Amyloid beta: Difference between revisions
From Proteopedia
Jump to navigationJump to search
Laura Olney (talk | contribs) No edit summary |
Laura Olney (talk | contribs) No edit summary |
||
| Line 16: | Line 16: | ||
==Neurotoxicity== | ==Neurotoxicity== | ||
'''Generation of Radicals''' | '''Generation of Radicals''' | ||
Amyloid beta produces reactive oxygen species, which induces oxidative stress and inflammation.<ref name="alz" /> | Amyloid beta produces reactive oxygen species, which induces oxidative stress and inflammation.<ref name="alz" /> | ||
'''Pore Formation''' | '''Pore Formation''' | ||
Amyloid beta can adhere to endothelial cell walls and create lesions, eventually a large deposite will cause cerrbral hemorrhage. The pores cause loss of calcium homeostasis and an influx of Ca2+ into neurons.<ref name="alz" /> | Amyloid beta can adhere to endothelial cell walls and create lesions, eventually a large deposite will cause cerrbral hemorrhage. The pores cause loss of calcium homeostasis and an influx of Ca2+ into neurons.<ref name="alz" /> | ||
'''Interaction with tau''' | '''Interaction with tau''' | ||
Tau proteins function to stabilize microtubules [[http://en.wikipedia.org/wiki/Tau_protein]]. Association between Tau proteins and amyloid beta results in dissociation of tau from microtubules which collapses the axonal structure leading to the death of neurons.<ref name="alz" /> | Tau proteins function to stabilize microtubules [[http://en.wikipedia.org/wiki/Tau_protein]]. Association between Tau proteins and amyloid beta results in dissociation of tau from microtubules which collapses the axonal structure leading to the death of neurons.<ref name="alz" /> | ||
'''Binding ApoE''' | '''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 Alzheimers. 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 Alzheimers. 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" /> | ||
'''Binding ABAD''' | '''Binding ABAD''' | ||
Amyloid beta-peptide binding alcohol dehydrogenase (ABAD) is an enzyme belonging to a family of short chain dehyndrogenase/reductases.. When amyloid beta binds to ABAD in the mitochondria there is increased mitochondiral disfunction, increased reactive oxygen species and oxidative stress.<ref name="alz" /> It has been found that by inhibiting amyloid beta from binding ADAB, using a decoy peptide, oxygen consumption is increased and the toxic effect are decreased. <ref>Inhibition of Amyloid-beta (A beta) peptide-binding alcohol dehydrogenase-A beta interaction reduces A beta accumulation and improves mitochondrial function in a mouse model of Alzheimer's disease: Yao, Jen et al.'' (2006). [http://dx.doi.org/10.1523/JNEUROSCI.4717-10.2011]</ref> | |||
Amyloid beta-peptide binding alcohol dehydrogenase (ABAD) is an enzyme belonging to a family of short chain dehyndrogenase/reductases.<ref>Amyloid β-Peptide-binding Alcohol Dehydrogenase Is a Component of the Cellular Response to Nutritional Stress: Yan, Shi Du et al.'' (2000). [http://www.jbc.org/content/275/35/27100.full DOI: 10.1074/jbc.M000055200]</ref> When amyloid beta binds to ABAD in the mitochondria there is increased mitochondiral disfunction, increased reactive oxygen species and oxidative stress.<ref name="alz" /> It has been found that by inhibiting amyloid beta from binding ADAB, using a decoy peptide, oxygen consumption is increased and the toxic effect are decreased. <ref>Inhibition of Amyloid-beta (A beta) peptide-binding alcohol dehydrogenase-A beta interaction reduces A beta accumulation and improves mitochondrial function in a mouse model of Alzheimer's disease: Yao, Jen et al.'' (2006). [http://dx.doi.org/10.1523/JNEUROSCI.4717-10.2011]</ref> | |||
'''Binding Catalase''' | '''Binding Catalase''' | ||
