BIOM30002 Lecture Notes - Lecture 34: Amyloid Beta, Slc1A2, Astrocyte
Document Summary
34: may 26 - molecular pathogenesis of alzheimer"s disease ii. App(cid:396)oa(cid:272)hes to u(cid:374)de(cid:396)sta(cid:374)di(cid:374)g the (cid:373)ole(cid:272)ula(cid:396) a(cid:374)d (cid:272)ellula(cid:396) (cid:271)iolog(cid:455) of alzhei(cid:373)e(cid:396)(cid:859)s disease. Some of the receptors the amyloid peptide interacts with. Pathways leading to neural dysfunction and memory loss in ad. Synaptic changes are critical for memory loss in ad. Mechanisms of synaptic impairment and/or neuronal cell dysfunction and death in ad brain: Accumulation of a peptide neurotoxicity is believed to be the most likely initiating factor in synaptic/neuronal dysfunction and death (amyloid cascade hypothesis) There are many alternative hypotheses, however these have not yet had the rigorous scientific support of the amyloid hypothesis. Oligomeric forms and possibly protofibrils derived from amyloid beta peptide are most toxic to neurons. Neurons treated with amyloid lose connections and die. Amyloid plaques feed amyloid back into toxic pathway. May occur outside cells so that ros damage cells from outside. Indirect oxidative stress e. g. through nmda type glutamate receptor modulation.
