scholarly journals CAN MOCA SCORES PREDICT AMYLOID PET SCAN POSITIVITY? SENSITIVITY AND SPECIFICITY ANALYSES IN A MEMORY CLINIC SAMPLE

2018 ◽  
Vol 2 (suppl_1) ◽  
pp. 136-136
Author(s):  
S Nair ◽  
S Ramaswamy ◽  
A Nair
2014 ◽  
Vol 10 ◽  
pp. P12-P12
Author(s):  
Gil Dan Rabinovici ◽  
Rik Ossenkoppele ◽  
Audrey Perrotin ◽  
Vincent Dore ◽  
William Jagust ◽  
...  

2021 ◽  
pp. 10.1212/CPJ.0000000000001049
Author(s):  
Tobias Langheinrich ◽  
Christopher Kobylecki ◽  
Matthew Jones ◽  
Jennifer C Thompson ◽  
Julie S Snowden ◽  
...  

A 65-year-old man was referred to a local memory clinic with memory complaints but clinical assessment found no abnormalities. When he presented two years later to our clinic social disinhibition, reduced empathy, poor judgment and hoarding had become obvious. He showed no insight. He had ischemic heart disease and was on preventive treatment. His mother died aged 97 suffering from dementia. Neurological examination was normal. During neuropsychological examination he exhibited verbal and behavioral disinhibition, inattention, emotional blunting and unconcern. He had prominent difficulties in abstraction, set shifting and sequencing with significant impact on memory tests (table1). A clinical diagnosis of behavioral variant FTD (bvFTD) was made. MRI (figure A) showed right more than left-sided temporal atrophy, bilateral frontal and milder parietal atrophy. Fluorodeoxyglucose (FDG)-PET (figure B) demonstrated fronto-temporal hypometabolism. Metabolism in the posterior cingulate was normal. He was homozygous for the APOE ε4 allele and negative for the C9orf72 expansion and mutations in MAPT, GRN, PSEN1, and APP. [18F]-Florbetapir PET (figure C) revealed increased tracer binding in all cortical regions corresponding to a centiloid value of 74%.


2020 ◽  
Vol 16 (S6) ◽  
Author(s):  
Megan E. O'Connell ◽  
Jennifer D. Walker ◽  
Kristen Jacklin ◽  
Carrie Ann Bourassa ◽  
Andrew Kirk ◽  
...  

2010 ◽  
Vol 4 (2) ◽  
pp. 138-144 ◽  
Author(s):  
Renata Eloah de Lucena Ferretti ◽  
Antonio Eduardo Damin ◽  
Sonia Maria Dozzi Brucki ◽  
Lilian Schafirovits Morillo ◽  
Tibor Rilho Perroco ◽  
...  

Abstract The diagnosis of normal cognition or dementia in the Brazilian Brain Bank of the Aging Brain Study Group (BBBABSG) has relied on postmortem interview with an informant. Objectives: To ascertain the sensitivity and specificity of postmortem diagnosis based on informant interview compared against the diagnosis established at a memory clinic. Methods: A prospective study was conducted at the BBBABSG and at the Reference Center for Cognitive Disorders (RCCD), a specialized memory clinic of the Hospital das Clínicas, University of São Paulo Medical School. Control subjects and cognitively impaired subjects were referred from the Hospital das Clínicas to the RCCD where subjects and their informants were assessed. The same informant was then interviewed at the BBBABSG. Specialists' panel consensus, in each group, determined the final diagnosis of the case, blind to other center's diagnosis. Data was compared for frequency of diagnostic equivalence. For this study, the diagnosis established at the RCCD was accepted as the gold standard. Sensitivity and specificity were computed. Results: Ninety individuals were included, 45 with dementia and 45 without dementia (26 cognitively normal and 19 cognitively impaired but non-demented). The informant interview at the BBBABSG had a sensitivity of 86.6% and specificity of 84.4% for the diagnosis of dementia, and a sensitivity of 65.3% and specificity of 93.7% for the diagnosis of normal cognition. Conclusions: The informant interview used at the BBBABSG has a high specificity and sensitivity for the diagnosis of dementia as well as a high specificity for the diagnosis of normal cognition.


Neurology ◽  
2020 ◽  
Vol 94 (18) ◽  
pp. e1916-e1928
Author(s):  
Heidi I.L. Jacobs ◽  
Jean C. Augustinack ◽  
Aaron P. Schultz ◽  
Bernard J. Hanseeuw ◽  
Joseph Locascio ◽  
...  

