In the usual case, the dementia syndrome is characterized by prominent amnesia with additional deficits in language and semantic knowledge, abstract reasoning, executive functions, attention, and visuospatial abilities ( Salmon & Bondi 1999). Consistent with these widespread neuropathological changes, the primary clinical manifestation of AD is a progressive global dementia syndrome that usually begins in later life (i.e., ages 60–70).
Neuropsychological Detection of Alzheimer's DiseaseĪlzheimer's disease is an age-related degenerative brain disorder characterized by neuronal atrophy, synapse loss, and the abnormal accumulation of amyloidogenic plaques and neurofibrillary tangles in medial temporal lobe limbic structures (e.g., entorhinal cortex, hippocampus) and the association cortices of the frontal, temporal, and parietal lobes ( Braak & Braak 1991).
The contributions of this research to the neuropsychological assessment of dementia are reviewed below. The cognitive manifestations of AD have been compared and contrasted to those of other age-related neurodegenerative disorders in order to improve differential diagnosis and provide information about the neurological basis of various cognitive abilities that are affected. The impact of aging on the ability to detect AD has been described, and subtle cognitive changes that might foreshadow the development of dementia in those with “preclinical” AD have been identified. This research has led to increased knowledge about the particular cognitive deficits that occur in the earliest stages of AD, and this has enhanced the ability to clinically diagnosis the disease early in its course. Neuropsychological research on dementia has focused on AD because it is the most common cause of dementia and is primarily defined by its impact on cognition. Accurate clinical diagnosis of dementia and its underlying cause is crucial for prognosis and the early and appropriate application of disease-specific treatments that are currently available or in development. This can be a particularly difficult task given the insidious onset and slow progression of most neurodegenerative diseases, but it is critically important given the lack of a reliable biological marker that can distinguish AD from normal aging or other neurodegenerative disorders that lead to dementia.
This interest is fueled by the need to accurately detect the onset of cognitive changes that signal the beginning of a progressive dementia syndrome and to differentiate among disorders with distinct etiologies and sites of pathology. The detection and characterization of cognitive deficits associated with age-related neurodegenerative diseases such as Alzheimer's disease (AD) is the focus of growing clinical research interest as increasing numbers of people survive into older age. Knowledge of these differences helps to clinically distinguish among various causes of dementia and provides useful models for understanding brain-behavior relationships that mediate cognitive abilities affected in various neurodegenerative diseases. Discrete patterns of cognitive deficits occur in AD and several neuropathologically distinct age-associated neurodegenerative disorders. Although decline in episodic memory is usually the earliest cognitive change that occurs prior to the development of the AD dementia syndrome, asymmetry in cognitive abilities may also occur in this “preclinical” phase of the disease and predict imminent dementia.
The qualitatively distinct pattern of deficits is less salient in very old AD patients than in younger AD patients. Quantitative and qualitative differences are apparent across many cognitive domains, but are especially obvious in episodic memory (particularly delayed recall), semantic knowledge, and some aspects of executive functions. Neuropsychological studies show that cognitive deficits associated with Alzheimer's disease (AD) are distinct from age-associated cognitive decline.
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