Abstract:
:Amyloid beta (Aβ) is implicated in Alzheimer's disease (AD) as an integral component of both neural toxicity and plaque formation. Brains of the longest-lived rodents, naked mole-rats (NMRs) approximately 32 years of age, had levels of Aβ similar to those of the 3xTg-AD mouse model of AD. Interestingly, there was no evidence of extracellular plaques, nor was there an age-related increase in Aβ levels in the individuals examined (2-20+ years). The NMR Aβ peptide showed greater homology to the human sequence than to the mouse sequence, differing by only 1 amino acid from the former. This subtle difference led to interspecies differences in aggregation propensity but not neurotoxicity; NMR Aβ was less prone to aggregation than human Aβ. Nevertheless, both NMR and human Aβ were equally toxic to mouse hippocampal neurons, suggesting that Aβ neurotoxicity and aggregation properties were not coupled. Understanding how NMRs acquire and tolerate high levels of Aβ with no plaque formation could provide useful insights into AD, and may elucidate protective mechanisms that delay AD progression.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Edrey YH,Medina DX,Gaczynska M,Osmulski PA,Oddo S,Caccamo A,Buffenstein Rdoi
10.1016/j.neurobiolaging.2013.03.032subject
Has Abstractpub_date
2013-10-01 00:00:00pages
2352-60issue
10eissn
0197-4580issn
1558-1497pii
S0197-4580(13)00151-6journal_volume
34pub_type
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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