Synapse impairment associated with enhanced apoptosis in post‐traumatic stress disorder

Xinzhao, Chen; Jiang, Yi-Fan; Wang, Jiayu; Liu, Yishu; Xiao, Menglei; Song, Congshan; Bai, Yu; Han, Nancy Yinuo; Han, Fang

doi:10.1002/syn.22134

Cited by 21 publications

(12 citation statements)

References 66 publications

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“…For example, LLD may be associated with reduced synaptic density 49 . Chronic stress, as in LLD, may lead to reduced spine density in the limbic system 50 , a central region for emotional regulation. Possibly, synaptic dysfunction in the hippocampus contributes to both affective and cognitive symptoms in depression 49 , which would be compatible with poorer memory in our LLD groups.…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal fluid markers for synaptic function and Alzheimer type changes in late life depression

Siafarikas

Kirsebom

Srivastava

et al. 2021

Sci Rep

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To explore markers for synaptic function and Alzheimer disease (AD) pathology in late life depression (LLD), predementia AD and normal controls (NC). A cross-sectional study to compare cerebrospinal fluid (CSF) levels of neurogranin (Ng), Beta-site amyloid-precursor-protein cleaving enzyme1 (BACE1), Ng/BACE1 ratio and Amyloid-β 42/40 ratio, phosphorylated-tau and total-tau in LLD with (LLD AD) or without (LLD NoAD) AD pathology, predementia AD and normal controls (NC). We included 145 participants (NC = 41; predementia AD = 66 and LLD = 38). LLD comprised LLD AD (n = 16), LLD NoAD (n = 19), LLD with non-AD typical changes (n = 3, excluded). LLD AD (pADJ < 0.05) and predementia AD (pADJ < 0.0001) showed significantly higher Ng than NC. BACE1 and Ng/BACE1 ratio were altered similarly. Compared to LLD NoAD, LLD AD showed significantly higher Ng (pADJ < 0.001), BACE1 (pADJ < 0.05) and Ng/BACE1 ratio (pADJ < 0.01). All groups had significantly lower Aβ 42/40 ratio than NC (predementia AD and LLD AD, p < 0.0001; LLD NoAD, p < 0.05). Both LLD groups performed similarly on tests of memory and executive function, but significantly poorer than NC. Synaptic function in LLD depended on AD pathology. LLD showed an association to Amyloid dysmetabolism. The LLD groups performed poorer cognitively than NC. LLD AD may be conceptualized as “predementia AD with depression”.

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Section: Discussionmentioning

confidence: 99%

Cerebrospinal fluid markers for synaptic function and Alzheimer type changes in late life depression

Siafarikas

Kirsebom

Srivastava

et al. 2021

Sci Rep

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“…Apoptosis involves the activation, expression and regulation of a series of genes and it differs from cell necrosis in morphology and biochemistry. The caspase family is a cysteine protease system with a specific aspartic cysteine that is a key player in apoptosis ( 17 , 18 ). To date, ≥14 caspase members have been implicated in apoptosis in mammals.…”

Section: Discussionmentioning

confidence: 99%

A steroid‑induced osteonecrosis model established using an organ‑on‑a‑chip platform

Liu

Sun

et al. 2021

Exp Ther Med

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Bone microvascular endothelial cells (BMECs) constitute the central part of the femoral head's intramural microenvironment network and have an essential role in the development of steroid-induced osteonecrosis of the femoral head. Recently, the rapid development of microfluidic technology has led to innovations in the fields of chemistry, medicine and life sciences. It is now possible to use microfluidics organ-on-a-chip techniques to assess osteonecrosis. In the present study, BMECs were cultured on a microfluidic organ-on-a-chip platform to explore the pathogenesis of femoral-head necrosis. The aim of the present study was to explore the effects of different interventions on BMECs and study the pathogenesis of steroid-induced osteonecrosis through a microfluidic organ-on-a-chip platform. Methods including SU-8 lithography were used to produce a microfluidic organ-on-a-chip and human umbilical vein endothelial cells (HUVECs) were used to test whether it was possible to culture cells on the chip. Subsequently, a set of methods were applied for the isolation, purification, culture and identification of BMECs. Hydroxyapatite (HA) was used for co-culture, dexamethasone was used at different concentrations as an intervention in the cells and icariin was used for protection. BMECs were isolated and cultured from the femoral head obtained following total hip arthroplasty and were then inoculated into the microfluidic organ-on-a-chip for further treatment. In part I of the experiment, HUVECs and BMECs both successfully survived on the chip and a comparison of the growth and morphology was performed. HA and BMECs were then co-cultured for comparison with the control group. The cell growth was observed by confocal microscopy after 24 h. In part II, the effects of different concentrations of glucocorticoid (0.4 or 0.6 mg/ml dexamethasone) and the protection of icariin were evaluated. The morphology of BMECs and the cleaved caspase-3/7 content were observed by immunofluorescence staining and confocal microscopy after 24 h. In the microfluidic organ-on-a-chip, the response of the cells was able to be accurately observed. In part I, at the same concentration of injected cells, BMECs exhibited improved viability compared with HUVECs (P<0.05). In addition, it was indicated that HA was not only able to promote the germination and growth of BMECs but also improve the survival of the cells (P<0.05). In part II, it was identified that dexamethasone was able to induce BMECs to produce cleaved caspase 3/7; the caspase 3/7 content was significantly higher than that in the blank control group (P<0.05) and a dose correlation was observed. Icariin was able to inhibit this process and protect the microvascular structure of BMECs. The content of cleaved caspase 3/7 in the icariin-protected group was significantly lower than that in the group without icariin (P<0.05). It was concluded that BMECs are more likely to survive than HUVECs and HA promoted the growth of BMECs on the microfluidic organ-on-a-chip platform. Glucocorticoid caused dama...

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“…Rats with experience of control over a stressor show increased dendritic spines within PL [ 47 ]. As discussed, experimental stressful experiences used to reproduce dysfunctional phenotypes in animal models foster increased structural neuroplasticity in striatal/limbic targets but reduced plasticity in PL [ 48 , 49 , 50 , 88 ] and the PL-DMS circuit is disrupted by the experience of these stressors [ 89 ]. Structural plasticity in the adult brain relies on the experience-dependent proliferation and pruning of dendritic spines within specific networks, leading to reorganization of connectivity between neuronal populations.…”

Section: Dopaminementioning

confidence: 99%

Role of Stress-Related Dopamine Transmission in Building and Maintaining a Protective Cognitive Reserve

2022

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This short review presents the hypothesis that stress-dependent dopamine (DA) transmission contributes to developing and maintaining the brain network supporting a cognitive reserve. Research has shown that people with a greater cognitive reserve are better able to avoid symptoms of degenerative brain changes. The paper will review evidence that: (1) successful adaptation to stressors involves development and stabilization of effective but flexible coping strategies; (2) this process requires dynamic reorganization of functional networks in the adult brain; (3) DA transmission is amongst the principal mediators of this process; (4) age- and disease-dependent cognitive impairment is associated with dysfunctional connectivity both between and within these same networks as well as with reduced DA transmission.

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Synapse impairment associated with enhanced apoptosis in post‐traumatic stress disorder

Cited by 21 publications

References 66 publications

Cerebrospinal fluid markers for synaptic function and Alzheimer type changes in late life depression

Cerebrospinal fluid markers for synaptic function and Alzheimer type changes in late life depression

A steroid‑induced osteonecrosis model established using an organ‑on‑a‑chip platform

Role of Stress-Related Dopamine Transmission in Building and Maintaining a Protective Cognitive Reserve

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