scholarly journals Molecular imaging and fluid biomarkers of Alzheimer’s disease neuropathology: an opportunity for integrated diagnostics

2021 ◽  
Author(s):  
Valentina Garibotto ◽  
Marina Boccardi ◽  
Arturo Chiti ◽  
Giovanni B. Frisoni
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Imaging ◽  
Integrated Diagnostics

scholarly journals Evaluation of the neuroprotective effect of taurine in Alzheimer’s disease using functional molecular imaging

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Se Jong Oh ◽  
Hae-June Lee ◽  
Ye Ji Jeong ◽  
Kyung Rok Nam ◽  
Kyung Jun Kang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Imaging ◽  
Neurodegenerative Disorder ◽  
Therapeutic Potential ◽  
Neuroprotective Effect ◽  
Treatment Options ◽  
Brain Uptake ◽  
Positron Emission ◽  
Taurine Treatment

Abstract Alzheimer’s disease (AD) is a chronic neurodegenerative disorder and the leading cause of dementia, but therapeutic treatment options are limited. Taurine has been reported to have neuroprotective properties against dementia, including AD. The present study aimed to investigate the treatment effect of taurine in AD mice by functional molecular imaging. To elucidate glutamate alterations by taurine, taurine was administered to 5xFAD transgenic mice from 2 months of age, known to apear amyloid deposition. Then, we performed glutamate positron emission tomography (PET) imaging studies for three groups (wild-type, AD, and taurine-treated AD, n = 5 in each group). As a result, brain uptake in the taurine-treated AD group was 31–40% higher than that in the AD group (cortex: 40%, p < 0.05; striatum: 32%, p < 0.01; hippocampus: 36%, p < 0.01; thalamus: 31%, p > 0.05) and 3–14% lower than that in the WT group (cortex: 10%, p > 0.05; striatum: 15%, p > 0.05; hippocampus: 14%, p > 0.05; thalamus: 3%, p > 0.05). However, we did not observe differences in Aβ pathology between the taurine-treated AD and AD groups in immunohistochemistry experiments. Our results reveal that although taurine treatment did not completely recover the glutamate system, it significantly increased metabolic glutamate receptor type 5 brain uptake. Therefore, taurine has therapeutic potential against AD.

Molecular Imaging in Alzheimer’s Disease

2011 ◽  
Vol 6 (1) ◽  
pp. 16
Author(s):  
Karl Herholz ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Imaging ◽  
Clinical Symptoms ◽  
Accurate Method ◽  
Imaging Biomarker ◽  
Pet Tracer ◽  
Specificity And Sensitivity ◽  
Positron Emission ◽  
Dementia Research

The most sensitive and accurate method for molecular imaging in human Alzheimer’s disease (AD) is positron emission tomography (PET). The most widely available PET tracer, which is also used in clinical oncology, is 18F-2-fluoro-2-deoxy-D-glucose (FDG). FDG is an imaging biomarker for early and differential diagnosis of AD. Even higher molecular specificity and sensitivity for detection of AD before dementia onset is provided by high-affinity ligands for fibrillary amyloid. 11C-Pittsburgh Compound B is widely being used in research laboratories, while new 18F-labelled ligands are currently undergoing formal clinical trials as amyloid imaging agents and are expected to become commercially available for clinical use in the near future. A large variety of tracers is being developed and used in dementia research for activated microglia and multiple neurotransmitter systems to study disease pathophysiology, biological correlates of clinical symptoms and new possibilities for treatment. Current studies in humans are investigating cholinergic, serotonergic and dopaminergic neurotransmission.

scholarly journals Molecular imaging in the diagnosis of Alzheimer's disease: visual assessment of [11C]PIB and [18F]FDDNP PET images

2010 ◽  
Vol 81 (8) ◽  
pp. 882-884 ◽  
Author(s):  
N. Tolboom ◽  
W. M. van der Flier ◽  
J. Boverhoff ◽  
M. Yaqub ◽  
M. P. Wattjes ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Imaging ◽  
Visual Assessment

scholarly journals Near-infrared fluorescence molecular imaging of amyloid beta species and monitoring therapy in animal models of Alzheimer’s disease

2015 ◽  
Vol 112 (31) ◽  
pp. 9734-9739 ◽  
Author(s):  
Xueli Zhang ◽  
Yanli Tian ◽  
Can Zhang ◽  
Xiaoyu Tian ◽  
Alana W. Ross ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Imaging ◽  
Amyloid Beta ◽  
Near Infrared ◽  
Imaging Data ◽  
Curcumin Analog ◽  
Near Infrared Fluorescence ◽  
Brain Extraction ◽  
Monitoring Therapy

