Advantages
- Improves cognitive function, learning, and memory in tauopathy models without altering protein levels
- Utilizes targeted intracranial delivery of AAV9 vector for efficient gene transfer to hippocampus and frontal cortex.
- Enhances synaptic plasticity and rescues long-term potentiation (LTP) deficits in affected brain regions.
Summary
Tau is a microtubule associated protein that has been linked to multiple neurodegenerative diseases, the most prevalent being Alzheimer’s disease (AD). In AD and other tauopathies, tau pathogenically aggregates, which contributesto the pathogenicity of the disease. Smallheat shock proteins (sHsp) are highly conserved, are highly expressed and respond quickly to stressful conditions. These sHsps have been shown to have increased expression with aging and to directly interact with autophagy-related proteins and to form complexes that help regulate aberrant proteins in the cell. Thismethod investigatesthe effects of Hsp22 wild-type and Hsp22 phosphomimetic mutant over expressionin the brains of tau transgenic miceon tau accumulation, cognitive function, synaptic plasticity, and neuronal health.The results show administration of both wild type Hsp22 and a mutant phosphomimetic Hsp22 were found to increase synaptic plasticity and long term potentiatingthus leading to increases in cognition, learning and memory in patients having a tauopathy such as Alzheimer’s disease.
The image shows that Hsp22 over expression improved reversal spatial learning in rTg4510 mice where mtHsp22 over expression significantly lowered the number of errors in rTg4510 mice compared to GFP controls, and mice with wtHsp22 over expression showed fewer errors than GFP controls.
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