Amyloid beta: Difference between revisions
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==Prevention and Treatment== | ==Prevention and Treatment== | ||
Only preliminary studies have begun on the prevention of Alzheimer's, and thus no true prevention has been determined but potential forms of prevention and risk factors have been identified. One promising preventative measure has been anti-inflammatory drugs. It is thought that preventing brain inflammation may be protecting patients with arthritis and taking anti-inflammatory drugs from Alzheimer's disease.<ref name="inf">PMID: 8757015</ref> | Only preliminary studies have begun on the prevention of Alzheimer's, and thus no true prevention has been determined but potential forms of prevention and risk factors have been identified. One promising preventative measure has been anti-inflammatory drugs. It is thought that preventing brain inflammation may be protecting patients with arthritis and taking anti-inflammatory drugs from Alzheimer's disease.<ref name="inf">PMID: 8757015</ref> Major risk factors seem to center around diet and exercise. Both mental and physical exercise are likely to play a role in maintaining mental stability. For instance it has been shown that individuals with raised systolic blood pressure and high serum cholesterol concentration, and in particular the combination of these risks, in midlife increase the risk of Alzheimer's disease in later life<ref name="risk">PMID: 11408299</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 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. | 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. | ||
