scholarly journals Differential effects of ischemic vascular disease and Alzheimer’s disease on brain atrophy and cognition

2015 ◽  
Vol 36 (1) ◽  
pp. 204-215 ◽  
Author(s):  
Ling Zheng ◽  
Harry V Vinters ◽  
Wendy J Mack ◽  
Michael W Weiner ◽  
Helena C Chui ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Infarction ◽  
Vascular Disease ◽  
Brain Atrophy ◽  
Cortical Atrophy ◽  
Elderly Persons ◽  
Indirect Pathway ◽  
Global Cognition

We previously reported that pathologic measures of arteriosclerosis (AS), cerebral infarction, and Alzheimer’s disease (AD) are independently correlated with cortical gray matter (CGM) atrophy measured by in vivo magnetic resonance imaging (MRI). Here, we use path analyses to model the associations between these three pathology measures and cognitive impairment, as mediated by CGM atrophy, after controlling for age and education. In this sample of 116 elderly persons followed longitudinally to autopsy (ischemic vascular disease (IVD) program project), differential patterns were observed between AS and atrophy/cognition versus AD and atrophy/cognition. The total effect of AD pathology on global cognition ( β = −0.61, s.e. = 0.06) was four times stronger than that of AS ( β = −0.15, s.e. = 0.08). The effect of AS on cognition appears to occur through cerebral infarction and CGM atrophy ( β = −0.13, s.e. = 0.04). In contrast, the effects of AD pathology on global cognition ( β = −0.50, s.e. = 0.07) occur through a direct pathway that is five times stronger than the indirect pathway acting through CGM atrophy ( β = −0.09, s.e. = 0.03). The strength of this direct AD pathway was not significantly mitigated by adding hippocampal volume to the model. AD pathology affects cognition not only through brain atrophy, but also via an unmeasured pathway that could be related to synaptic dysfunction before the development of cortical atrophy.

P1-009: A Data-Driven Comparison of the Progression of Brain Atrophy in Posterior Cortical Atrophy and Alzheimer's Disease

2016 ◽  
Vol 12 ◽  
pp. P401-P402
Author(s):  
Razvan Valentin Marinescu ◽  
Alexandra L. Young ◽  
Neil P. Oxtoby ◽  
Nicholas C. Firth ◽  
Marco Lorenzi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Atrophy ◽  
Data Driven ◽  
Cortical Atrophy ◽  
Posterior Cortical Atrophy

scholarly journals Functional signature of conversion in Mild Cognitive Impairment patients

2018 ◽  
Author(s):  
Stefano Delli Pizzi ◽  
Miriam Punzi ◽  
Stefano L Sensi ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Brain Atrophy ◽  
Cortical Atrophy ◽  
Study Cohort ◽  
Dramatic Decline ◽  
Healthy Control ◽  
Cortical Regions

AbstractThe entorhinal-hippocampal circuit is a strategic hub for memory but also the first site to be affected in the Alzheimer’s Disease (AD)-related pathology. We investigated MRI patterns of brain atrophy and functional connectivity in a study cohort obtained from the Alzheimer’s Disease Neuroimaging Initiative database including healthy control (HC), Mild Cognitive Impairment (MCI), and AD subjects. MCI individuals were clinically evaluated 24 months after the MRI scan, and the group further divided into a subset of subjects who either did (c-MCI) or did not (nc-MCI) convert to AD. Compared to HC subjects, AD patients exhibited a collapse of long-range connectivity from the hippocampus and entorhinal cortex, pronounced cortical/sub-cortical atrophy, and a dramatic decline in cognitive performances. c-MCI patients showed entorhinal and hippocampal hypo-connectivity, no signs of cortical thinning but evidence of right hippocampus atrophy. On the contrary, nc-MCI patients showed lack of brain atrophy, largely preserved cognitive functions, hippocampal and entorhinal hyper-connectivity with selected neocortical/sub-cortical regions mainly involved in memory processing and brain meta-stability. This hyper-connectivity can represent an early compensatory strategy to overcome the progression of cognitive impairment. This functional signature can also be employed for the diagnosis of c-MCI subjects.