Near-infrared fluorescence (NIRF) molecular imaging has been widely applied to monitoring therapy of cancer and other diseases in preclinical studies; however, this technology has not been applied successfully to monitoring therapy for Alzheimer’s disease (AD). Although several NIRF probes for detecting amyloid beta (Aβ) species of AD have been reported, none of these probes has been used to monitor changes of Aβs during therapy. In this article, we demonstrated that CRANAD-3, a curcumin analog, is capable of detecting both soluble and insoluble Aβ species. In vivo imaging showed that the NIRF signal of CRANAD-3 from 4-mo-old transgenic AD (APP/PS1) mice was 2.29-fold higher than that from age-matched wild-type mice, indicating that CRANAD-3 is capable of detecting early molecular pathology. To verify the feasibility of CRANAD-3 for monitoring therapy, we first used the fast Aβ-lowering drug LY2811376, a well-characterized beta-amyloid cleaving enzyme-1 inhibitor, to treat APP/PS1 mice. Imaging data suggested that CRANAD-3 could monitor the decrease in Aβs after drug treatment. To validate the imaging capacity of CRANAD-3 further, we used it to monitor the therapeutic effect of CRANAD-17, a curcumin analog for inhibition of Aβ cross-linking. The imaging data indicated that the fluorescence signal in the CRANAD-17–treated group was significantly lower than that in the control group, and the result correlated with ELISA analysis of brain extraction and Aβ plaque counting. It was the first time, to our knowledge, that NIRF was used to monitor AD therapy, and we believe that our imaging technology has the potential to have a high impact on AD drug development.

Molecular Imaging and Magnetic Resonance Imaging in Early Diagnosis of Alzheimer's Disease

2008 ◽  
Vol 21 (6) ◽  
pp. 755-771
Author(s):  
O. Schillaci ◽  
L. Travascio ◽  
C. Bruni ◽  
G. Bazzocchi ◽  
A. Testa ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Imaging ◽  
Magnetic Resonance ◽  
Early Diagnosis ◽  
Neurodegenerative Disorder ◽  
The Elderly ◽  
Resonance Imaging ◽  
New Techniques ◽  
Molecular Imaging Agents

Alzheimer's disease (AD), a progressive neurodegenerative disorder, is the most common cause of dementia in the elderly. Magnetic resonance (MR) or computed tomography (CT) imaging is recommended for routine evaluation of dementias. The development of molecular imaging agents and the new techniques of MR for AD are critically important for early diagnosis, neuropathogenesis studies and assessing treatment efficacy in AD. Neuroimaging using nuclear medicine techniques such as SPECT, PET and MR spectroscopy has the potential to characterize the biomarkers for Alzheimer's disease. The present review summarizes the results of radionuclide imaging and MR imaging in AD.

scholarly journals Molecular imaging of Alzheimer’s disease–related gamma-secretase in mice and nonhuman primates

2020 ◽  
Vol 217 (12) ◽  
Author(s):  
Yulong Xu ◽  
Changning Wang ◽  
Hsiao-Ying Wey ◽  
Yingxia Liang ◽  
Zude Chen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Imaging ◽  
Amyloid Β ◽  
Transgenic Animals ◽  
Gamma Secretase ◽  
Functional Conservation ◽  
Aβ42 Peptide ◽  
Molecular Brain ◽  
The Brain

The pathogenesis of Alzheimer’s disease (AD) is primarily driven by brain accumulation of the amyloid-β-42 (Aβ42) peptide generated from the amyloid-β precursor protein (APP) via cleavages by β- and γ-secretase. γ-Secretase is a prime drug target for AD; however, its brain regional expression and distribution remain largely unknown. Here, we are aimed at developing molecular imaging tools for visualizing γ-secretase. We used our recently developed γ-secretase modulators (GSMs) and synthesized our GSM-based imaging agent, [11C]SGSM-15606. We subsequently performed molecular imaging in rodents, including AD transgenic animals, and macaques, which revealed that our probe displayed good brain uptake and selectivity, stable metabolism, and appropriate kinetics and distribution for imaging γ-secretase in the brain. Interestingly, rodents and macaques shared certain brain areas with high γ-secretase expression, suggesting a functional conservation of γ-secretase. Collectively, we have provided the first molecular brain imaging of γ-secretase, which may not only accelerate our drug discovery for AD but also advance our understanding of AD.

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