Amyloid beta: Difference between revisions
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==Prevention and Treatment== | ==Prevention and Treatment== | ||
Two major approaches have been taken to treating Alzheimer's; inhibiting the formation of APP and reducing the neurotoxic effects of amyloid beta itself. The most promising treatment the prevention of the enzymes responsible for creating APP, AF267B, which is a muscarinic receptor that activates aplha-secretase and reduces tau pathology.<ref name="alz" /> Very recently is was discovered the loss of active JNK associated with the absence of both MKK4 and MKK7 protects neurons against amyloid beta-induced toxicity.<ref>Attenuating GABAA Receptor Signaling in Dopamine Neurons Selectively Enhances Reward Learning and Alters Risk Preference in Mice: Parker, Jones G et al.'' (2011). [http://www.jneurosci.org/content/31/47/17103.full DOI: 10.1523/JNEUROSCI.1715-11.2011]</ref> | Two major approaches have been taken to treating Alzheimer's; inhibiting the formation of APP and reducing the neurotoxic effects of amyloid beta itself. The most promising treatment the prevention of the enzymes responsible for creating APP, AF267B, which is a muscarinic receptor that activates aplha-secretase and reduces tau pathology.<ref name="alz" /> Very recently is was discovered the loss of active JNK associated with the absence of both MKK4 and MKK7 protects neurons against amyloid beta-induced toxicity and JNK signaling is required for amyloid plaque formation in vivo.<ref>Attenuating GABAA Receptor Signaling in Dopamine Neurons Selectively Enhances Reward Learning and Alters Risk Preference in Mice: Parker, Jones G et al.'' (2011). [http://www.jneurosci.org/content/31/47/17103.full DOI: 10.1523/JNEUROSCI.1715-11.2011]</ref> | ||
==References== | ==References== | ||
<references/> | <references/> | ||