Odor Identification Deficits in MCI and Alzheimer's Disease
Odor Identification Deficits in MCI and Alzheimer's Disease
Tests of odor identification (OI) can discriminate neurodegenerative diseases, such as Alzheimer's disease (AD) from normal aging, with high sensitivity and specificity. The first observed olfactory deficit in patients with AD is not the ability to detect various odors, but to identify them correctly.
Olfactory deficits have also frequently been reported in mild cognitive impairment (MCI), and there seem to be no significant differences between non-amnestic and amnestic MCI (aMCI) regarding OI performance. Interestingly, studies using the Brief Smell Identification Test (B-SIT) show that both probable AD patients and MCI subtypes score throughout the range of the test, thereby indicating that some probable AD and MCI patients have a relatively intact OI ability. OI ability can therefore not be used to distinguish patients with MCI from those with AD. The reason why some patients retain OI ability longer than others is unknown, and we wished to investigate this further in the present study.
Pathological changes in different areas of the olfactory system have been suggested to cause the deficits of OI function in patients with AD, as well as other forms of dementia. The OI deficit has been shown to correlate with the number of tangles in the entorhinal cortex and hippocampus in AD pathology. Neuroimaging studies support a particular role for the medial temporal lobe in OI in healthy controls, and in normal aging the activity during OI decreases in these areas with age. Cross-sectional and longitudinal volumetric studies have demonstrated a strong correlation between volume of the hippocampus and OI ability in AD. Other non-CNS factors possibly affecting olfaction in AD include deposits of tau protein and beta-amyloid in the olfactory epithelium, and a reduced number of mitral cells and axonal loss in the olfactory tract. OI performance has been shown to be associated with cognitive speed, verbal fluency, and memory in healthy controls and MCI/AD patients.
There is currently little information regarding factors that differentiate patients with comparatively intact compared to impaired OI function in early AD, though OI has been found to predict conversion of MCI to AD. The main goal of this study was therefore to explore the relationship between the integrity of OI function, cognitive measures, and brain structure volume in healthy elderly individuals, compared to patients with aMCI or early AD. We also wished to examine whether differences in cognitive measures and brain structure volumes could be detected when patients were divided according to their OI ability.
Background
Tests of odor identification (OI) can discriminate neurodegenerative diseases, such as Alzheimer's disease (AD) from normal aging, with high sensitivity and specificity. The first observed olfactory deficit in patients with AD is not the ability to detect various odors, but to identify them correctly.
Olfactory deficits have also frequently been reported in mild cognitive impairment (MCI), and there seem to be no significant differences between non-amnestic and amnestic MCI (aMCI) regarding OI performance. Interestingly, studies using the Brief Smell Identification Test (B-SIT) show that both probable AD patients and MCI subtypes score throughout the range of the test, thereby indicating that some probable AD and MCI patients have a relatively intact OI ability. OI ability can therefore not be used to distinguish patients with MCI from those with AD. The reason why some patients retain OI ability longer than others is unknown, and we wished to investigate this further in the present study.
Pathological changes in different areas of the olfactory system have been suggested to cause the deficits of OI function in patients with AD, as well as other forms of dementia. The OI deficit has been shown to correlate with the number of tangles in the entorhinal cortex and hippocampus in AD pathology. Neuroimaging studies support a particular role for the medial temporal lobe in OI in healthy controls, and in normal aging the activity during OI decreases in these areas with age. Cross-sectional and longitudinal volumetric studies have demonstrated a strong correlation between volume of the hippocampus and OI ability in AD. Other non-CNS factors possibly affecting olfaction in AD include deposits of tau protein and beta-amyloid in the olfactory epithelium, and a reduced number of mitral cells and axonal loss in the olfactory tract. OI performance has been shown to be associated with cognitive speed, verbal fluency, and memory in healthy controls and MCI/AD patients.
There is currently little information regarding factors that differentiate patients with comparatively intact compared to impaired OI function in early AD, though OI has been found to predict conversion of MCI to AD. The main goal of this study was therefore to explore the relationship between the integrity of OI function, cognitive measures, and brain structure volume in healthy elderly individuals, compared to patients with aMCI or early AD. We also wished to examine whether differences in cognitive measures and brain structure volumes could be detected when patients were divided according to their OI ability.
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