Activation of K+ channels and suppression of neuronal activity by secreted beta-amyloid-precursor protein

Article Abstract:

The abnormal K+ channel properties in Alzheimer's disease patients are due to irregularities in the processing of beta-amyloid precursor protein (beta-APP) or the secreted forms of beta-APP (sAPP). APPs regulate the neuronal excitability, which modulates the developmental and synaptic plasticity in the nervous system. The action of sAPPs is mediated by cGMP and protein dephosphorylation, as a cGMP antagonist and a phosphate inhibitor suppresses the activation of K+ channels by cGMP.

Potassium channels, Neuroplasticity

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Pathways towards and away from Alzheimer's disease

Article Abstract:

Alzheimer's disease is neurodegenerative disorder that is passed on in the genes. There are no treatments for this but scientists are beginning to understand the cellular and molecular alterations that are responsible for the neuron's demise.

Neurons, Genes

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Ballads of a protien quartet

Article Abstract:

The fate of neurons in the developing brain and in Alzheimer's disease may lie with a four-protein complex that regulates the cleavage of two molecules spanning the cell membrane. The role of each protein is now being unveiled.

Proteins

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