P1098
Poster Presentations: Tuesday, July 18, 2017
Table 1 SUVR values with respect to cerebellum grey for few example ROIs (with and without grey mask) of an example early AD subject
produce cognitive decline, and drives amyloid-independent brain atrophy during the earliest stage of disease.
SUVRcerebellum_grey Without GM mask With GM mask Regions
Ab
Tau
Ab
Tau
Cortical Parahippocampus Ambiens Gyrus Parahippocampus Subiculum Gyrus Frontal Lobe Anterior Cingulate Gyrus Middle Temporal Gyrus Amygdala Thalamus Cerebellum
1.7897 1.2681 1.3130 1.8248 1.9104 1.8238 1.2430 1.4182 1.0728
1.5178 1.6853 1.3581 1.5478 1.5855 1.8219 1.4781 1.1118 1.0025
1.8212 1.3254 1.3370 1.8935 1.9517 1.8442 1.2978 1.3671 1
1.5639 1.7746 1.3928 1.6043 1.6038 1.8713 1.6159 1.1611 1
P3-366
CEREBROVASCULAR RESISTANCE AND CEREBRAL AMYLOIDOSIS: EFFECTS ON COGNITIVE DECLINE, CORTICAL ATROPHY AND PROGRESSION TO DEMENTIA
Belinda Yew, Daniel A. Nation, University of Southern California, Los Angeles, CA, USA. Contact e-mail:
[email protected] Background: Vascular risk factors have been increasingly implicated in Alzheimer’s disease (AD). Blood pressure and decreased cerebral blood flow (CBF) are of particular interest given their links to AD biomarkers and clinical progression. We therefore hypothesized that elevated ratio of blood pressure to CBF, indicative of cerebrovascular resistance, would predict amyloid retention, cognitive decline, cortical thinning, and progression to dementia over a 2-year period, independent of neuronal metabolism. Methods: Older adults with (n ¼ 33) and without (n ¼ 199) AD underwent arterial spin labeling magnetic resonance imaging to measure regional CBF in brain regions susceptible to aging and AD. An estimated cerebrovascular resistance index (CVRi) was then calculated as the ratio of mean arterial pressure to regional CBF. Positron emission tomography with florbetapir-fluorine-18 (18F) and fludeoxyglucose was used to quantify amyloid retention and neuronal metabolism, respectively. Non-demented participants were classified as Ab– or Ab+ based on florbetapir-indexed amyloid load. Cognitive performance was evaluated via annual assessments of global cognition, memory, and executive function. Linear mixed models and regression were used to assess CVRi prediction of cognitive performance, amyloid, and atrophy over 2 years. CVRi prediction of progression to dementia was evaluated using logistic regression. Results: CVRi was significantly elevated in nondemented Ab+ versus Ab– participants, with further elevation observed in AD patients. CVRi group differences were also of greater statistical effect size and encompassed a greater number of brain regions, than those for CBF alone, including frontal, parietal, temporal, and hippocampal areas. Cognitive decline over 2-year follow-up was accelerated by elevated baseline CVRi, particularly for amyloid-positive individuals. Higher CVRi was also associated with elevated inferior temporal amyloid retention and cortical thinning 2 years later. Finally, increased CVRi predicted greater progression to dementia, beyond that attributable to amyloid-positivity. Conclusions: Findings suggest that increased cerebrovascular resistance may represent a previously unrecognized contributor to Alzheimer’s disease that is independent of neuronal hypometabolism, predates changes in brain perfusion, exacerbates and works synergistically with amyloidosis to
P3-367
THE SUBCORTICAL INTRINSIC ACTIVITY ABNORMALITY UNDERLYING THE SPATIAL NAVIGATION DEFICIT IN MILD COGNITIVE IMPAIRMENT: A RESTINGSTATE FMRI STUDY
Bing Zhang1, Zhao Qing2, Zuzana Nedelska3,4,5, Jakub Hort6,7, 1 Department of Radiology, The Drum Tower Hospital of Nanjing University Medical School, Nanjing, China; 2Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China, Nanjing, China; 3 International Clinical Research Center, St. Anne’s University Hospital Brno, Brno, Czech Republic; 4Memory Clinic, Department of Neurology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic; 5Charles University in Prague, Prague, Czech Republic; 6St. Anne’s University Hospital Brno, Brno, Czech Republic; 7 Charles University in Prague and Motol University Hospital, Prague, Czech Republic. Contact e-mail:
[email protected] Background: To explore how and if intrinsic activity in subcortical navigation network is underlying the spatial navigation impairment in mild cognitive impairment (MCI) patients. Methods: 22 MCI patients (12 males, 70 years611) and 21 normal controls (NC, 7 males, 64 years611) were finally included. All participants provided signed consent, and the local research ethics committee approved the study. Computer simulated tasks were used to evaluate the spatial navigation ability, T1 weight image was used to segment the subcortical regions and three resting-state functional MRI measure, including amplitude of low frequency fluctuation (ALFF), fractional ALFF (fALFF) and regional homogeneity (ReHo) within these regions was extracted. Statistical analyses were applied for comparison between groups and correlation between these measures and task performances. Results: The ReHo in right hippocampus (0.13560.025 vs 0.11860.026, p¼0.01), pallidum (0.13760.032 vs 0.11660.031, p¼0.04), amygdala (0.13260.029 vs 0.11260.029, p¼0.01) and thalamus (0.14960.030 vs 0.13460.026, p¼0.03) were significantly reduced in mild cognitive impairment (MCI) patients. The MCI vs. NC group showed a significant interaction effect on correlation between ReHo and allocentric spatial navigation ability in right hippocampus (F¼4.44, p¼0.04), pallidum (F¼8.97, p¼0.01) and thalamus (F¼5.95, p¼0.02), namely, the correlation are significantly disturbed in MCI patients. Conclusions: Our results demonstrated MCI can alter the subcortical intrinsic activity alteration disturb its association with the spatial navigation ability. It suggested that the intrinsic activities could be early biomarkers of spatial navigation impairment in MCI, and provided novel insights of “cognitive reserve” in human brain degeneration.
P3-368
TEMPORAL LOBE ATROPHY IN MCI ADULTS WITH OR WITHOUT DEPRESSIVE SYMPTOMS AND IN PATIENTS WITH LATE-LIFE DEPRESSION
Camille Parent1, Simon Duchesne2,3,4,5, Carol Hudon6,7, 1Universite Laval, Quebec, QC, Canada; 2Departement de Radiologie et Medecine Nucleaire, Universite Laval, Quebec, QC, Canada; 3True Positive Medical Devices Inc., Quebec, QC, Canada; 4Institut Universitaire en Sante Mentale de Quebec, Quebec, QC, Canada; 5Faculty of Medicine, University Laval, Quebec, QC, Canada; 6Universite Laval, Quebec, QC, Canada; 7Institut Universitaire en Sante Mentale de Quebec, Quebec, QC, Canada. Contact e-mail:
[email protected]
