Anaemia and cerebrospinal fluid biomarkers of Alzheimer’s pathology in cognitively normal elders: the CABLE study

Abstract Background Anaemia has been reported to be associated with cognitive decline and Alzheimer’s disease (AD), but the associations between anaemia and cerebrospinal fluid (CSF) AD biomarkers are still unknown. This study aimed to investigate the associations between anaemia and CSF AD biomarkers. Methods Participants were included from the Chinese Alzheimer’s Biomarker and LifestylE (CABLE) study. The associations of anaemia and its severity with CSF AD biomarkers including β-amyloid 1–42 (Aβ42), total tau (t-tau) and phosphorylated tau (p-tau) were analysed by multiple linear regression models. Adjusted for age, gender, educational levels, APOE ε4 alleles, comorbidities (history of coronary heart disease, history of stroke, hypertension, diabetes mellitus, dyslipidaemia) and glomerular filtration rate. Results A total of 646 cognitively normal older adults, consisting of 117 anaemia patients and 529 non-anaemia individuals, were included in this study. Anaemia patients had lower levels of CSF Aβ42 than individuals without anaemia (p = 0.035). Besides, participants with more severe anaemia had lower CSF Aβ42 levels (p = 0.045). No significant association of anaemia with CSF t-tau and p-tau levels was found. Conclusion Cross-sectionally, anaemia was associated with lower CSF Aβ42 levels. These findings consolidated the causal close relationship between anaemia and AD.

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Midlife Stress in Relation to Late-Life Cerebrospinal Fluid Biomarkers of Alzheimer’s Disease: A 25-Year Follow-Up Study

Dementia and Geriatric Cognitive Disorders ◽

10.1159/000490885 ◽

2018 ◽

Vol 46 (1-2) ◽

pp. 90-99 ◽

Cited By ~ 4

Author(s):

Lena Johansson ◽

Silke Kern ◽

Henrik Zetterberg ◽

Kaj Blennow ◽

Anne Börjesson-Hansson ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cerebrospinal Fluid ◽

Psychological Stress ◽

Late Life ◽

Csf Biomarkers ◽

Linear Regression Models ◽

Cerebrospinal Fluid Biomarkers ◽

T Tau

Background/Aims: Psychological stress has previously been associated with higher risk of developing late-life dementia, especially Alzheimer’s disease (AD). This study tested whether longstanding midlife stress is related to cerebrospinal fluid (CSF) biomarkers of late-life AD, such as tau protein and amyloid beta (Aβ). Methods: The study included 79 nondemented females from the Prospective Population Study of Women in Gothenburg, Sweden, who responded to a standardized stress question at baseline (mean age 49 years) and underwent a lumbar puncture at follow-up 25 years later. Multiple linear regression models analyzed the relationships between midlife psychological stress and late-life CSF measures of total tau (t-tau), phosphorylated tau (p-tau), Aβ40, and Aβ42. Results: Longstanding stress in midlife was associated with higher levels of CSF t-tau (β = 0.64, p = 0.01) and Aβ40 (β = 0.60, p = 0.02) in late life. No associations were found between midlife stress and levels of p-tau or Aβ42. Conclusion: The findings suggest that longstanding stress stimulates unspecific neurodegenerative processes, but not the core processes of AD, at least not in the early phase of the disease. The association with higher concentration of CSF t-tau may reflect neural degeneration and the association with higher Aβ40 may be an early sign of Aβ overproduction or cerebrovascular processes in the brain.

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History of cigarette smoking in cognitively-normal elders is associated with elevated cerebrospinal fluid biomarkers of oxidative stress

Drug and Alcohol Dependence ◽

10.1016/j.drugalcdep.2014.06.030 ◽

2014 ◽

Vol 142 ◽

pp. 262-268 ◽

Cited By ~ 16

Author(s):

Timothy C. Durazzo ◽

Niklas Mattsson ◽

Michael W. Weiner ◽

Magdalena Korecka ◽

John Q. Trojanowski ◽

...

Keyword(s):

Oxidative Stress ◽

Cerebrospinal Fluid ◽

Cigarette Smoking ◽

Cognitively Normal ◽

Cerebrospinal Fluid Biomarkers ◽

History Of ◽

Biomarkers Of Oxidative Stress

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Evidence that iron accelerates Alzheimer’s pathology: a CSF biomarker study

Journal of Neurology Neurosurgery & Psychiatry ◽

10.1136/jnnp-2017-316551 ◽

2017 ◽

Vol 89 (5) ◽

pp. 456-460 ◽

Cited By ~ 26

Author(s):

Scott Ayton ◽

Ibrahima Diouf ◽

Ashley Ian Bush

Keyword(s):

