Serum amyloid β protein in young and elderly depression: a pilot study

Kita, Yohei; Baba, Hajime; Maeshima, Hitoshi; Nakano, Yoshitaka; Suzuki, Tomohiko; Arai, Heii

doi:10.1111/j.1479-8301.2009.00293.x

Cited by 34 publications

(22 citation statements)

References 27 publications

(50 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mean age of LLMD subjects in this cohort was 73.8±8.5 years and the sample was comprised of homebound elderly with multiple concomitant chronic diseases. Additionally, the same difference in Aβ40/Aβ42 ratio was found in a cross-sectional study on 60 Japanese inpatient young and old depressed subjects [80], in which serum Aβ40 levels were significantly higher in young depressed patients compared to young controls (<60 years) and the Aβ40/Aβ42 ratio was significantly higher in both young and elderly depressed (≥60 years) patients compared to non-depressed controls (mean age of LLMD: 68.2±5.6 years), although the Hamilton Rating Scale for Depression (HAM-D)[81] score did not correlate by itself with Aβ40, Aβ42 levels or Aβ40/42 ratio. These findings were replicated on a larger sample of 193 inpatient young (<40 years), middle age (≥40 to <65) and old depressed subjects (≥65) and 413 controls.…”

Section: Resultssupporting

confidence: 65%

Soluble Amyloid-β . Levels and Late-Life Depression

Osorio¹,

Gumb²,

Pomara³

2014

CPD

View full text Add to dashboard Cite

Late-Life Major Depression (LLMD) is a complex heterogeneous disorder that has multiple pathophysiological mechanisms such as medical comorbidity, vascular-related factors and Alzheimer’s disease (AD). There is an association between LLMD and AD, with LLMD possibly being a risk factor for, or early symptom of AD and vascular dementia. Whether depression is an etiologic risk factor for dementia, or part of the dementia prodrome remains controversial. AD has a long prodromal period with the neuropathologic features of the disease preceding the onset of clinical symptoms by as much as 15–20 years. Clinicopathological studies have provided robust support for the importance of Aβ42 in the pathogenesis of AD, but several other risk factors have also been identified. Given the relationship between Aβ42 and AD, a potential relationship between Aβ42 and LLMD would improve the understanding of the association between LLMD and AD. We reviewed 15 studies that analyzed the relationship between soluble Aβ42 and LLMD. For studies looking at plasma and/or cerebrospinal fluid (CSF) levels of Aβ42, the relationship between LLMD and soluble Aβ42 was equivocal, with some studies finding elevated Aβ42 levels associated with LLMD and others finding the opposite, decreased levels of Aβ42 associated with LLMD. It may be that there is poor reliability in the diagnosis of depression in late life, or variability in the criteria and the scales used, or subtypes of depression in late life such as early vs. late onset depression, vascular-related depression, and preclinical/comorbid depression in AD. The different correlations associated with each of these factors would be causing the inconsistent results for soluble Aβ42 levels in LLMD, but it is also possible that these patterns derive from disease stage-dependent differences in the trajectory of CSF Aβ42 during older age, or changes in neuronal activity or the sleep/wake cycle produced by LLMD that influence Aβ42 dynamics.

show abstract

Section: Resultssupporting

confidence: 65%

Soluble Amyloid-β . Levels and Late-Life Depression

Osorio¹,

Gumb²,

Pomara³

2014

CPD

View full text Add to dashboard Cite

show abstract

“…Other studies evaluated the plasma levels of Aβ peptides. Most studies found a significant reduction of plasma Aβ 42 and increased Aβ 40 :Aβ 42 ratio in LLD; although non-significant results have also been reported (Sun et al , 2008; Baba et al , 2012; Benitez et al , 2009; Kita et al , 2009). …”

Section: Introductionmentioning

confidence: 96%

Plasma and cerebrospinal fluid amyloid-β levels in late-life depression: A systematic review and meta-analysis

