Friendly

THE NEUROPSYCHOLOGY OF ALZHEIMER'S AND PARKINSON'S DISEASE.

It is well established that neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD) pose major public health concern in the world's aging population. PD and AD are thought to be among the most common forms of neurodegenerative disorders affecting almost 1 in a 100 individuals in the age range of 70-90 years (Launer et al, 1999). The exact pathology and etiology of both diseases still remains elusive, despite several risk factors being identified (Mok et al., 2004). Among well-known risk factors one can identify a variety of genetic polymorphisms, endocrine diseases, oxidative stress, infection and inflammation, diabetes, smoking, head trauma, vitamin deficiencies, and nutritional problems (Launer et al, 1999). The lack of knowledge concerning the fundamental nature of this disease warrants further research and academic scrutiny.

The Cognitive Neuropsychology of Alzheimer's disease

Alzheimer's disease (AD) is thought to be a progressive neurodegenerative condition of still complex and unknown aetiology, and indeed one of the most common forms of dementia (Becker, 2004). This disorder was discovered by the German psychiatrist Alois Alzheimer in 1906. Although this disease is well characterized neuropathologically, it is still difficult to accurately diagnose it in its entirety (Becker, 2004). In this respect, it has been postulated that due to the subtle signs of AD it is sometimes not differentiated from features characteristic of other central nervous system disorders (Bondi et al, 2003). Among the features of AD one can identify symptoms such as severe amnesia, language deficits, and decline visuospatial abilities (Netsky, 1983). It should also be evident that there are more than 50 different causes of brain dysfunction associated with AD, and the disease itself can only be diagnosed through verification of characteristic neurodegenerative abnormalities such as neurofibrillary tangles (Khachaturian, 1985). In this respect, evidence from structural and functional neuroimaging has revealed that advanced AD is thought to implicate neurofibrially tangles, loss of neurons and synapses, as well as the presence of neuritic plaques (Tuokko, Kristjansson & Miller, 1995; Wright & Persad, 2007).

Despite the fact that the cause of AD remains unknown, one can still identify a number of risk factors. For instance, to present, age is thought to be the single most important risk factor, specifically between the ages of 65 and 85 (Katzman & Kawas, 1994). Furthermore, it is thought that diagnosis of Alzheimer's also requires the presence of clinically significant impairments in two or more cognitive domains (McKhann et al, 2011). Epidemiological studies have consistently demonstrated that people who are normally classified with Mild Cognitive Impairment (MCI) show considerably high conversion rates to AD (Busse et al., 2006; Gauthier et al., 2006; Jak et al., 2009; Loewenstein, Acevedo, Agron, & Duara, 2007; Tuokko & McDowell, 2006). In turn, MCI has been shown to be a reliable precursor stage to the development of Alzheimer's disease (Summers & Saunders, 2012). Summers and Saunders (2012) found that patterns of impairments on verbal and visual episodic memory, working memory, short-term memory, and attentional processing can be strong prognostic indicators of development of AD. However, MCI has also attracted some criticism from some who argued that at an individual level MCI may not be as stable as initially thought given that longitudinal studies have shown that a substantial proportion of participants with cognitive deficits reverted to normal level of cognition (Busse et al., 2006; Gauthier et al., 2006). Similarly, other studies (see Summers & Saunders, 2012) suggested that cognitive deficits such as amnestic impairment alone lack of predictive validity and reliability when it comes to identifying risk of developing AD.

