Investigating Pathological Features of Alzheimer’s Disease in Human and Mouse Brain Tissue with Visible Light Optical Coherence Microscopy

2018 ◽  
Author(s):  
Antonia Lichtenegger ◽  
Martina Muck ◽  
Pablo Eugui ◽  
Danielle Harper ◽  
Marco Augustin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Visible Light ◽  
Brain Tissue ◽  
Mouse Brain ◽  
Optical Coherence ◽  
Pathological Features ◽  
Optical Coherence Microscopy ◽  
Human And Mouse

scholarly journals Assessment of pathological features in Alzheimer’s disease brain tissue with a large field-of-view visible-light optical coherence microscope

2018 ◽  
Vol 5 (03) ◽  
pp. 1 ◽  
Author(s):  
Antonia Lichtenegger ◽  
Martina Muck ◽  
Pablo Eugui ◽  
Danielle J. Harper ◽  
Marco Augustin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Visible Light ◽  
Brain Tissue ◽  
Field Of View ◽  
Large Field ◽  
Optical Coherence ◽  
Pathological Features

scholarly journals Spectroscopic imaging with spectral domain visible light optical coherence microscopy in Alzheimer’s disease brain samples

2017 ◽  
Vol 8 (9) ◽  
pp. 4007 ◽  
Author(s):  
Antonia Lichtenegger ◽  
Danielle J. Harper ◽  
Marco Augustin ◽  
Pablo Eugui ◽  
Martina Muck ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Visible Light ◽  
Spectroscopic Imaging ◽  
Spectral Domain ◽  
Optical Coherence ◽  
Optical Coherence Microscopy

scholarly journals Visualization of neuritic plaques in Alzheimer’s disease by polarization-sensitive optical coherence microscopy

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Bernhard Baumann ◽  
Adelheid Woehrer ◽  
Gerda Ricken ◽  
Marco Augustin ◽  
Christian Mitter ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Optical Coherence ◽  
Neuritic Plaques ◽  
Optical Coherence Microscopy

scholarly journals Abnormal brain cholesterol homeostasis in Alzheimer’s disease—a targeted metabolomic and transcriptomic study

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Vijay R. Varma ◽  
H. Büşra Lüleci ◽  
Anup M. Oommen ◽  
Sudhir Varma ◽  
Chad T. Blackshear ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Tissue ◽  
Cholesterol Metabolism ◽  
Cholesterol Biosynthesis ◽  
Cholesterol Homeostasis ◽  
Transcriptomic Data ◽  
Brain Cholesterol ◽  
Cholesterol Levels

AbstractThe role of brain cholesterol metabolism in Alzheimer’s disease (AD) remains unclear. Peripheral and brain cholesterol levels are largely independent due to the impermeability of the blood brain barrier (BBB), highlighting the importance of studying the role of brain cholesterol homeostasis in AD. We first tested whether metabolite markers of brain cholesterol biosynthesis and catabolism were altered in AD and associated with AD pathology using linear mixed-effects models in two brain autopsy samples from the Baltimore Longitudinal Study of Aging (BLSA) and the Religious Orders Study (ROS). We next tested whether genetic regulators of brain cholesterol biosynthesis and catabolism were altered in AD using the ANOVA test in publicly available brain tissue transcriptomic datasets. Finally, using regional brain transcriptomic data, we performed genome-scale metabolic network modeling to assess alterations in cholesterol biosynthesis and catabolism reactions in AD. We show that AD is associated with pervasive abnormalities in cholesterol biosynthesis and catabolism. Using transcriptomic data from Parkinson’s disease (PD) brain tissue samples, we found that gene expression alterations identified in AD were not observed in PD, suggesting that these changes may be specific to AD. Our results suggest that reduced de novo cholesterol biosynthesis may occur in response to impaired enzymatic cholesterol catabolism and efflux to maintain brain cholesterol levels in AD. This is accompanied by the accumulation of nonenzymatically generated cytotoxic oxysterols. Our results set the stage for experimental studies to address whether abnormalities in cholesterol metabolism are plausible therapeutic targets in AD.

scholarly journals 1700 nm optical coherence microscopy enables minimally invasive, label-free, in vivo optical biopsy deep in the mouse brain

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Jun Zhu ◽  
Hercules Rezende Freitas ◽  
Izumi Maezawa ◽  
Lee-way Jin ◽  
Vivek J. Srinivasan
Keyword(s):  
Minimally Invasive ◽  
Mouse Brain ◽  
Numerical Aperture ◽  
Optical Biopsy ◽  
Optical Coherence ◽  
Label Free ◽  
Optical Coherence Microscopy ◽  
Minimal Invasiveness ◽  
Cortical Regions

AbstractIn vivo, minimally invasive microscopy in deep cortical and sub-cortical regions of the mouse brain has been challenging. To address this challenge, we present an in vivo high numerical aperture optical coherence microscopy (OCM) approach that fully utilizes the water absorption window around 1700 nm, where ballistic attenuation in the brain is minimized. Key issues, including detector noise, excess light source noise, chromatic dispersion, and the resolution-speckle tradeoff, are analyzed and optimized. Imaging through a thinned-skull preparation that preserves intracranial space, we present volumetric imaging of cytoarchitecture and myeloarchitecture across the entire depth of the mouse neocortex, and some sub-cortical regions. In an Alzheimer’s disease model, we report that findings in superficial and deep cortical layers diverge, highlighting the importance of deep optical biopsy. Compared to other microscopic techniques, our 1700 nm OCM approach achieves a unique combination of intrinsic contrast, minimal invasiveness, and high resolution for deep brain imaging.

Learning Deficits Accompanied by Microglial Proliferation After the Long-Term Post-Injection of Alzheimer’s Disease Brain Extract in Mouse Brains

2021 ◽  
Vol 79 (4) ◽  
pp. 1701-1711
Author(s):  
Tetsuo Hayashi ◽  
Shotaro Shimonaka ◽  
Montasir Elahi ◽  
Shin-Ei Matsumoto ◽  
Koichi Ishiguro ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Brain ◽  
Functional Decline ◽  
Brain Regions ◽  
Insoluble Fraction ◽  
Brain Extract ◽  
Post Injection ◽  
Learning Deficits

Background: Human tauopathy brain injections into the mouse brain induce the development of tau aggregates, which spread to functionally connected brain regions; however, the features of this neurotoxicity remain unclear. One reason may be short observational periods because previous studies mostly used mutated-tau transgenic mice and needed to complete the study before these mice developed neurofibrillary tangles. Objective: To examine whether long-term incubation of Alzheimer’s disease (AD) brain in the mouse brain cause functional decline. Methods: We herein used Tg601 mice, which overexpress wild-type human tau, and non-transgenic littermates (NTg) and injected an insoluble fraction of the AD brain into the unilateral hippocampus. Results: After a long-term (17–19 months) post-injection, mice exhibited learning deficits detected by the Barnes maze test. Aggregated tau pathology in the bilateral hippocampus was more prominent in Tg601 mice than in NTg mice. No significant changes were observed in the number of Neu-N positive cells or astrocytes in the hippocampus, whereas that of Iba-I-positive microglia increased after the AD brain injection. Conclusion: These results potentially implicate tau propagation in functional decline and indicate that long-term changes in non-mutated tau mice may reflect human pathological conditions.

Sign in / Sign up

Export Citation Format

Share Document