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Plasma transferrin and hemopexin are associated with altered A beta uptake and cognitive decline in Alzheimer's disease pathology

Artikel i vetenskaplig tidskrift
Författare A. Ashraf
Nicholas J. Ashton
P. Chatterjee
K. Goozee
K. K. Shen
J. Fripp
D. Ames
C. Rowe
C. L. Masters
V. Villemagne
A. Hye
R. N. Martins
P. W. So
Publicerad i Alzheimers Research & Therapy
Volym 12
Nummer/häfte 1
ISSN 1758-9193
Publiceringsår 2020
Publicerad vid Wallenberglaboratoriet
Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Språk en
Länkar dx.doi.org/10.1186/s13195-020-00634...
Ämnesord Alzheimer's disease, Cognitively normal, Cognitive impairment, Heme, Hemoglobin, Iron, Mild cognitive impairment, Proteomics, Transferrin, amyloid-beta, cerebrospinal-fluid, hemoglobin alpha, iron homeostasis, heme, expression, neurons, peptides, tau, identification, Neurosciences & Neurology
Ämneskategorier Neurovetenskaper

Sammanfattning

Background Heme and iron homeostasis is perturbed in Alzheimer's disease (AD); therefore, the aim of the study was to examine the levels and association of heme with iron-binding plasma proteins in cognitively normal (CN), mild cognitive impairment (MCI), and AD individuals from the Australian Imaging, Biomarker and Lifestyle Flagship Study of Ageing (AIBL) and Kerr Anglican Retirement Village Initiative in Ageing Health (KARVIAH) cohorts. Methods Non-targeted proteomic analysis by high-resolution mass spectrometry was performed to quantify relative protein abundances in plasma samples from 144 CN individuals from the AIBL and 94 CN from KARVIAH cohorts and 21 MCI and 25 AD from AIBL cohort. ANCOVA models were utilized to assess the differences in plasma proteins implicated in heme/iron metabolism, while multiple regression modeling (and partial correlation) was performed to examine the association between heme and iron proteins, structural neuroimaging, and cognitive measures. Results Of the plasma proteins implicated in iron and heme metabolism, hemoglobin subunit beta (p = 0.001) was significantly increased in AD compared to CN individuals. Multiple regression modeling adjusted for age, sex, APOE epsilon 4 genotype, and disease status in the AIBL cohort revealed lower levels of transferrin but higher levels of hemopexin associated with augmented brain amyloid deposition. Meanwhile, transferrin was positively associated with hippocampal volume and MMSE performance, and hemopexin was negatively associated with CDR scores. Partial correlation analysis revealed lack of significant associations between heme/iron proteins in the CN individuals progressing to cognitive impairment. Conclusions In conclusion, heme and iron dyshomeostasis appears to be a feature of AD. The causal relationship between heme/iron metabolism and AD warrants further investigation.

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