scholarly journals Development of silicon fluoride acceptor (SiFA)-conjugated antibodies targeting TREM2 and Poly-GA repeats as new tracers for PET imaging of neurodegenerative diseases

2021 ◽  
Vol 96-97 ◽  
pp. S37
Author(s):  
Monireh Shojaei ◽  
Christian Haass ◽  
Dieter Edbauer ◽  
Kai Schlepckow ◽  
Peter Bartenstein ◽  
...  
2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Anne-Claire Dupont ◽  
Bérenger Largeau ◽  
Denis Guilloteau ◽  
Maria Joao Santiago Ribeiro ◽  
Nicolas Arlicot

In vivo exploration of neurodegenerative diseases by positron emission tomography (PET) imaging has matured over the last 20 years, using dedicated radiopharmaceuticals targeting cellular metabolism, neurotransmission, neuroinflammation, or abnormal protein aggregates (beta-amyloid and intracellular microtubule inclusions containing hyperphosphorylated tau). The ability of PET to characterize biological processes at the cellular and molecular levels enables early detection and identification of molecular mechanisms associated with disease progression, by providing accurate, reliable, and longitudinally reproducible quantitative biomarkers. Thus, PET imaging has become a relevant imaging method for monitoring response to therapy, approved as an outcome measure in bioclinical trials. The aim of this paper is to review and discuss the current inputs of PET in the assessment of therapeutic effectiveness in neurodegenerative diseases connected by common pathophysiological mechanisms, including Parkinson’s disease, Huntington’s disease, dementia, amyotrophic lateral sclerosis, multiple sclerosis, and also in psychiatric disorders. We also discuss opportunities for PET imaging to drive more personalized neuroprotective and therapeutic strategies, taking into account individual variability, within the growing framework of precision medicine.


2008 ◽  
Vol 4 ◽  
pp. T542-T542
Author(s):  
Qiao-Xin Li ◽  
Katrina M. Laughton ◽  
Steve J. Collins ◽  
Victor L. Villemagne ◽  
Christopher C. Rowe ◽  
...  

Author(s):  
Elizabeth C. Mormino ◽  
Tyler N. Toueg ◽  
Carmen Azevedo ◽  
Jessica B. Castillo ◽  
Wanjia Guo ◽  
...  

2014 ◽  
Vol 43 (19) ◽  
pp. 6683-6691 ◽  
Author(s):  
Lin Zhu ◽  
Karl Ploessl ◽  
Hank F. Kung

Amyvid/PET imaging of a living brain detects β-amyloid plaque deposition, a risk factor for developing Alzheimer's disease.


MedChemComm ◽  
2015 ◽  
Vol 6 (12) ◽  
pp. 2184-2193 ◽  
Author(s):  
Vadim Bernard-Gauthier ◽  
Justin J. Bailey ◽  
Arturo Aliaga ◽  
Alexey Kostikov ◽  
Pedro Rosa-Neto ◽  
...  

Dysregulation of tropomyosin receptor kinases (TrkA/B/C) expression and signalling is recognized as a hallmark of numerous neurodegenerative diseases including Parkinson's, Huntington's and Alzheimer's disease.


2011 ◽  
Vol 3 (1) ◽  
pp. 111-119 ◽  
Author(s):  
Alex Sik Chung Ching ◽  
Bertrand Kuhnast ◽  
Annelaure Damont ◽  
Dirk Roeda ◽  
Bertrand Tavitian ◽  
...  

2013 ◽  
Vol 55 ◽  
pp. 119-131 ◽  
Author(s):  
Bernadette Carroll ◽  
Graeme Hewitt ◽  
Viktor I. Korolchuk

Autophagy is a process of lysosome-dependent intracellular degradation that participates in the liberation of resources including amino acids and energy to maintain homoeostasis. Autophagy is particularly important in stress conditions such as nutrient starvation and any perturbation in the ability of the cell to activate or regulate autophagy can lead to cellular dysfunction and disease. An area of intense research interest is the role and indeed the fate of autophagy during cellular and organismal ageing. Age-related disorders are associated with increased cellular stress and assault including DNA damage, reduced energy availability, protein aggregation and accumulation of damaged organelles. A reduction in autophagy activity has been observed in a number of ageing models and its up-regulation via pharmacological and genetic methods can alleviate age-related pathologies. In particular, autophagy induction can enhance clearance of toxic intracellular waste associated with neurodegenerative diseases and has been comprehensively demonstrated to improve lifespan in yeast, worms, flies, rodents and primates. The situation, however, has been complicated by the identification that autophagy up-regulation can also occur during ageing. Indeed, in certain situations, reduced autophagosome induction may actually provide benefits to ageing cells. Future studies will undoubtedly improve our understanding of exactly how the multiple signals that are integrated to control appropriate autophagy activity change during ageing, what affect this has on autophagy and to what extent autophagy contributes to age-associated pathologies. Identification of mechanisms that influence a healthy lifespan is of economic, medical and social importance in our ‘ageing’ world.


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