scholarly journals Aβ alters the connectivity of olfactory neurons in the absence of amyloid plaques in vivo

2012 ◽  
Vol 3 (1) ◽  
Author(s):  
Luxiang Cao ◽  
Benjamin R. Schrank ◽  
Steve Rodriguez ◽  
Eric G. Benz ◽  
Thomas W. Moulia ◽  
...  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eugene Kim ◽  
Davide Di Censo ◽  
Mattia Baraldo ◽  
Camilla Simmons ◽  
Ilaria Rosa ◽  
...  

AbstractAmyloid plaques are a hallmark of Alzheimer’s disease (AD) that develop in its earliest stages. Thus, non-invasive detection of these plaques would be invaluable for diagnosis and the development and monitoring of treatments, but this remains a challenge due to their small size. Here, we investigated the utility of manganese-enhanced MRI (MEMRI) for visualizing plaques in transgenic rodent models of AD across two species: 5xFAD mice and TgF344-AD rats. Animals were given subcutaneous injections of MnCl2 and imaged in vivo using a 9.4 T Bruker scanner. MnCl2 improved signal-to-noise ratio but was not necessary to detect plaques in high-resolution images. Plaques were visible in all transgenic animals and no wild-types, and quantitative susceptibility mapping showed that they were more paramagnetic than the surrounding tissue. This, combined with beta-amyloid and iron staining, indicate that plaque MR visibility in both animal models was driven by plaque size and iron load. Longitudinal relaxation rate mapping revealed increased manganese uptake in brain regions of high plaque burden in transgenic animals compared to their wild-type littermates. This was limited to the rhinencephalon in the TgF344-AD rats, while it was most significantly increased in the cortex of the 5xFAD mice. Alizarin Red staining suggests that manganese bound to plaques in 5xFAD mice but not in TgF344-AD rats. Multi-parametric MEMRI is a simple, viable method for detecting amyloid plaques in rodent models of AD. Manganese-induced signal enhancement can enable higher-resolution imaging, which is key to visualizing these small amyloid deposits. We also present the first in vivo evidence of manganese as a potential targeted contrast agent for imaging plaques in the 5xFAD model of AD.


2011 ◽  
Vol 21 (14) ◽  
pp. 4193-4196 ◽  
Author(s):  
Mengchao Cui ◽  
Masahiro Ono ◽  
Hiroyuki Kimura ◽  
Boli Liu ◽  
Hideo Saji

Author(s):  
Gabriel Lepousez ◽  
Mariana Alonso ◽  
Sebastian Wagner ◽  
Benjamin W. Gallarda ◽  
Pierre-Marie Lledo

2015 ◽  
Vol 44 (7) ◽  
pp. 1807-1819 ◽  
Author(s):  
Matteo Staderini ◽  
María Antonia Martín ◽  
Maria Laura Bolognesi ◽  
J. Carlos Menéndez

Near infrared (NIR) imaging is a promising and non-invasive method to visualize amyloid plaquesin vivo.


2012 ◽  
Vol 8 (4S_Part_4) ◽  
pp. P156-P156
Author(s):  
Thomas Wisniewski ◽  
Jialin Li ◽  
Dung Minh Hoang ◽  
Hong Xu ◽  
Yanjie Sun ◽  
...  

Author(s):  
Einar M. Sigurdsson ◽  
Youssef Zaim Wadghiri ◽  
Marcin Sadowski ◽  
James I. Elliott ◽  
Yongsheng Li ◽  
...  

2019 ◽  
Vol 44 (5) ◽  
pp. 327-338 ◽  
Author(s):  
Takuya Noda ◽  
Hideaki Shiga ◽  
Kentaro Yamada ◽  
Masayuki Harita ◽  
Yukari Nakamura ◽  
...  
Keyword(s):  

2004 ◽  
Vol 24 (2) ◽  
pp. 247-256 ◽  
Author(s):  
Nobuyuki Okamura ◽  
Takahiro Suemoto ◽  
Tsuyoshi Shiomitsu ◽  
Masako Suzuki ◽  
Hiroshi Shimadzu ◽  
...  

2006 ◽  
Vol 18 (s1) ◽  
pp. S3-S16 ◽  
Author(s):  
Agneta Nordberg

The pathological processes that lead to Alzheimer's disease (AD) begin decades before the onset of dementia. Brain abnormalities in genetically susceptible individuals have been observed even in young adults. Patients with AD differ from normal elderly patients in brain morphology and neurochemistry. Important observations include increasing appearance of amyloid plaques and neurofibrillary tangles, progressive loss of hippocampal volume, reduced cerebral glucose utilization, inflammatory processes, glial activation, and impairment of cholinergic function with losses of nicotinic acetylcholine receptors. These changes appear to begin in the asymptomatic stages and continue as cognition and then function and behavior are disrupted. Mild cognitive impairment (MCI) may be the first cognitive manifestation of this pathogenic process moderated by ongoing compensatory neurochemical mechanisms in the cholinergic system. Recent advances in positron emission tomography imaging techniques, including the development of the Pittsburgh B compound (PIB), allow in vivo visualization of amyloid plaques. These techniques have the potential to enable brain amyloid load to be monitored over time and to be related to brain function. Emerging evidence suggests that β-amyloid may interact with nicotinic receptors. This interaction may have clinically significant downstream effects and may mediate amyloid neurotoxicity. The cholinesterase inhibitors may have multiple actions, depending on the stage of the disease, from very mild to severe.


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