Journal of Alzheimer's disease : JAD
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Cerebral amyloid angiopathy-related inflammation (CAA-ri) represents the most readily responsive form of CAA, if diagnosed and treated early. Although CAA-ri typically presents with a monophasic pattern, recurrences have been occasionally reported. ⋯ Our observations highlight the importance of not underestimating any new neurological symptoms in patients who have already experienced an episode of CAA-ri. Although the frequency of CAA-ri recurrences is rare, in cases of suspected relapse, a prompt clinical and radiological follow-up should be considered in order to obtain a timely diagnosis and treatment, having a potential strong impact on patients' clinical outcome.
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Comparative Study
More atrophy of deep gray matter structures in frontotemporal dementia compared to Alzheimer's disease.
The involvement of frontostriatal circuits in frontotemporal dementia (FTD) suggests that deep gray matter structures (DGM) may be affected in this disease. ⋯ Nucleus accumbens, caudate nucleus, and globus pallidus were more severely affected in FTD than in AD and SC. The associations between cognition and DGM structures varied between the diagnostic groups. The observed difference in volume of these DGM structures supports the idea that next to frontal cortical atrophy, DGM structures, as parts of the frontal circuits, are damaged in FTD rather than in AD.
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Comparative Study
Mirror Image of the Amyloid-β Species in Cerebrospinal Fluid and Cerebral Amyloid in Alzheimer's Disease.
Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) accumulation in brain that is paralleled by Aβ(1-42) reduction in cerebrospinal fluid (CSF). We analyzed the pattern of Aβ peptides, including the N- and C-terminal truncated fragments, in brain and CSF from two familial and one sporadic AD cases. We found that (i) each patient is characterized by a distinct Aβ profile in CSF and brain deposits and (ii) the CSF Aβ pattern mirrors the Aβ profile of cerebral amyloid. These results suggest the existence of different molecular AD subtypes which can be recognized by CSF analysis, enabling patient stratification.
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We have employed structural equation models to explicitly distinguish functional status, and therefore "dementia-relevant" variance in cognitive task performance (i.e., "δ"). We previously associated δ with cytokines and other serum biomarkers in a well characterized Alzheimer's disease cohort, the Texas Alzheimer's Research and Care Consortium. ⋯ Most of these associations are again specific to Non-Hispanic White participants. These findings have yet to be validated in other cohorts, but may suggest cross-ethnic differences in dementia's pathobiological mechanisms between Hispanic Mexican-Americans and Non-Hispanic Whites.
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There is growing evidence that the human brain is a large scale complex network. The structural network is reported to be disrupted in cognitively impaired patients. However, there have been few studies evaluating the effects of amyloid and small vessel disease (SVD) markers, the common causes of cognitive impairment, on structural networks. ⋯ Greater white matter hyperintensity volumes or lacunae numbers were significantly associated with decreased network integration (increased shortest path length, decreased global efficiency) and increased network segregation (increased clustering coefficient, increased transitivity, increased modularity). Decreased network integration or increased network segregation were associated with poor performances in attention, language, visuospatial, memory, and frontal-executive functions. Our results suggest that SVD alters white matter network integration and segregation, which further predicts cognitive dysfunction.