Amyloid beta: Difference between revisions

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==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 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> Some potential targets for treatment include inhibiting beta sheet formation, creating molecules with high affinity for the self recognition region to prevent oligomerization, and tau pathology.

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 it 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> Some potential targets for treatment include inhibiting beta sheet formation, creating molecules with high affinity for the self recognition region to prevent oligomerization, and tau pathology.

==References==

Amyloid beta: Difference between revisions

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 ==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 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> Some potential targets for treatment include inhibiting beta sheet formation, creating molecules with high affinity for the self recognition region to prevent oligomerization, and tau pathology.
+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 it 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> Some potential targets for treatment include inhibiting beta sheet formation, creating molecules with high affinity for the self recognition region to prevent oligomerization, and tau pathology.
 ==References==
 <references/>