Nascimento

Silva

Malloy-Diniz

et al. 2015

Journal of Psychiatric Research

View full text Add to dashboard Cite

This study aimed to evaluate differences in plasma and cerebrospinal fluid (CSF) levels of Aβ peptides in older adults with late-life depression compared to non-depressed older controls. We conducted a systematic review and meta-analysis of the literature using PubMed, Web of science and Scopus databases with no search limits for publication dates or languages. Two independent reviewers extracted data and assessed quality. Six hundred references were retrieved, and we included 12 studies in the meta-analysis after eligibility screening. Older adults with late-life depression (LLD) had a higher plasma Aβ40:Aβ42 ratio compared to non-depressed participants (SMD= 1.10, CI95% [0.28; 1.96], p=0.01), and marginally significant reduction of CSF Aβ42 levels (SMD= −1.12, CI95% [−2.47; 0.22], p=0.1). The present results evidence that older adults with depression have significant differences in Aβ metabolism, in the same direction observed in individuals with AD. These differences in the Aβ metabolism may help identify a subgroup of subjects with LLD at higher risk of developing AD.

show abstract

“…The plaques typically consist of 39–42 amino acid A fragments, and the plasma ratio of 42 and 40 amino acids long fragments (A42/A40) is suggested of being useful for identifying the risk of developing mild cognitive impairment and AD [2], [3]. Based on the classification of amino acids by Branden and Tooze [4], 25 amino acids out of the total 42 have hydrophobic side chains in A42.…”

Section: Introductionmentioning

confidence: 99%

Effects of Transmitters and Amyloid-Beta Peptide on Calcium Signals in Rat Cortical Astrocytes: Fura-2AM Measurements and Stochastic Model Simulations

Toivari

Manninen

Nahata³

et al. 2011

PLoS ONE

View full text Add to dashboard Cite

BackgroundTo better understand the complex molecular level interactions seen in the pathogenesis of Alzheimer's disease, the results of the wet-lab and clinical studies can be complemented by mathematical models. Astrocytes are known to become reactive in Alzheimer's disease and their ionic equilibrium can be disturbed by interaction of the released and accumulated transmitters, such as serotonin, and peptides, including amyloid- peptides (A). We have here studied the effects of small amounts of A25–35 fragments on the transmitter-induced calcium signals in astrocytes by Fura-2AM fluorescence measurements and running simulations of the detected calcium signals.Methodology/Principal FindingsIntracellular calcium signals were measured in cultured rat cortical astrocytes following additions of serotonin and glutamate, or either of these transmitters together with A25–35. A25–35 increased the number of astrocytes responding to glutamate and exceedingly increased the magnitude of the serotonin-induced calcium signals. In addition to A25–35-induced effects, the contribution of intracellular calcium stores to calcium signaling was tested. When using higher stimulus frequency, the subsequent calcium peaks after the initial peak were of lower amplitude. This may indicate inadequate filling of the intracellular calcium stores between the stimuli. In order to reproduce the experimental findings, a stochastic computational model was introduced. The model takes into account the major mechanisms known to be involved in calcium signaling in astrocytes. Model simulations confirm the principal experimental findings and show the variability typical for experimental measurements.Conclusions/SignificanceNanomolar A25–35 alone does not cause persistent change in the basal level of calcium in astrocytes. However, even small amounts of A25–35, together with transmitters, can have substantial synergistic effects on intracellular calcium signals. Computational modeling further helps in understanding the mechanisms associated with intracellular calcium oscillations. Modeling the mechanisms is important, as astrocytes have an essential role in regulating the neuronal microenvironment of the central nervous system.

show abstract

Serum amyloid β protein in young and elderly depression: a pilot study

Cited by 34 publications

References 27 publications

Soluble Amyloid-β . Levels and Late-Life Depression

Soluble Amyloid-β . Levels and Late-Life Depression

Plasma and cerebrospinal fluid amyloid-β levels in late-life depression: A systematic review and meta-analysis

Effects of Transmitters and Amyloid-Beta Peptide on Calcium Signals in Rat Cortical Astrocytes: Fura-2AM Measurements and Stochastic Model Simulations

Contact Info

Product

Resources

About

Serum amyloid β protein in young and elderly depression: a pilot study

Cited by 34 publications

References 27 publications

Soluble Amyloid-&#946; . Levels and Late-Life Depression

Soluble Amyloid-&#946; . Levels and Late-Life Depression

Plasma and cerebrospinal fluid amyloid-β levels in late-life depression: A systematic review and meta-analysis

Effects of Transmitters and Amyloid-Beta Peptide on Calcium Signals in Rat Cortical Astrocytes: Fura-2AM Measurements and Stochastic Model Simulations

Contact Info

Product

Resources

About

Soluble Amyloid-β . Levels and Late-Life Depression

Soluble Amyloid-β . Levels and Late-Life Depression