TY - JOUR
T1 - Comparison of symptomatic and asymptomatic persons with primary age-related tauopathy
AU - Besser, Lilah M.
AU - Crary, John F.
AU - Mock, Charles
AU - Kukull, Walter A.
N1 - Funding Information:
The NACC database is funded by NIA/NIH grant U01 AG016976. NACC data are contributed by the NIA-funded ADCs: P30 AG019610 (principal investigator [PI] Eric Reiman, MD), P30 AG013846 (PI Neil Kowall, MD), P50 AG008702 (PI Scott Small, MD), P50 AG025688 (PI Allan Levey, MD, PhD), P50 AG047266 (PI Todd Golde, MD, PhD), P30 AG010133 (PI Andrew Saykin, PsyD), P50 AG005146 (PI Marilyn Albert, PhD), P50 AG005134 (PI Bradley Hyman, MD, PhD), P50 AG016574 (PI Ronald Petersen, MD, PhD), P50 AG005138 (PI Mary Sano, PhD), P30 AG008051 (PI Steven Ferris, PhD), P30 AG013854 (PI M. Marsel Mesulam, MD), P30 AG008017 (PI Jeffrey Kaye, MD), P30 AG010161 (PI David Bennett, MD), P50 AG047366 (PI Victor Henderson, MD, MS), P30 AG010129 (PI Charles DeCarli, MD), P50 AG016573 (PI Frank LaFerla, PhD), P50 AG016570 (PI Marie-Francoise Chesselet, MD, PhD), P50 AG005131 (PI Douglas Galasko, MD), P50 AG023501 (PI Bruce Miller, MD), P30 AG035982 (PI Russell Swerdlow, MD), P30 AG028383 (PI Linda Van Eldik, PhD), P30 AG010124 (PI John Trojanowski, MD, PhD), P50 AG005133 (PI Oscar Lopez, MD), P50 AG005142 (PI Helena Chui, MD), P30 AG012300 (PI Roger Rosenberg, MD), P50 AG005136 (PI Thomas Montine, MD, PhD), P50 AG033514 (PI Sanjay Asthana, MD, FRCP), P50 AG005681 (PI John Morris, MD), and P50 AG047270 (PI Stephen Strittmatter, MD, PhD). We also acknowledge the following funding sources: NIH grants R01 NS095252 (PI Dr. Crary) and R01AG054008 (PI Dr. Crary) and Alzheimer’s Association NIRG-15-363188 (PI Dr. Crary).
Publisher Copyright:
© 2017 American Academy of Neurology.
PY - 2017/10/17
Y1 - 2017/10/17
N2 - Objective: To conduct a clinicopathologic study to characterize clinical and neuropathologic features associated with cognitive impairment in participants with no neuritic amyloid plaques (primary age-related tauopathy [PART] definite) and sparse neuritic plaques (amyloid sparse). Methods: Using the National Alzheimer's Coordinating Center database, we identified 377 individuals who were PART definite (n = 170) or amyloid sparse (n = 207), clinically examined within 1 year of death, and autopsied at 1 of 26 National Institute on Aging-funded Alzheimer's Disease Centers. Factors associated with the odds of being symptomatic (global Clinical Dementia Rating [CDR] score >0) were identified with multivariable logistic regression. Results: PART-definite participants less often had a high Braak neurofibrillary tangle stage V or VI (4%) compared to amyloid sparse participants (28%, p < 0.001). Of the PART-definite participants, 98 were symptomatic and 72 asymptomatic according to their global CDR scores. PART-definite participants were less often symptomatic (58%) compared with amyloid sparse participants (80%, p < 0.001). Within the PART-definite group, independent predictors of symptomatic status included depression (adjusted odds ratio [aOR] 4.20, 95% confidence interval [CI] 2.15-8.19), Braak stage (aOR 1.42, 95% CI 1.04-1.95), and history of stroke (aOR 8.09, 95% CI 2.63-24.82). Within the amyloid sparse group, independent predictors of symptomatic status included education (aOR 0.80, 95% CI 0.65-0.99), Braak stage (aOR 1.91, 95% CI 1.07-3.43), and amyloid angiopathy (aOR 2.75, 95% CI 1.14-6.64). Conclusions: These findings support the hypothesis that participants with PART have an amyloid-independent dementing Alzheimer disease-like temporal lobe tauopathy.
AB - Objective: To conduct a clinicopathologic study to characterize clinical and neuropathologic features associated with cognitive impairment in participants with no neuritic amyloid plaques (primary age-related tauopathy [PART] definite) and sparse neuritic plaques (amyloid sparse). Methods: Using the National Alzheimer's Coordinating Center database, we identified 377 individuals who were PART definite (n = 170) or amyloid sparse (n = 207), clinically examined within 1 year of death, and autopsied at 1 of 26 National Institute on Aging-funded Alzheimer's Disease Centers. Factors associated with the odds of being symptomatic (global Clinical Dementia Rating [CDR] score >0) were identified with multivariable logistic regression. Results: PART-definite participants less often had a high Braak neurofibrillary tangle stage V or VI (4%) compared to amyloid sparse participants (28%, p < 0.001). Of the PART-definite participants, 98 were symptomatic and 72 asymptomatic according to their global CDR scores. PART-definite participants were less often symptomatic (58%) compared with amyloid sparse participants (80%, p < 0.001). Within the PART-definite group, independent predictors of symptomatic status included depression (adjusted odds ratio [aOR] 4.20, 95% confidence interval [CI] 2.15-8.19), Braak stage (aOR 1.42, 95% CI 1.04-1.95), and history of stroke (aOR 8.09, 95% CI 2.63-24.82). Within the amyloid sparse group, independent predictors of symptomatic status included education (aOR 0.80, 95% CI 0.65-0.99), Braak stage (aOR 1.91, 95% CI 1.07-3.43), and amyloid angiopathy (aOR 2.75, 95% CI 1.14-6.64). Conclusions: These findings support the hypothesis that participants with PART have an amyloid-independent dementing Alzheimer disease-like temporal lobe tauopathy.
UR - http://www.scopus.com/inward/record.url?scp=85031407413&partnerID=8YFLogxK
U2 - 10.1212/WNL.0000000000004521
DO - 10.1212/WNL.0000000000004521
M3 - Article
C2 - 28916532
AN - SCOPUS:85031407413
SN - 0028-3878
VL - 89
SP - 1707
EP - 1715
JO - Neurology
JF - Neurology
IS - 16
ER -