ObjectiveTo identify the hippocampal subregions linking initial amyloid and tau pathology to memory performance in clinically normal older individuals, reflecting preclinical Alzheimer disease (AD).MethodsA total of 127 individuals from the Harvard Aging Brain Study (mean age 76.22 ± 6.42 years, 68 women [53.5%]) with a Clinical Dementia Rating score of 0, a flortaucipir tau-PET scan, a Pittsburgh compound B amyloid-PET scan, a structural MRI scan, and cognitive testing were included. From these images, we calculated neocortical, hippocampal, and entorhinal amyloid pathology; entorhinal and hippocampal tau pathology; and the volumes of 6 hippocampal subregions and total hippocampal volume. Memory was assessed with the selective reminding test. Mediation and moderation analyses modeled associations between regional markers and memory. Analyses included covariates for age, sex, and education.ResultsNeocortical amyloid, entorhinal tau, and presubiculum volume univariately associated with memory performance. The relationship between neocortical amyloid and memory was mediated by entorhinal tau and presubiculum volume, which was modified by hippocampal amyloid burden. With other biomarkers held constant, presubiculum volume was the only marker predicting memory performance in the total sample and in individuals with elevated hippocampal amyloid burden.ConclusionsThe presubiculum captures unique AD-related biological variation that is not reflected in total hippocampal volume. Presubiculum volume may be a promising marker of imminent memory problems and can contribute to understanding the interaction between incipient AD-related pathologies and memory performance. The modulation by hippocampal amyloid suggests that amyloid is a necessary, but not sufficient, process to drive neurodegeneration in memory-related regions.


2016 ◽  
Vol 12 ◽  
pp. P19-P20
Author(s):  
Arno de Wilde ◽  
Wiesje M. van der Flier ◽  
Femke H. Bouwman ◽  
Rik Ossenkoppele ◽  
Wiesje Pelkmans ◽  
...  

Neurology ◽  
2018 ◽  
Vol 91 (9) ◽  
pp. e859-e866 ◽  
Author(s):  
Andrew J. Aschenbrenner ◽  
Brian A. Gordon ◽  
Tammie L.S. Benzinger ◽  
John C. Morris ◽  
Jason J. Hassenstab

ObjectiveTo examine the independent and interactive influences of neuroimaging biomarkers on retrospective cognitive decline.MethodsA total of 152 middle-aged and older adult participants with at least 2 clinical and cognitive assessments, a Clinical Dementia Rating score of 0 or 0.5, and a flortaucipir (18F-AV-1451) tau PET scan, a florbetapir (18F-AV-45) amyloid PET scan, and a structural MRI scan were recruited from the Knight Alzheimer Disease Research Center at Washington University in St. Louis. Cognition was assessed with standard measures reflecting episodic memory, executive functioning, semantic fluency, and processing speed.ResultsResults from retrospective longitudinal analyses showed that each biomarker had a univariate association with the global cognitive composite; however, when each marker was analyzed in a single statistical model, only tau was a significant predictor of global cognitive decline. There was an interaction between tau and amyloid such that tau-related cognitive decline was worse in individuals with high amyloid. There was also an interaction with hippocampal volume indicating that individuals with high levels of all 3 pathologies exhibited the greatest declines in cognition. Additional analyses within each cognitive domain indicated that tau had the largest negative influence on tests of episodic memory and executive functioning.ConclusionsTogether, these results suggest that increasing levels of tau most consistently relate to declines in cognition preceding biomarker collection. These findings support models of Alzheimer disease (AD) staging that suggest that elevated β-amyloid alone may be insufficient to produce cognitive change in individuals at risk for AD and support the use of multiple biomarkers to stage AD progression.


Neurology ◽  
2021 ◽  
pp. 10.1212/WNL.0000000000012775
Author(s):  
Suzanne Schindler ◽  
Yan Li ◽  
Virginia D. Buckles ◽  
Brian Andrew Gordon ◽  
Tammie L.S. Benzinger ◽  
...  

Objective:To predict when cognitively normal individuals with brain amyloidosis will develop symptoms of Alzheimer disease (AD).Methods:Brain amyloid burden was measured by amyloid PET with Pittsburgh compound B. The mean cortical standardized uptake value ratio (SUVR) was transformed into a timescale using longitudinal data.Results:Amyloid accumulation was evaluated in 236 individuals who underwent more than one amyloid PET scan. The average age was 66.5 ± 9.2 years and twelve individuals (5%) had cognitive impairment at their baseline amyloid PET scan. A tipping point in amyloid accumulation was identified at a low level of amyloid burden (SUVR 1.2), after which nearly all individuals accumulated amyloid at a relatively consistent rate until reaching a high level of amyloid burden (SUVR 3.0). The average time between levels of amyloid burden was used to estimate the age at which an individual reached SUVR 1.2. Longitudinal clinical diagnoses for 180 individuals were aligned by the estimated age at SUVR 1.2. In the twenty-two individuals who progressed from cognitively normal to a typical AD dementia syndrome, the estimated age at which an individual reached SUVR 1.2 predicted the age at symptom onset (R2=0.54, p<0.0001, root mean square error (RMSE) 4.5 years); the model was more accurate after exclusion of three likely misdiagnoses (R2=0.84, p<0.0001, RMSE of 2.8 years).Conclusions:The age of symptom onset in sporadic AD is strongly correlated with the age that an individual reaches a tipping point in amyloid accumulation.


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