However, it is still difficult to identify which patients are at a preclinical phase given that there is a variety of overlapping cognitive impairments in AD. One can also identify some level of comorbidity associated with the AD. For instance, it has been postulated that depression may co-occur with AD (Pfenning, Littman & Bauer, 2007). The fact that depression symptoms can overlap with AD symptoms can sometimes lead to mischaracterization of cognitive deficits as preclinical AD. It is also interesting to notice that depression can indeed be a strong predictor of AD. For instance, a number of studies have found that depressive symptoms and depression in general predicts cognitive decline and AD (Jorm, 2001; Ownby et al, 2006). Two broad theories emerged from studies connecting depression to AD; (1) Depression is thought to increase the risk for AD by damaging the hippocampus (Sapolsky, Krey & McEwan, 1986). (2) Depression can potentially be an early indicator of AD (Andreescu et al, 2008). It is also interesting to notice that given that both accounts received strong empirical support, and this factor can lead one to speculate that both explanations could be combined when explaining the relationship between depression and AD. According to the hypothesis postulated by Sapolsky (1996) it would appear that chronic stressors and depression are related to prolonged activation of hypothalamic-pituitary-adrenal (HPA) axis. In turn, it is thought that the HPA axis engages the pituitary and adrenal glands, as well as the hypothalamus. The hypothalamus releases vasopressin and corticotropin-releasing hormone in response to stress. The pituitary gland then releases adrenocorticotropic hormone (ACTH), which consequently stimulates adrenal gland to release corticosteroids like cortisol (McEwen, 1999). It could be argued that long-term exposure to stress during depressive episodes could lead to prolonged high levels of cortisol associated with shrinking and cell death in the hippocampus (McEwen, 1999).

The hypothesis proposed by Andreescu et al (2008) also postulates that smaller hippocampal volumes can be a strong prognostic indicator for neuronal loss in depressed individuals. Nonetheless, one should note that the two aforementioned approaches (prodrome hypothesis and glucocorticoid cascade hypothesis) diverge in their predictions about the extent to what individuals develop late-life depression as an early symptom of AD (see Brommelhoff et al, 2009) or that depression simply acts as a risk factor for development of AD (van Reekum et al, 1999). There are overlapping symptoms in depression and AD. For example, it appears that depressed patients are at higher risk of AD. However, it is not easy to distinguish between the two disorders given that they have a range of overlapping symptoms (Marin, Sewell, & Schlechter, 2002). One important distinction that should be made is that although neuropsychological impairment in depression could be successfully treated, the same cannot be said about neuropsychological impairment in AD (Marin, Sewell, & Schlechter, 2002). In terms of treatment, it has been argued that it will have its best effect when starting as early as possible, specially before irreversible brain damage has occurred (Gauthier, 2005).

The Cognitive Neuropsychology of Parkinson's disease

Similar to Alzheimer's disease, Parkinson's disease (PD) is a very common neurodegenerative disorder which can affect 100-150 individuals per 100,000 inhabitants (Tandberg et al, 1995). Again, just like AD, the exact nature and specific aetiology of PD remains unknown in most cases. It is thought that PD is present in all countries which prevalence studies have been systematically conducted (Tandberg et al, 1995). In terms of gender differences, it is thought that PD is equally prevalent in men as it is in women (Zhang & Roman, 1993). Despite the nature of PD being quite elusive, a number of risk factors have been identified as potential prognostic indicator of PD development. These include genetic factors, head trauma, vascular disease, infections, and sub-clinical intoxications (Duvoisin, 1993; Rybicki, Johnson, Uman, & Gorell, 1993; Tipton, McCrodden, & Sullivan, 1993). In terms of key features, PD is primarily characterized by rigidity, postural instability, bradykinesia, and resting tremor (Braak et al., 2004). From a pathological view point, it is well established that PD is defined as loss of dopaminergic neurons in the substantia nigra. In addition, PD is also characterized by formation of [alpha]-synuclein positive Lewy bodies within remaining neurons (Braak et al., 2004). One should also note that in addition to degeneration of the dopaminergic system, one can also identify other affected neurotransmitter systems. These include the cholinergic system (nucleus basasils of Meynert), the serotonergic system, and the noradrenergic system (Jellinger, 1999). In addition, one should note that PD is also marked by cortical changes and presence of Lewy bodies, amyloid plaques and neurofibrillary tangles (NFT [Jellinger, Seppi, Wenning & Poewe, 2002]). In terms of diagnosis of PD, it is thought that clinicians rely considerably on patients' medical history and clinical examination (Larsen, Dupont, & Tandberg, 1994). It is also interesting to notice that Neuroimaging studies have found that visualization of dopamine transporter by means of photon emission computed tomography (SPECT) could play a key role in diagnosis of PD (Walker et al, 2004).