Elevated Tau PET Signal Depends on Abnormal Amyloid Levels and Correlates with Cognitive Impairment in Elderly Persons without Dementia

2020 ◽  
Vol 78 (1) ◽  
pp. 395-404 ◽  
Author(s):  
Rui-Qi Zhang ◽  
Shi-Dong Chen ◽  
Xue-Ning Shen ◽  
Yu-Xiang Yang ◽  
Jia-Ying Lu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Executive Function ◽  
Amyloid Β ◽  
Amyloid Pet ◽  
Elderly Persons ◽  
Cross Sectional ◽  
Memory Decline ◽  
Tau Pet

Background: The recent developed PET ligands for amyloid-β (Aβ) and tau allow these two neuropathological hallmarks of Alzheimer’s disease (AD) to be mapped and quantified in vivo and to be examined in relation to cognition. Objective: To assess the associations among Aβ, tau, and cognition in non-demented subjects. Methods: Three hundred eighty-nine elderly participants without dementia from the Alzheimer’s Disease Neuroimaging Initiative underwent tau and amyloid PET scans. Cross-sectional comparisons and longitudinal analyses were used to evaluate the relationship between Aβ and tau accumulation. The correlations between biomarkers of both pathologies and performance in memory and executive function were measured. Results: Increased amyloid-PET retention was associated with greater tau-PET retention in widespread cortices. We observed a significant tau increase in the temporal composite regions of interest over 24 months in Aβ+ but not Aβ– subjects. Finally, tau-PET retention but not amyloid-PET retention significantly explained the variance in memory and executive function. Higher level of tau was associated with greater longitudinal memory decline. Conclusion: These findings suggested PET-detectable Aβ plaque pathology may be a necessary antecedent for tau-PET signal elevation. Greater tau-PET retention may demonstrate poorer cognition and predict prospective memory decline in non-demented subjects.

P2-169: NEUROFIBRILLARY TANGLES PREDICT IN VIVO CORTICAL ATROPHY IN PRIMARY PROGRESSIVE APHASIA WITH ALZHEIMER'S DISEASE

2006 ◽  
Vol 14 (7S_Part_13) ◽  
pp. P733-P733
Author(s):  
Daniel T. Ohm ◽  
Garam Kim ◽  
Tamar Gefen ◽  
Alfred Rademaker ◽  
Sandra Weintraub ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Tangles ◽  
Primary Progressive Aphasia ◽  
Cortical Atrophy ◽  
Progressive Aphasia ◽  
Primary Progressive

scholarly journals Neuropathologic basis of in vivo cortical atrophy in the aphasic variant of Alzheimer's disease

2019 ◽  
Vol 30 (2) ◽  
pp. 332-344 ◽  
Author(s):  
Daniel T. Ohm ◽  
Angela J. Fought ◽  
Alfred Rademaker ◽  
Garam Kim ◽  
Jaiashre Sridhar ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cortical Atrophy

scholarly journals Relationship between cortical iron and tau aggregation in Alzheimer’s disease

Brain ◽  
2020 ◽  
Vol 143 (5) ◽  
pp. 1341-1349 ◽  
Author(s):  
Nicola Spotorno ◽  
Julio Acosta-Cabronero ◽  
Erik Stomrud ◽  
Björn Lampinen ◽  
Olof T Strandberg ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Critical Role ◽  
Disease Process ◽  
Amyloid Β ◽  
Cortical Atrophy ◽  
Tau Pet ◽  
Tau Aggregation ◽  
The Relationship

Abstract A growing body of evidence suggests that the dysregulation of neuronal iron may play a critical role in Alzheimer’s disease. Recent MRI studies have established a relationship between iron accumulation and amyloid-β aggregation. The present study provides further insight demonstrating a relationship between iron and tau accumulation using magnetic resonance-based quantitative susceptibility mapping and tau-PET in n = 236 subjects with amyloid-β pathology (from the Swedish BioFINDER-2 study). Both voxel-wise and regional analyses showed a consistent association between differences in bulk magnetic susceptibility, which can be primarily ascribed to an increase in iron content, and tau-PET signal in regions known to be affected in Alzheimer’s disease. Subsequent analyses revealed that quantitative susceptibility specifically mediates the relationship between tau-PET and cortical atrophy measures, thus suggesting a modulatory effect of iron burden on the disease process. We also found evidence suggesting the relationship between quantitative susceptibility and tau-PET is stronger in younger participants (age ≤ 65). Together, these results provide in vivo evidence of an association between iron deposition and both tau aggregation and neurodegeneration, which help advance our understanding of the role of iron dysregulation in the Alzheimer’s disease aetiology.

