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

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 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.

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.

scholarly journals Cognitive Reserve Proxies, Alzheimer Pathologies, and Cognition

2020 ◽  
Author(s):  
Kang Ko ◽  
Dahyun Yi ◽  
Min Soo Byun ◽  
Jun Ho Lee ◽  
So Yeon Jeon ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Cognitive Reserve ◽  
Cognitive Activity ◽  
Moderating Effect ◽  
Cortical Atrophy ◽  
Moderating Effects ◽  
The Relationship

Abstract BackgroundLimited information is available regarding which of the commonly used cognitive reserve (CR) proxies are more appropriate to precisely reflect moderation effect for the relationship between a specific Alzheimer’s disease (AD) pathology and cognitive decline. We examined the moderating effects of the frequently used four CR proxies [i.e., education, premorbid intelligence quotient (pIQ), occupational complexity (OC), and lifetime cognitive activity (LCA)] on the relationships between various in vivo AD pathologies and cognitive decline. MethodsThis study included 361 older adults (268 cognitively unimpaired, 52 mild cognitive impairment with beta-amyloid (Aβ) deposition, 41 AD dementia with Aβ deposition). All participants underwent multi-modal brain imaging including [11C] Pittsburgh Compound B positron emission tomography (PET), [18F] Fluorodeoxyglucose-PET, and magnetic resonance imaging to measure AD pathologies as well as comprehensive clinical and neuropsychological assessments. Information on education, pIQ estimated with an adult reading test, OC, and LCA was obtained. The Consortium to Establish a Registry for Alzheimer's Disease neuropsychological battery total score (CERAD-TS) was used as the cognitive measure. We used linear regression model predicting cognition to examine the interactions of each CR proxy and each AD pathology.ResultsAmong the CR proxies, only education significantly moderated the relationship between Aβ deposition and CERAD-TS. Education, pIQ, and LCA, but not OC, showed moderating effect on the relationship between AD-signature cerebral hypometabolism and CERAD-TS. In contrast, only OC had a significant moderating effect on the relationship between cortical atrophy of the AD-signature regions and CERAD-TS. ConclusionsThe present findings suggest that the proposed CR proxies have different moderating effects on the relationships between specific AD pathologies and cognitive decline. To investigate CR or related issues, it is necessary to select a proper CR proxy considering the target brain pathology.

Sign in / Sign up

Export Citation Format

Share Document