Amyloid beta: Difference between revisions

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'''Binding ApoE'''

Apolipoprotein E is normally involved in lipoprotein metabolism and transfer but it has been shown to play a role in the development of Alzheimer's. ApoE4 has the most affinity for amyloid beta and uses the low-density lipoprotein-related protein receptor to internalize amyloid beta into neurons it also promotes the production od amyloid beta by stimulating APP recycling. It is also theorized that apolipoproteins promote the aggregation of amyloid beta into toxic oligomers.<ref name="alz" />

Apolipoprotein E is normally involved in lipoprotein metabolism and transfer but it has been shown to play a role in the development of Alzheimer's. ApoE4 has the most affinity for amyloid beta and uses the low-density lipoprotein-related protein receptor to internalize amyloid beta into neurons. It also promotes the production of amyloid beta by stimulating APP recycling. It is also theorized that apolipoproteins promote the aggregation of amyloid beta into toxic oligomers.<ref name="alz" />

'''Binding ABAD'''

Line 37:

'''Binding Catalase'''

Catalase normally functions to convert hydrogen peroxide to hydrogen and water. If amyloid beta complexes with catalase at residues 31-35 ~~catalase~~ can no longer breakdown the toxic molecule. Is it thought that the inactivation of catalase is due to the insertion of the sulfur side chain of methionine into the catalytic site.<ref name="alz" />

Catalase normally functions to convert hydrogen peroxide to hydrogen and water. If amyloid beta complexes with catalase at residues 31-35 it can no longer breakdown the toxic molecule. Is it thought that the inactivation of catalase is due to the insertion of the sulfur side chain of methionine into the catalytic site.<ref name="alz" />

==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> 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>.

Only preliminary studies have begun on the prevention of Alzheimer's. 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. By taking anti-inflammatory drugs, it is thought that patients with arthritis may decrease/prevent brain inflammation which may prevent some of the stress that leads to 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 in midlife with raised systolic blood pressure and high serum cholesterol concentration, and in particular the combination of these risks, 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 is the prevention of the enzymes responsible for creating APP, AF267B. This is a muscarinic receptor that activates alpha-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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@@ Line 29: / Line 29: @@
 '''Binding ApoE'''
-Apolipoprotein E is normally involved in lipoprotein metabolism and transfer but it has been shown to play a role in the development of Alzheimer's. ApoE4 has the most affinity for amyloid beta and uses the low-density lipoprotein-related protein receptor to internalize amyloid beta into neurons it also promotes the production od amyloid beta by stimulating APP recycling. It is also theorized that apolipoproteins promote the aggregation of amyloid beta into toxic oligomers.<ref name="alz" />
+Apolipoprotein E is normally involved in lipoprotein metabolism and transfer but it has been shown to play a role in the development of Alzheimer's. ApoE4 has the most affinity for amyloid beta and uses the low-density lipoprotein-related protein receptor to internalize amyloid beta into neurons. It also promotes the production of amyloid beta by stimulating APP recycling. It is also theorized that apolipoproteins promote the aggregation of amyloid beta into toxic oligomers.<ref name="alz" />
 '''Binding ABAD'''
@@ Line 37: / Line 37: @@
 '''Binding Catalase'''
-Catalase normally functions to convert hydrogen peroxide to hydrogen and water. If amyloid beta complexes with catalase at residues 31-35 catalase can no longer breakdown the toxic molecule. Is it thought that the inactivation of catalase is due to the insertion of the sulfur side chain of methionine into the catalytic site.<ref name="alz" />
+Catalase normally functions to convert hydrogen peroxide to hydrogen and water. If amyloid beta complexes with catalase at residues 31-35 it can no longer breakdown the toxic molecule. Is it thought that the inactivation of catalase is due to the insertion of the sulfur side chain of methionine into the catalytic site.<ref name="alz" />
 ==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> 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>.
+Only preliminary studies have begun on the prevention of Alzheimer's. 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. By taking anti-inflammatory drugs, it is thought that patients with arthritis may decrease/prevent brain inflammation which may prevent some of the stress that leads to 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 in midlife with raised systolic blood pressure and high serum cholesterol concentration, and in particular the combination of these risks, 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 is the prevention of the enzymes responsible for creating APP, AF267B. This is a muscarinic receptor that activates alpha-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/>