Disease Process ◽

Threshold Value ◽

Simulation Modelling ◽

Longitudinal Changes ◽

Accelerated Depreciation ◽

History Of ◽

Amyloid Aβ ◽

Β Amyloid ◽

Using Data ◽

Alzheimer’S Pathology

ObjectiveTo investigate whether cerebrospinal fluid (CSF) ferritin (reporting brain iron) is associated with longitudinal changes in CSF β-amyloid (Aβ) and tau.MethodsMixed-effects models of CSF Aβ1-42 and tau were constructed using data from 296 participants who had baseline measurement of CSF ferritin and annual measurement of CSF tau and Aβ1-42 for up to 5 years.ResultsIn subjects with biomarker-confirmed Alzheimer’s pathology, high CSF ferritin (>6.2 ng/mL) was associated with accelerated depreciation of CSF Aβ1-42 (reporting increased plaque formation; p=0.0001). CSF ferritin was neither associated with changes in CSF tau in the same subjects, nor longitudinal changes in CSF tau or Aβ1-42 in subjects with low baseline pathology. In simulation modelling of the natural history of Aβ deposition, which we estimated to occur over 31.4 years, we predicted that it would take 12.6 years to reach the pathology threshold value of CSF Aβ from healthy normal levels, and this interval is not affected by CSF ferritin. CSF ferritin influences the fall in CSF Aβ over the next phase, where high CSF ferritin accelerated the transition from threshold preclinical Aβ levels to the average level of Alzheimer’s subjects from 18.8 to 10.8 years.ConclusionsIron might facilitate Aβ deposition in Alzheimer’s and accelerate the disease process.

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Association of serum Apolipoprotein B with cerebrospinal fluid biomarkers of Alzheimer’s pathology

Annals of Clinical and Translational Neurology ◽

10.1002/acn3.51153 ◽

2020 ◽

Vol 7 (10) ◽

pp. 1766-1778

Author(s):

Hao Hu ◽

Lan Tan ◽

Yan‐Lin Bi ◽

Wei Xu ◽

Lin Tan ◽

...

Keyword(s):

Cerebrospinal Fluid ◽

Apolipoprotein B ◽

Cerebrospinal Fluid Biomarkers ◽

Alzheimer’S Pathology

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Cerebrospinal fluid biomarkers of β-amyloid metabolism and neuronal damage in epileptic seizures

European Journal of Neurology ◽

10.1111/ene.12336 ◽

2013 ◽

Vol 21 (3) ◽

pp. 486-491 ◽

Cited By ~ 9

Author(s):

P. Shahim ◽

R. Rejdak ◽

P. Ksiazek ◽

K. Blennow ◽

H. Zetterberg ◽

...

Keyword(s):

Cerebrospinal Fluid ◽

Neuronal Damage ◽

Epileptic Seizures ◽

Cerebrospinal Fluid Biomarkers ◽

Amyloid Metabolism ◽

Β Amyloid

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Cerebrospinal Fluid Biomarkers for Dementia with Lewy Bodies

International Journal of Alzheimer s Disease ◽

10.4061/2010/536538 ◽

2010 ◽

Vol 2010 ◽

pp. 1-17 ◽

Cited By ~ 7

Author(s):

Elizabeta B. Mukaetova-Ladinska ◽

Rachael Monteith ◽

Elaine K. Perry

Keyword(s):

Cerebrospinal Fluid ◽

Dementia With Lewy Bodies ◽

Lewy Bodies ◽

Low Frequency ◽

Csf Biomarkers ◽

Term Care ◽

Clinical Criteria ◽

Cerebrospinal Fluid Biomarkers ◽

The Uk ◽

T Tau

More than 750,000 of the UK population suffer from some form of cognitive impairment and dementia. Of these, 5–20% will have Dementia with Lewy Bodies (DLB). Clinico-pathological studies have shown that it is the low frequency of DLB clinical core features that makes the DLB diagnosis hardly recognisable during life, and easily misdiagnosed for other forms of dementia. This has an impact on the treatment and long-term care of the affected subjects. Having a biochemical test, based on quantification of a specific DLB biomarker within Cerebrospinal Fluid (CSF) could be an effective diagnostic method to improve the differential diagnosis. Although some of the investigated DLB CSF biomarkers are well within the clinical criteria for sensitivity and specificity (90%), they all seem to be confounded by the contradictory data for each of the major groups of biomarkers (-synuclein, tau and amyloid proteins). However, a combination of CSF measures appear to emerge, that may well be able to differentiate DLB from other dementias: -synuclein reduction in early DLB, a correlation between CSF -synuclein and A42 measures (characteristic for DLB only), and t-tau and p-tau181 profile (differentiating AD from DLB).

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