Like AD, PD and its etiology is also characterized by much heterogeneity (Foltynie et al, 2005). In this respect, one can identify a range of different patients, including those with rapid disease progression, those with tremor and non-tremor dominant and patients belonging to the younger onset class (Giovannini et al, 1991). For instance, when looking at PD patients with young onset of the disease, it would appear that they are characterized by having a much slower rate of progression of Parkinson's. In addition, the young onset patients also have slightly greater potential to develop motor fluctuations (Gibb & Lees, 1988). This factor could in fact be a consequence of prolonged exposure to levodopa (Hughes, Daniel, Blankson & Lees, 1993). It is also interesting to notice that the tremor dominant subgroup has less cognitive impairment (Zetusky et al, 1985) and slower rate of PD progression (Jankovic et al, 1990). In contrast, it would appear that patients in the non-tremor category have mild executive impairment and are affected by mild depression (Wenning et al, 1994). Finally, patients who experience rapid progression of the disease sometimes exhibit no signs of cognitive impairments (Morrish, Sawle, & Brooks, 1995).

In terms of general cognitive functioning in PD affected patients it should be noted that contrary to what was previously assumed, cognitive impairment is very common even in very early PD (Foltynie et al, 2004). In addition, it has been argued that even if cognitive impairments are not immediately apparent, they are, nonetheless detectable through neuropsychological tests (Muslimovic, Post, Speelman, & Schmand, 2005). Furthermore, with the progression of PD there are a substantial amount of patients which develop dementia (Emre, 2003). Moreover, among other neuropsychological symptoms one can also identify visual hallucinations and apathy may also be found among the most common (Aarsland & Karlsen, 1999). In this way, Parkinson's disease has become increasingly recognized as not only a mere movement disorder, but also as a neuropsychiatric disorder. In this way, studies have consistently demonstrated the clinical importance of the aforementioned symptoms, as this provides useful insights for planning and caring for patients affected by PD (Schrag, Jahanshahi, & Quinn, 2000; Aarsland, Larsen, Tandberg, & Laake, 2000).

It is also worth mentioning that the neurocircuitry of the basal ganglia has been implicated in the etiology of PD (Obeso et al, 2000). In this respect, it is thought that 'motor circuit' of the basal ganglia nuclei is directly related to movement problems such as the ones observed in PD (Obeso et al, 2000). Furthermore, when comparing AD and PD patients, it would also appear that PD patients perform better at explicit learning tasks compared to AD patients. Additionally, PD patients are significantly more impaired in implicit learning tasks compared to AD patients (Bondi & Kaszniak, 1991). This raises some important issues concerning the neural circuitry underpinning explicit and implicit learning in both PD and AD patients.

CONCLUSION

It appears that there are a number of similarities between AD and PD. Although the two are not related, both PD and AD have an onset that is late in life (normally after the age of 50). In addition, both diseases are neurodegenerative, and progressive, leading to damage of neurons, and becoming increasingly worse as time goes by. Among similarities between

AD and PD one should also note that both diseases led to dementia, and severe impairment of executive functioning. Despite the causes for both AD and PD being elusive, one could argue that future studies should seek to integrate more multidisciplinary approaches as means of getting further insights into to the underlying etiology of both AD and PD. In this respect, it is thought that Biopsychosocial approaches could offer some useful insights into examining both disorders in greater detail, as well as positioning them within a much broader context.

REFERENCES

Aarsland, D., & Karlsen, K. (1999). Neuropsychiatric aspects of Parkinson's disease. Current Psychiatry Reports. Vol.1, (1), pp. 61-68.

Aarsland, D., Larsen, J. P., Tandberg, E., & Laake, K. (2000). Predictors of nursing home placement in Parkinson's disease: A population-based, prospective study. Journal of the American Geriatrics Society, Vol.48, (8), pp. 938-942.

