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An Open Question: Is the A2A Adenosine Receptor a Novel Target for Alzheimer’s Disease Treatment?
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An Open Question: Is the A2A Adenosine Receptor a Novel Target for Alzheimer’s Disease Treatment?
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Journal Article
An Open Question: Is the A2A Adenosine Receptor a Novel Target for Alzheimer’s Disease Treatment?
2021
Overview
[...]the disease begins decades earlier with amyloid accumulation in the neocortex but amyloid deposition, which is very common even in physiological aging, is not sufficient to cause AD. [...]oligomers can reduce blood flow in brain capillaries and induce hyperphosphorylation of the AD-relevant epitopes of TAU protein (Selkoe and Hardy 2016;Nortley et al., 2019). [...]Aβ load triggers neurodegeneration through oligomers which induce unbalanced activation of neuronal kinases resulting in excessive production of pTAU that, in turn, aggregates in pTAU toxic oligomers and spreads from its initial location in allocortex to neocortex. On the basis of the neuropathological picture, several biomarkers have been developed for the in vivo definition of the pathology. [...]the ATN system (Amyloid-TAU-Neurodegeneration) has been set up including 1) estimate of the amyloid load: Aβ decrease in cerebrospinal fluid (CSF) and/or Aβ cortical accumulation at amyloid-PET; 2) pTAU valuation: pTAU increase in CSF and/or pTAU cortical accumulation at TAU-PET; 3) extent of neurodegeneration: atrophic pattern at brain MRI and/or hypometabolism at FDG-PET and/or increase of total-TAU in CSF (Jack et al., 2018b;Chételat et al., 2020). [...]amyloid reduction is only one aspect of the therapeutic approach and there is increasing attention to non-amyloid targets with 121 agents having clinical trials in course for the treatment of AD (Cummings et al., 2020).
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