P3-274: High CSF TAU is Related to Reduced Hippocampal Volume and Subjective Cognitive Decline in Healthy Elderly with Amyloid Pathology

2016 ◽  
Vol 12 ◽  
pp. P939-P940
Author(s):  
Alexa Pichet Binette ◽  
Jacob W. Vogel ◽  
Vladimir S. Fonov ◽  
Jennifer Tremblay-Mercier ◽  
Cécile Madjar ◽  
...  
2016 ◽  
Vol 12 ◽  
pp. P102-P103
Author(s):  
Alexa Pichet Binette ◽  
Jacob W. Vogel ◽  
Vladimir S. Fonov ◽  
Cécile Madjar ◽  
Jennifer Tremblay-Mercier ◽  
...  

2015 ◽  
Vol 11 (7S_Part_7) ◽  
pp. P315-P316
Author(s):  
Jacob W. Vogel ◽  
Monika Varga Doležalová ◽  
Renaud La Joie ◽  
Shawn Marks ◽  
Allison Fero ◽  
...  

2014 ◽  
Vol 10 ◽  
pp. P58-P59
Author(s):  
Audrey Perrotin ◽  
Florence Mézenge ◽  
Brigitte Landeau ◽  
Stéphanie Egret ◽  
Vincent de La Sayette ◽  
...  

2019 ◽  
Vol 75 (7) ◽  
pp. 1382-1392 ◽  
Author(s):  
Marie Caillaud ◽  
Carol Hudon ◽  
Benjamin Boller ◽  
Simona Brambati ◽  
Simon Duchesne ◽  
...  

Abstract Objective The concepts of mild cognitive impairment (MCI) and subjective cognitive decline (SCD) have been proposed to identify individuals in the early stages of Alzheimer’s disease (AD), or other neurodegenerative diseases. One approach to validate these concepts is to investigate the relationship between pathological brain markers and cognition in those individuals. Method We included 126 participants from the Consortium for the Early Identification of Alzheimer’s disease-Quebec (CIMA-Q) cohort (67 SCD, 29 MCI, and 30 cognitively healthy controls [CH]). All participants underwent a complete cognitive assessment and structural magnetic resonance imaging. Group comparisons were done using cognitive data, and then correlated with hippocampal volumes and white matter hyperintensities (WMHs). Results Significant differences were found between participants with MCI and CH on episodic and executive tasks, but no differences were found when comparing SCD and CH. Scores on episodic memory tests correlated with hippocampal volumes in both MCI and SCD, whereas performance on executive tests correlated with WMH in all of our groups. Discussion As expected, the SCD group was shown to be cognitively healthy on tasks where MCI participants showed impairment. However, SCD’s hippocampal volume related to episodic memory performances, and WMH to executive functions. Thus, SCD represents a valid research concept and should be used, alongside MCI, to better understand the preclinical/prodromal phase of AD.


Neurology ◽  
2017 ◽  
Vol 89 (19) ◽  
pp. 2002-2009 ◽  
Author(s):  
Jacob W. Vogel ◽  
Monika Varga Doležalová ◽  
Renaud La Joie ◽  
Shawn M. Marks ◽  
Henry D. Schwimmer ◽  
...  

Objective:To assess in a longitudinal study whether subjective cognitive decline (SCD) and brain β-amyloid (Aβ) contribute unique information to cognitive decline.Methods:One hundred thirty-six healthy elderly from the Berkeley Aging Cohort Study were followed up for a mean of 4 years. SCD and affective measures were generated from the Geriatric Depression Scale (GDS) with factor analysis on data from a larger set of 347 healthy, nondepressed (GDS <11) elderly individuals. Cognition was summarized with previously validated factor scores. Pittsburgh compound B (PiB)-PET scans were acquired to determine the presence (PiB+) or absence (PiB−) of Aβ pathology. Mixed models were used to assess the independent and interactive effects of SCD, affective features, PiB status, and time on cognition, with adjustment for demographic variables.Results:SCD score demonstrated good construct validity compared to an existing measure of subjective memory and was partially explained by several lower-order measurements. Mixed models revealed that SCD interacted with PiB status to predict change in episodic memory and global cognition over time, with adjustment for affective features. PiB+ individuals with more severe SCD demonstrated the steepest cognitive decline. Worse SCD predicted faster decline in working memory independently of PiB status. No such effects were seen for affective scores when adjusted for SCD.Conclusions:PiB+ individuals with SCD are at greatest risk of cognitive decline. Evidence for amyloid alone is not sufficient to indicate risk of rapid cognitive decline in healthy elderly. Effects of GDS on cognitive decline in nondepressed cohorts may be driven by SCD rather than subsyndromal depression.


2014 ◽  
Vol 10 ◽  
pp. P58-P58 ◽  
Author(s):  
Audrey Perrotin ◽  
Stéphanie Egret ◽  
Florence Mézenge ◽  
Brigitte Landeau ◽  
Vincent de La Sayette ◽  
...  

2020 ◽  
Author(s):  
Nira Cedres ◽  
Patricia Diaz-Galvan ◽  
Lucio Diaz-Flores ◽  
J-Sebastian Muehlboeck ◽  
Yaiza Molina ◽  
...  

