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Preclinical amyloid pathology biomarker positivity: effects on tau pathology and neurodegeneration

Journal article
Authors Kina Höglund
Silke Kern
Anna Zettergren
Anne Börjesson-Hanson
Henrik Zetterberg
Ingmar Skoog
Kaj Blennow
Published in Translational Psychiatry
Volume 7
ISSN 2158-3188
Publication year 2017
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Centre for Ageing and Health (Agecap)
Language en
Keywords mild cognitive impairment, cerebrospinal-fluid levels, acid-binding, protein, apoe epsilon-4 allele, alzheimers-disease, a-beta, diagnostic-criteria, nondemented individuals, vascular dementia, apolipoprotein-e, Psychiatry, een b, 1993, zeitschrift fur gerontologie, v26, p163, lstein mf, 1975, journal of psychiatric research, v12, p189
Subject categories Psychiatry


Brain autopsy and biomarker studies indicate that the pathology of Alzheimer's disease (AD) is initiated at least 10-20 years before clinical symptoms. This provides a window of opportunity to initiate preventive treatment. However, this emphasizes the necessity for biomarkers that identify individuals at risk for developing AD later in life. In this cross-sectional study, originating from three epidemiologic studies in Sweden (n = 1428), the objective was to examine whether amyloid pathology, as determined by low cerebrospinal fluid (CSF) concentration of the 42 amino acid form of beta-amyloid (A beta 42), is associated with biomarker evidence of other pathological changes in cognitively healthy elderly. A total of 129 patients were included and CSF levels of A beta 42, total tau, tau phosphorylated at threonine 181 (p-tau), neurogranin, VILIP-1, VEGF, FABP3, A beta 40, neurofilament light, MBP, orexin A, BDNF and YKL-40 were measured. Among these healthy elderly, 35.6% (N=46) had CSF A beta 42 levels below 530 pg ml(-1). These individuals displayed significantly higher CSF concentrations of t-tau (P < 0.001), p-tau (181) (P < 0.001), neurogranin (P = 0.009) and FABP3 (P = 0.044) compared with amyloid-negative individuals. Our study indicates that there is a subpopulation among healthy older individuals who have amyloid pathology along with signs of ongoing neuronal and synaptic degeneration, as well as tangle pathology. Previous studies have demonstrated that increase in CSF tau and p-tau is a specific sign of AD progression that occurs downstream of the deposition of A beta. On the basis of this, our data suggest that these subjects are at risk for developing AD. We also confirm the association between APOE epsilon 4 and amyloid pathology in healthy older individuals.

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