Saturday, 29 June 2013

New work out of Columbia University Medical Center has demonstrated that a protein called caspase-2 is a key...


New work out of Columbia University Medical Center has demonstrated that a protein called caspase-2 is a key regulator of a signaling pathway that leads to cognitive decline in Alzheimer’s disease – that associated with beta-amyloid.
The findings, made in a mouse model of Alzheimer’s, suggest that inhibiting this protein could prevent the neuronal damage. Here, the leftmost image–WT (wildtype), or normal, mice–shows normal branching of neuronal dendrites. The mice with Alzheimer’s disease (J20) show significant dendritic loss. When caspase-2 was deleted from mice with Alzheimer’s (J20/Casp2KO), dendritic branching was normal–demonstrating that removal of caspase-2 can protect neurons in the presence of amyloid beta. These images are taken at 14 months.

More info: http://newsroom.cumc.columbia.edu/2013/06/25/protein-identified-that-contributes-to-cognitive-decline-in-alzheimers/

1 comment:

  1. I would be interested to see long term effects of caspase-2 supression. Since caspases are also regulators of programmed cell death, I would be curious to see if tumor progression occurs in its absense. Sounds interesting though.

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