The pathophysiology of Alzheimer’s disease (AD) is characterized by chronic, progressive neurodegeneration. One of the most obvious pathological feature of AD is the accumulation of soluble amyloid beta (Aβ) peptides in the brain. In this work, pridopidine, a selective sigma-1 receptor (S1R) antagonist, will be tested whether it ameliorates synaptic deficits induced by Aβ 1–42. If one can confirm detrimental effects of Aβ 1-42 oligomers on long-term potentiation (LTP) in the CA1 region of murine hippocampal slices, pridopidine will be co-treated in an attempt to reverse LTP deficits.
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The pathophysiology of Alzheimer’s disease (AD) is characterized by chronic, progressive neurodegeneration. One of the most obvious pathological feature of AD is the accumulation of soluble amyloid beta (Aβ) peptides in the brain. In this work, pridopidine, a selective sigma-1 receptor (S1R) antagonist, will be tested whether it ameliorates synaptic deficits induced by Aβ 1–42. If one can confirm detrimental effects of Aβ 1-42 oligomers on long-term potentiation (LTP) in the CA1 region of murine...
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