Journal
NEURODEGENERATIVE DISEASES
Volume 13, Issue 2-3, Pages 163-165Publisher
KARGER
DOI: 10.1159/000355063
Keywords
Alzheimer's disease; Biomarkers; Cerebrospinal fluid; Neuroimaging; Maternal family history; Sleep disordered breathing; ApoE4, mechanisms
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Funding
- NCATS NIH HHS [UL1 TR000038] Funding Source: Medline
- NHLBI NIH HHS [HL118624-01, R01 HL118624, K24 HL109156] Funding Source: Medline
- NIA NIH HHS [R01 AG035137, RC2 AG036502, R01 AG012101, AG035137, P30 AG008051, R21 AG032554, R01 AG013616, AG036502, AG13616, AG032554, AG022374, AG008051, R01 AG022374, AG12101] Funding Source: Medline
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Background: The pathophysiological process of Alzheimer's disease (AD) begins many years before the emergence of clinical symptoms (preclinical AD). A hypothetical biomarker progression in the pathogenesis of AD has been suggested, beginning with the deposition of amyloid-beta (A beta) and followed by increases in neurofibrillary tangles, synaptic loss, hippocampal atrophy, and lastly, cognitive impairment. Objective: We explored the effect of several risk factors for AD on the pattern of AD biomarker expression in normal subjects. Methods: AD biomarker evidence was examined at baseline in 96 cognitively normal elderly subjects with none or at least one of the following: ApoE4+ allele, a maternal history of AD (mFHx), sleep-disordered breathing (SDB), and longitudinal evidence of decline to mild cognitive impairment or AD (decliners) at follow-up. Results: Decliners and ApoE4+ subjects presented with expected reduced cerebrospinal fluid A beta 42, elevated P-tau and T-tau. In addition, decliners had fluorodeoxyglucose positron emission tomography hypometabolism in the medial temporal lobe. Individuals with mFHx demonstrated no A beta 42 effect, but had elevations in P-tau and T-tau. SDB was found to be associated with elevated A beta 42, P-tau and T-tau, as well as with reduced medial temporal lobe glucose metabolic rates. Conclusion: Our results indicate a heterogeneous biomarker expression, suggesting diversity of AD pathways in at-risk presymptomatic subjects. (C) 2013 S. Karger AG, Basel
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