Andreescu, C., Butters, M. A., Begley, A., Rajji, T., Wu, M., Meltzer, C. C. & Aizenstein, H. (2008). Gray matter changes in late life depression--a structural MRI analysis. Neuropsychopharmacology, Vol.33, pp. 2566-2572.

Becker, J. (2004). Cognitive neuropsychology of Alzheimer's disease. Oxford: Oxford University Press.

Bondi, M. W., & Kaszniak, A. W. (1991). Implicit and explicit memory in Alzheimer's disease and Parkinson's disease. Journal of Clinical and Experimental Neuropsychology, Vol.13, (2), pp. 339-358.

Bondi, M. W., Houston, W. S., Salmon, D. P., Corey-Bloom, J., Katzman, R., Thal, L. J., & Delis, D. C. (2003). Neuropsychological deficits associated with Alzheimer's disease in the very-old: Discrepancies in raw vs. standardized scores. Journal of the International Neuropsychological Society, Vol.9, (5), pp. 783-795.

Braak, H., Ghebremedhin, E., Rub, U., Bratzke, H., & Del Tredici, K. (2004). Stages in the development of Parkinson's disease-related pathology. Cell and Tissue Research, Vol.318, (1), pp. 121-134.

Brommelhoff, J. A., Gatz, M., Johansson, B., McArdle, J. J., Fratiglioni, L., & Pedersen, N. L. (2009). Depression as a risk factor or prodomal feature for dementia? Findings in a population-based sample of Swedish twins. Psychology and Aging, Vol. 24, pp. 373-384.

Busse, A., Hensel, A., Guhne, U., Angermeyer, M. C., & Riedel-Heller, S. G. (2006). Mild cognitive impairment: Long-term course of four clinical subtypes. Neurology, Vol.67, pp. 2176-2185

Duvoisin, R. C. (1993). The genetics of Parkinson's disease. A review. Advances in Neurology, Vol.60, pp. 306-315

Emre, M. (2003) What causes mental dysfunction in Parkinson's disease? Movement Disorders. Vol.18, (6), pp. 63-71

Gauthier, S. G. (2005). Alzheimer's disease: The benefits of early treatment. European Journal of Neurology, Vol.12, pp. 11-16.

Gauthier, S., Reisberg, B., Zaudig, M., Petersen, R. C., Ritchie, K., Broich, K.,Winblad, B. (2006). Mild cognitive impairment. The Lancet, Vol.367, pp. 1262-1270

Gibb, W. R., & Lees, A. J. (1988). A comparison of clinical and pathological features of young- and old-onset Parkinson's disease. Neurology, Vol.38, (9), pp. 1402-1406.

Giovannini, P., Piccolo, I., Genitrini, S., Soliveri, P., Girotti, F., Geminiani, G., Scigliano, G., & Caraceni, T. (1991). Early-onset Parkinson's disease. Movement Disorders. Vol.6, (1), pp. 36-42.

Hughes, A. J., Daniel, S. E., Blankson, S., & Lees, A. J. (1993). A clinicopathologic study of 100 cases of Parkinson's disease. Archives of Neurology, Vol.50, (2), pp. 140-148.

Jak, A. J., Urban, S., McCauley, A., Bangen, K. J., Delano-Wood, L., Corey-Bloom, J., & Bondi, W. (2009). Profile of hippocampal volumes and stroke risk varies by neuropsychological definition of mild cognitive impairment. Journal of the International Neuropsychological Society, Vol.15, pp. 890-897

Jankovic, J., McDermott, M., Carter, J., Gauthier, S., Goetz, C., Golbe, L., Huber, S., Koller, W., Olanow, C., Shoulson, I., & et al. (1990). Variable expression of Parkinson's disease: a base-line analysis of the DATATOP cohort. The Parkinson Study Group. Neurology, Vol.40, (10), pp. 1529-1534

Jellinger, K. A. (1999a). Neuroptahological correlates of mental dysfunction in Parkinson's disease: un update. In E. C. Wolters, Scheltens, P., Berendse, H.W. (Ed.), Mental dysfunction in Parkinson's disease: II (pp. 82-105). Utrecht: Academic Pharmaceutic Production

Jellinger, K. A., Seppi, K., Wenning, G. K., & Poewe, W. (2002). Impact of coexistent Alzheimer pathology on the natural history of Parkinson's disease. Journal of Neural Transmission, Vol.109, (3), pp. 329-339.

