scholarly journals Tanshinone IIA reduces the risk of Alzheimer’s disease by inhibiting iNOS, MMP-2 and NF-κBp65 transcription and translation in the temporal lobes of rat models of Alzheimer’s disease

2014 ◽  
Vol 10 (2) ◽  
pp. 689-694 ◽  
Author(s):  
PING JIANG ◽  
CHUNBO LI ◽  
ZHENGHUA XIANG ◽  
BINGHUA JIAO
2021 ◽  
pp. 1-11
Author(s):  
Adam S. Bernstein ◽  
Steven Z. Rapcsak ◽  
Michael Hornberger ◽  
Manojkumar Saranathan ◽  

Background: Increasing evidence suggests that thalamic nuclei may atrophy in Alzheimer’s disease (AD). We hypothesized that there will be significant atrophy of limbic thalamic nuclei associated with declining memory and cognition across the AD continuum. Objective: The objective of this work was to characterize volume differences in thalamic nuclei in subjects with early and late mild cognitive impairment (MCI) as well as AD when compared to healthy control (HC) subjects using a novel MRI-based thalamic segmentation technique (THOMAS). Methods: MPRAGE data from the ADNI database were used in this study (n = 540). Healthy control (n = 125), early MCI (n = 212), late MCI (n = 114), and AD subjects (n = 89) were selected, and their MRI data were parcellated to determine the volumes of 11 thalamic nuclei for each subject. Volumes across the different clinical subgroups were compared using ANCOVA. Results: There were significant differences in thalamic nuclei volumes between HC, late MCI, and AD subjects. The anteroventral, mediodorsal, pulvinar, medial geniculate, and centromedian nuclei were significantly smaller in subjects with late MCI and AD when compared to HC subjects. Furthermore, the mediodorsal, pulvinar, and medial geniculate nuclei were significantly smaller in early MCI when compared to HC subjects. Conclusion: This work highlights nucleus specific atrophy within the thalamus in subjects with early and late MCI and AD. This is consistent with the hypothesis that memory and cognitive changes in AD are mediated by damage to a large-scale integrated neural network that extends beyond the medial temporal lobes.


Author(s):  
Briana S. Last ◽  
Batool Rizvi ◽  
Adam M. Brickman

Structural magnetic resonance imaging (MRI) is a powerful tool to visualize and quantitate morphological and pathological features of the aging brain. Most work that has used structural MRI to study Alzheimer’s disease (AD) focused on the spatial distribution of atrophic changes associated with disease. These studies consistently show focal atrophy beginning in medial temporal lobes in early and presymptomatic stages of AD before spreading globally throughout the cortical mantle. Normal cognitive aging—aging in the absence of major neurodegenerative disease—on the other hand follows and anterior-to-posterior gradient of atrophic change. In addition to atrophic changes, conventional structural MRI can be used to appreciate markers of small and large vessel cerebrovascular disease, including white matter hyperintensities (WMHs), cerebral microbleeds, and infarction. Studies that have examined cerebrovascular changes associated with AD also show a consistent relationship with risk and severity of clinical AD, particularly with regard to lobar microbleeds and posterior WMH. It is unclear whether cerebrovascular changes play an independent role in the clinical expression of AD or whether it is more mechanistically related, reflecting a core feature of the disease. This chapter reviews recent work on regional atrophy in AD and normal aging, as well as work on small and large cerebrovascular disease in AD.


2019 ◽  
Vol 26 (3) ◽  
pp. 139-152 ◽  
Author(s):  
Kai  Hu ◽  
Yafeng  Li ◽  
Huifen  Yu ◽  
Yanhui Hu

Neuroreport ◽  
2016 ◽  
Vol 27 (12) ◽  
pp. 883-893 ◽  
Author(s):  
Bei-Ling Lu ◽  
Jian Li ◽  
Jun Zhou ◽  
Wen-Wen Li ◽  
Heng-Fei Wu

1996 ◽  
Vol 39 (7) ◽  
pp. 658
Author(s):  
B.deS. Frederick ◽  
A. Satlin ◽  
D. Yurgelun-Todd ◽  
P.F. Renshaw

2007 ◽  
Vol 32 (10) ◽  
pp. 1709-1717 ◽  
Author(s):  
Ismet Tahirovic ◽  
Emin Sofic ◽  
Aida Sapcanin ◽  
Ismet Gavrankapetanovic ◽  
Lidija Bach-Rojecky ◽  
...  

1992 ◽  
Vol 94 (1) ◽  
pp. 82
Author(s):  
P. Scheltens ◽  
D. Leys ◽  
F. Barkhof ◽  
H.C. Weinstein ◽  
E.C. Wolters ◽  
...  

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