The brain structural and cognitive basis of odor identification deficits in mild cognitive impairment and Alzheimer’s disease
1 Department of Circulation and Medical Imaging, Norwegian University of Science and Technology (NTNU), Trondheim, Norway
2 Department of Geriatrics, St. Olav’s Hospital, University Hospital of Trondheim, Trondheim, Norway
3 Department of Neuroscience, Medical Faculty, Pb. 8905, Norwegian University of Science and Technology (NTNU), Trondheim, 7491, Norway
4 Department of Neurology, St. Olav’s Hospital, University Hospital of Trondheim, Trondheim, Norway
5 Norwegian Centre for Ageing and Health, Department of Geriatric Medicine, Oslo University Hospital, Oslo, Norway
6 Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway
7 Department of Medical Imaging, St. Olav’s Hospital, University Hospital of Trondheim, Trondheim, Norway
BMC Neurology 2014, 14:168 doi:10.1186/s12883-014-0168-1Published: 26 August 2014
The objectives of this study were to explore the relationship between olfactory impairment, cognitive measures, and brain structure volumes in healthy elderly individuals, compared to patients with amnestic mild cognitive impairment (aMCI) or early Alzheimer’s disease (AD). The primary aim was to elucidate possible differences in cognitive scores and brain structure volumes between aMCI/AD patients with relatively intact odor identification (OI) ability and those with reduced ability.
Twelve patients with aMCI, six with early AD, and 30 control subjects were included. OI abilities were assessed with the Brief Smell Identification Test (B-SIT) and Sniffin Sticks Identification Test (SSIT). Neuropsychological tests of executive functions and memory were performed. Brain structural volumes were obtained from T1 weighted 3D MRI at 3 Tesla. Statistical comparisons between the patients with aMCI and AD indicated no significant differences in performance on most tests. Since the groups were small and AD patients were in an early phase of disease, all patients were subsequently considered together as a single group for studying OI. Patients were subdivided into relatively intact (scores >50%) and reduced OI (≤ 50% score) on the olfactory tests.
The aMCI/AD group with reduced OI ability, as measured by both B-SIT and SSIT, had significantly smaller hippocampal volume as compared to the patient group with OI scores > 50%. There was a significant association between OI scores and hippocampal volume in the patient (not the control) group. Similar changes with tests of executive function and memory were not found. Low OI scores on B-SIT were associated with conversion from aMCI to AD in patients. The reduced OI patient group was significantly faster on Rey complex figure copying than the fairly intact OI group.
The results from this pilot study suggest that the reduction in the size of hippocampus in connection with early AD is associated more with loss of OI ability rather than loss of memory, thus demonstrating that impaired OI is an early marker of medial temporal lobe degeneration.