Glycogenesis by Mark Cicade (CC-BY-SA-4.0)
In a previous post we took a very brief look at the suggested relationship between glycogen synthase and a regulator of this enzyme – glycogen synthase kinase 3. We also looked at some of the evidence implicating GSK 3 in Alzheimer’s Disease from Small and Duff’s 2008 paper on the Dual Pathway Hypothesis (DPH).
In this post we will revisit the paper by Beurel and colleagues from 2014. In the 6 years since Small and Duff’s paper there have been further relevant findings about the relationship between GSK 3 and Alzheimer’s Disease. Beurel and colleagues look at this evidence independently of the DPH.
Beurel note that
- GSK 3 is linked to Amyloid Beta peptide production
- GSK 3 is linked to Tau pathology
- GSK 3 is linked to apoptosis
- GSK 3 inhibitors improve cognition in models of Alzheimer’s Disease
- The prevalence of Dementia in people with Bipolar Disorder taking Lithium is examined
- The use of GSK inhibitors in Alzheimer’s Type Dementia is discussed
To avoid ambiguity, it is important to note that Lithium is not licensed in the UK for the treatment of Alzheimer’s Type Dementia. Indeed for this to be the case, it would need to have positive results from specialised trials and to have passed through regulatory approval. This is not the case at the time of writing. The discussion above is being investigated in a research setting.
Beurel and colleagues have written a very detailed paper and the interested reader can learn much about GSK 3 beyond the focus on Alzheimer’s Disease discussed here. However in terms of Alzheimer’s Disease the six lines of evidence above are interesting and add further detail to Small and Duff’s hypothesis.
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