Jorm, A. F. (2001). History of depression as a risk factor for dementia: An updated review. Australian and New Zealand Journal of Psychiatry, Vol.35, pp. 776-781.

Khachaturian, Z. S. (1985). Diagnosis of Alzheimer's disease. Archives of Neurology, Vol. 42(11), pp. 1097-1105.

Larsen, J. P., Dupont, E., & Tandberg, E. (1994). Clinical diagnosis of Parkinson's disease. Proposal of diagnostic subgroups classified at different levels of confidence. Acta Neurologica Scandinavica, Vol. 89(4), pp. 242-251

Launer LJ, Andersen K, Dewey ME, Letenneur L, Ott A, Amaducci LA, Brayne C, Copeland JR, Dartigues JF, Kragh-Sorensen P, Lobo A, Martinez-Lage JM, Stijnen T, Hofman A. (1999) Rates and risk factors for dementia and Alzheimer's disease: results from EURODEM pooled analyses. EURODEM Incidence Research Group and Work Groups. European Studies of Dementia. Neurology. Vol.52, pp. 78-84

Loewenstein, D. A., Acevedo, A., Agron, J., & Duara, R. (2007). Stability of neurocognitive impairment in different subtypes of mild cognitive impairment. Dementia and Geriatric Cognitive Disorders, Vol.23, pp. 82-86

Marin, D., Sewell, M. & Schlechter, A. (2002). Alzheimer's disease: Accurate and early diagnosis in the primary care setting. Geriatrics, Vol.57, 36-40

Morrish, P. K., Sawle, G. V. & Brooks, D. J. (1995). Clinical and [18F] dopa PET findings in early Parkinson's disease. Journal of Neurological Neurosurgical Psychiatry, Vol.59, (6), pp. 597-600

Muslimovic, D., Post, B., Speelman, J. D., & Schmand, B. (2005) Cognitive profile of patients with newly diagnosed Parkinson disease. Neurology, Vol.65, (8), pp. 1239-1245

Netsky, M. G. (1983). Alzheimer's Disease. A Report of Progress in Research. Journal of Neuropathology & Experimental Neurology, Vol. 42(1), Vol.108-109.

Obeso, J. A., Rodriguez-Oroz, M. C., Rodriguez, M., Lanciego, J. L., Artieda, J., Gonzalo, N., & Olanow, C. W. (2000). Pathophysiology of the basal ganglia in Parkinson's disease. Trends in Neurosciences, Vol.23, pp. 8-pp. 19.

Ownby, R. L., Crocco, E., Acevedo, A., John, V., & Loewenstein, D. (2006). Depression and risk for Alzheimer disease. Systematic review, meta-analysis, and meta-regression analysis. Archives of General Psychiatry, Vol.63, pp. 530-538.

Pfennig, A., Littmann, E., & Bauer, M. (2007). Neurocognitive impairment and dementia in mood disorders. The Journal of Neuropsychiatry and Clinical Neurosciences, Vol.19, (4), pp. 373-382.
COPYRIGHT 2017 Oxford Mosaic Publications Limited
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2017 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Pereira, Mauro Ramos De Jesus
Publication:Journal of Social and Psychological Sciences
Article Type:Report
Date:Jan 1, 2017
Words:2965
Previous Article:UNDERSTANDING THE NATURE AND AETIOLOGY OF SCHIZOPHRENIA.
Next Article:WHAT IS THE RELATIONSHIP BETWEEN WORKING MEMORY AND A HEIGHTENED SENSE OF AROUSAL?
Topics:

Terms of use | Privacy policy | Copyright © 2020 Farlex, Inc. | Feedback | For webmasters