Abstract AIMS: To investigate the interplay between gray matter (GM) and white matter (WM) neurodegeneration in subjective cognitive decline (SCD), including thickness across the whole cortical mantle, hippocampal volume, and integrity across the whole WM. METHODS: We included 225 cognitively unimpaired individuals from a community-based cohort, of whom 123 endorsed one or more subjective cognitive complaints. GM neurodegeneration was assessed through measures of cortical thickness across the whole mantle and hippocampal volume. WM neurodegeneration was assessed through measures of mean diffusivity (MD) across the whole WM skeleton. Mediation analysis and multiple linear regression were conducted to investigate the interplay between the measures of GM and WM neurodegeneration.RESULTS: A higher number of complaints was associated with reduced hippocampal volume, cortical thinning in several frontal and temporal areas and the insula, and higher MD across the WM skeleton, with a tendency to spare the occipital lobe. SCD-related cortical thinning and increased MD were associated with each other and jointly contributed to the complaints, but the contribution of cortical thinning to SCD was stronger.CONCLUSIONS: Neurodegeneration processes affecting the GM and WM seem to be associated with each other in SCD and include brain areas other than those typically targeted by Alzheimer’s disease (AD). Our findings suggest that SCD may be a sensitive behavioral marker of heterogeneous brain pathologies in individuals recruited from the community.


Neurology ◽  
2019 ◽  
Vol 92 (5) ◽  
pp. e395-e405
Author(s):  
Olga Voevodskaya ◽  
Konstantinos Poulakis ◽  
Pia Sundgren ◽  
Danielle van Westen ◽  
Sebastian Palmqvist ◽  
...  

ObjectiveTo investigate the association between longitudinal changes in proton magnetic resonance spectroscopy (MRS) metabolites and amyloid pathology in individuals without dementia, and to explore the relationship between MRS and cognitive decline.MethodsIn this longitudinal multiple time point study (a subset of the Swedish BioFINDER), we included cognitively healthy participants, individuals with subjective cognitive decline, and individuals with mild cognitive impairment. MRS was acquired serially in 294 participants (670 individual spectra) from the posterior cingulate/precuneus. Using mixed-effects models, we assessed the association between MRS and baseline β-amyloid (Aβ), and between MRS and the longitudinal Mini-Mental State Examination, accounting for APOE, age, and sex.ResultsWhile baseline MRS metabolites were similar in Aβ positive (Aβ+) and negative (Aβ−) individuals, in the Aβ+ group, the estimated rate of change was +1.9%/y for myo-inositol (mI)/creatine (Cr) and −2.0%/y for N-acetylaspartate (NAA)/mI. In the Aβ− group, mI/Cr and NAA/mI yearly change was −0.05% and +1.2%; however, this was not significant across time points. The mild cognitive impairment Aβ+ group showed the steepest MRS changes, with an estimated rate of +2.93%/y (p = 0.07) for mI/Cr and −3.55%/y (p < 0.01) for NAA/mI. Furthermore, in the entire cohort, we found that Aβ+ individuals with low baseline NAA/mI had a significantly higher rate of cognitive decline than Aβ+ individuals with high baseline NAA/mI.ConclusionWe demonstrate that the longitudinal change in mI/Cr and NAA/mI is associated with underlying amyloid pathology. MRS may be a useful noninvasive marker of Aβ-related processes over time. In addition, we show that in Aβ+ individuals, baseline NAA/mI may predict the rate of future cognitive decline.


2021 ◽  
Vol 13 ◽  
Author(s):  
Qian Chen ◽  
Sichu Wu ◽  
Xin Li ◽  
Yi Sun ◽  
Wenqian Chen ◽  
...  

Individuals with subjective cognitive decline (SCD) are at higher risk of incipient Alzheimer's disease (AD). Spatial navigation (SN) impairments in AD dementia and mild cognitive impairment patients have been well-documented; however, studies investigating SN deficits in SCD subjects are still lacking. This study aimed to explore whether basal forebrain (BF) and entorhinal cortex (EC) atrophy contribute to spatial disorientation in the SCD stage. In total, 31 SCD subjects and 24 normal controls were enrolled and administered cognitive scales, a 2-dimensional computerized SN test, and structural magnetic resonance imaging (MRI) scanning. We computed the differences in navigation distance errors and volumes of BF subfields, EC, and hippocampus between the SCD and control groups. The correlations between MRI volumetry and navigation distance errors were also calculated. Compared with the controls, the SCD subjects performed worse in both egocentric and allocentric navigation. The SCD group showed volume reductions in the whole BF (p &lt; 0.05, uncorrected) and the Ch4p subfield (p &lt; 0.05, Bonferroni corrected), but comparable EC and hippocampal volumes with the controls. In the SCD cohort, the allocentric errors were negatively correlated with total BF (r = −0.625, p &lt; 0.001), Ch4p (r = −0.625, p &lt; 0.001), total EC (r = −0.423, p = 0.031), and left EC volumes (r = −0.442, p = 0.024), adjusting for age, gender, years of education, total intracranial volume, and hippocampal volume. This study demonstrates that SN deficits and BF atrophy may be promising indicators for the early detection of incipient AD patients. The reduced BF volume, especially in the Ch4p subfield, may serve as a structural basis for allocentric disorientation in SCD subjects independent of hippocampal atrophy. Our findings may have further implications for the preclinical diagnosis and intervention for potential AD patients.


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