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Preclinical amyloid pathology biomarker positivity: effects on tau pathology and neurodegeneration
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- Höglund, Kina, 1976 (author)
- Gothenburg University,Göteborgs universitet,Centrum för åldrande och hälsa (AgeCap),Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Centre for Ageing and Health (Agecap),Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
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- Kern, Silke (author)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Centrum för åldrande och hälsa (AgeCap),Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry,Centre for Ageing and Health (Agecap)
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- Zettergren, Anna, 1978 (author)
- Gothenburg University,Göteborgs universitet,Centrum för åldrande och hälsa (AgeCap),Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Centre for Ageing and Health (Agecap),Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
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- (creator_code:org_t)
- 2017-01-10
- 2017
- English.
- In: Translational Psychiatry. - : Springer Science and Business Media LLC. - 2158-3188. ; 7
- Journal article (peer-reviewed)
Abstract
Subject headings
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- 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.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Psykiatri (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Psychiatry (hsv//eng)
Keyword
- 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
Publication and Content Type
- ref (subject category)
- art (subject category)
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- University of Gothenburg
- Karolinska Institutet
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