Cranial irradiation significantly reduces beta amyloid plaques in the brain and improves cognition in a murine model of Alzheimer’s Disease (AD)

2016 ◽  
Vol 118 (3) ◽  
pp. 579-580 ◽  
Author(s):  
Brian Marples ◽  
Mackenzie McGee ◽  
Sean Callan ◽  
Scott E. Bowen ◽  
Bryan J. Thibodeau ◽  
...  
The Analyst ◽  
2019 ◽  
Vol 144 (23) ◽  
pp. 7049-7056 ◽  
Author(s):  
Emerson A. Fonseca ◽  
Lucas Lafetá ◽  
Renan Cunha ◽  
Hudson Miranda ◽  
João Campos ◽  
...  

We have found different Raman signatures of AB fibrils and in brain tissues from unmixed analysis, providing a detailed image of amyloid plaques in the brain, with the potential to be used as biomarkers.


Metallomics ◽  
2016 ◽  
Vol 8 (8) ◽  
pp. 782-789 ◽  
Author(s):  
Zhong-Hao Zhang ◽  
Chen Chen ◽  
Qiu-Yan Wu ◽  
Rui Zheng ◽  
Qiong Liu ◽  
...  

Effects on Aβ production and the probable connection among selenoenzymes, GSK3β and Aβ pathology by selenomethionine treatment in AD mice.


2019 ◽  
pp. S445-S451 ◽  
Author(s):  
H. Svobodová ◽  
D. Kosnáč ◽  
Z. Balázsiová ◽  
H. Tanila ◽  
P.O. Miettinen ◽  
...  

Iron is very important element for functioning of the brain. Its concentration changes with aging the brain or during disease. The aim of our work was the histological examination of content of ferritin and free iron (unbound) in brain cortex in association with Aβ plaques from their earliest stages of accumulation in amyloid plaque forming APP/PS1 transgenic mice. Light microscopy revealed the onset of plaques formation at 8-monthage. Detectable traces of free iron and no ferritin were found around plaques at this age, while the rate of their accumulation in and around Aβ plaques was elevated at 13 months of age. Ferritin accumulated mainly on the edge of Aβ plaques, while the smaller amount of free iron was observed in the plaque-free tissue, as well as in and around Aβ plaques. We conclude that free iron and ferritin accumulation follows the amyloid plaques formation. Quantification of cortical iron and ferritin content can be an important marker in the diagnosis of Alzheimer’s disease.


2020 ◽  
Vol 39 (12) ◽  
pp. 4060-4070
Author(s):  
Imran Saied ◽  
Tughrul Arslan ◽  
Siddharthan Chandran ◽  
Colin Smith ◽  
Tara Spires-Jones ◽  
...  

Nano Research ◽  
2016 ◽  
Vol 9 (7) ◽  
pp. 2190-2201 ◽  
Author(s):  
Giulio Sancini ◽  
Roberta Dal Magro ◽  
Francesca Ornaghi ◽  
Claudia Balducci ◽  
Gianluigi Forloni ◽  
...  

2019 ◽  
Author(s):  
Maria V. Pulina ◽  
Maya Hopkins ◽  
Vahram Haroutunian ◽  
Paul Greengard ◽  
Victor Bustos

ABSTRACTIntroductionThe levels and distribution of amyloid deposits in the brain does not correlate well with Alzheimer’s disease (AD) progression. Therefore, it is likely that Amyloid-precursor-protein proteolytic fragments other than beta-amyloid contribute to the onset of AD.MethodsWe developed a sensitive assay adapted to the detection of C99, the direct precursor of beta-amyloid. Three postmortem groups were studied: control with normal and stable cognition; subjects with moderate AD, and individuals with severe AD. The amount of C99 and beta-amyloid was quantified and correlated with the severity of AD.ResultsC99 accumulates in vulnerable neurons, and its levels correlate with the degree of cognitive impairment in patients suffering from AD. In contrast, beta-amyloid levels are increased in both vulnerable and resistant brain areas.DiscussionThese results raise the possibility that C99, rather than beta-amyloid plaques, is responsible for the death of nerve cells in Alzheimer’s disease.


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