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10.3233/JAD-170585 http://scihub22266oqcxt.onion/10.3233/JAD-170585 C5869994!5869994!29036828     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Alzheimers+Dis ä ; 62 (3): 1403-16 Nephropedia Template TP {{tp|p=29036828|t=ä. Mitochondria and Mitochondrial Cascades in Alzheimer?s Disease |pdf=|usr=}}{{29036828}} gab.com Text Mitochondria and Mitochondrial Cascades in Alzheimer s Disease JO: J Alzheimers Dis http://www.kidney.de/pget.php?&tw=1&pmid=29036828 #FOAvip Decades of research indicate mitochondria from Alzheimer?s disease (AD) patients differ from those of non-AD individuals. Initial studies revealed structural differences, and subsequent studies showed functional deficits. Observations of structure and function changes prompted investigators to consider the consequences, significance, and causes of AD-related mitochondrial dysfunction. Currently, extensive research argues mitochondria may mediate, drive, or contribute to a variety of AD pathologies. The perceived significance of these mitochondrial changes continues to grow, and many currently believe AD mitochondrial dysfunction represents a reasonable therapeutic target. Debate continues over the origin of AD mitochondrial changes. Some argue amyloid-? (A?) induces AD mitochondrial dysfunction, a view that does not challenge the amyloid cascade hypothesis and that may in fact help explain that hypothesis. Alternatively, data indicate mitochondrial dysfunction exists independent of A?, potentially lies upstream of A? deposition, and suggest a primary mitochondrial cascade hypothesis that assumes mitochondrial pathology hierarchically supersedes A? pathology. Mitochondria, therefore, appear at least to mediate or possibly even initiate pathologic molecular cascades in AD. This review considers studies and data that inform this area of AD research. Twit Text FOAVip Mitochondria and Mitochondrial Cascades in Alzheimer s Disease ????J Alzheimers Dis http://www.kidney.de/pget.php?&tw=1&pmid=29036828 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29036828 #FOAvip English Wikipedia <ref>{{Cite pmid|29036828}}</ref> Mitochondria and Mitochondrial Cascades in Alzheimer?s Disease #MMPMID29036828 Swerdlow RH J Alzheimers Dis ä[]; 62 (3): 1403-16 PMID29036828show ga Decades of research indicate mitochondria from Alzheimer?s disease (AD) patients differ from those of non-AD individuals. Initial studies revealed structural differences, and subsequent studies showed functional deficits. Observations of structure and function changes prompted investigators to consider the consequences, significance, and causes of AD-related mitochondrial dysfunction. Currently, extensive research argues mitochondria may mediate, drive, or contribute to a variety of AD pathologies. The perceived significance of these mitochondrial changes continues to grow, and many currently believe AD mitochondrial dysfunction represents a reasonable therapeutic target. Debate continues over the origin of AD mitochondrial changes. Some argue amyloid-? (A?) induces AD mitochondrial dysfunction, a view that does not challenge the amyloid cascade hypothesis and that may in fact help explain that hypothesis. Alternatively, data indicate mitochondrial dysfunction exists independent of A?, potentially lies upstream of A? deposition, and suggest a primary mitochondrial cascade hypothesis that assumes mitochondrial pathology hierarchically supersedes A? pathology. Mitochondria, therefore, appear at least to mediate or possibly even initiate pathologic molecular cascades in AD. This review considers studies and data that inform this area of AD research. äMitochondria and Mitochondrial Cascades in Alzheimer?s Disease (epmc).pdf DeepDyve Pubget Overpricing