P1-278: In vivo mapping of incremental cortical atrophy from health to overt Alzheimer's disease

2008 ◽  
Vol 4 ◽  
pp. T298-T298
Author(s):  
Annapaola Prestia ◽  
Paul M. Thompson ◽  
Francesca Sabattoli ◽  
Michela Pievani ◽  
Giovanni B. Frisoni
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cortical Atrophy

In vivo mapping of incremental cortical atrophy from incipient to overt Alzheimer’s disease

2009 ◽  
Vol 256 (6) ◽  
pp. 916-924 ◽  
Author(s):  
Giovanni B. Frisoni ◽  
Annapaola Prestia ◽  
Paul E. Rasser ◽  
Matteo Bonetti ◽  
Paul M. Thompson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cortical Atrophy

scholarly journals Frontal presentation of Alzheimer's disease: A series of patients with biological evidence by CSF biomarkers

2013 ◽  
Vol 7 (1) ◽  
pp. 66-74 ◽  
Author(s):  
Leonardo Cruz de Souza ◽  
Maxime Bertoux ◽  
Aurélie Funkiewiez ◽  
Dalila Samri ◽  
Carole Azuar ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cortical Atrophy ◽  
Csf Biomarkers ◽  
Post Mortem ◽  
Posterior Cortical Atrophy ◽  
Biological Profile ◽  
Atypical Presentations ◽  
Alzheimer Pathology

ABSTRACT Besides its typical amnesic presentation, focal atypical presentations of Alzheimer's disease (AD) have been described in neuropathological studies. These phenotypical variants of AD (so-called "atypical AD") do not follow the typical amnestic pattern and include non-amnestic focal cortical syndromes, such as posterior cortical atrophy and frontal variant AD. These variants exhibit characteristic histological lesions of Alzheimer pathology at post-mortem exam. By using physiopathological markers, such as cerebrospinal fluid markers, it is now possible to establish in vivo a biological diagnosis of AD in these focal cortical syndromes. We report a series of eight patients who were diagnosed with behavioural variant frontotemporal dementia based on their clinical, neuropsychological and neuroimaging findings, while CSF biomarkers showed an AD biological profile, thus supporting a diagnosis of frontal variant of AD.

scholarly journals Retinal thinning of inner sub-layers is associated with cortical atrophy in a mouse model of Alzheimer’s disease: a longitudinal multimodal in vivo study

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Samuel Chiquita ◽  
Elisa J. Campos ◽  
João Castelhano ◽  
Mário Ribeiro ◽  
José Sereno ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Visual Cortex ◽  
Mouse Model ◽  
Cortical Atrophy ◽  
Therapeutic Monitoring ◽  
Lower Phase ◽  
Additional Tool ◽  
Model Of Alzheimer’S Disease

Abstract Background It has been claimed that the retina can be used as a window to study brain disorders. However, concerning Alzheimer’s disease (AD), it still remains controversial whether changes occurring in the brain and retina are associated. We aim to understand when changes start appearing in the retina and brain, how changes progress, and if they are correlated. Methods We carried out a unique longitudinal study, at 4, 8, 12, and 16 months of age, in a triple transgenic mouse model of AD (3×Tg-AD), which mimics pathological and neurobehavioral features of AD, as we have already shown. Retinal structure and physiology were evaluated in vivo using optical coherence tomography and electroretinography. Brain visual cortex structure was evaluated in vivo using magnetic resonance imaging. Results The retinal thickness of 3×Tg-AD decreased, at all time points, except for the outer nuclear layer, where the opposite alteration was observed. Amplitudes in scotopic and photopic responses were increased throughout the study. Similarly, higher amplitude and lower phase values were observed in the photopic flicker response. No differences were found in the activity of retinal ganglion cells. Visual cortex gray matter volume was significantly reduced. Conclusions Our results show that this animal model shows similar neural changes in the retina and brain visual cortex, i.e., retinal and brain thinning. Moreover, since similar changes occur in the retina and brain visual cortex, these observations support the possibility of using the eye as an additional tool (noninvasive) for early AD diagnosis and therapeutic monitoring.

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