Brain ureido degenerative protein modifications are associated with neuroinflammation and proteinopathy in Alzheimer’s disease with cerebrovascular disease

Gallart‐Palau, Xavier; Serra, Aida; Lee, Benjamin Sian Teck; Xue, Guangpu; Sze, Siu Kwan

doi:10.1186/s12974-017-0946-y

Cited by 40 publications

(31 citation statements)

References 81 publications

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“…Brain tissues (approximately 40 mg/group) including the white matter from BCAS and sham animals were retained for molecular analysis . Details of the proteomic analysis using the TMT6‐based LC‐MS/MS are provided in Supporting Information.…”

Section: Methodsmentioning

confidence: 99%

Carotid artery disease in post‐stroke survivors and effects of enriched environment on stroke pathology in a mouse model of carotid artery stenosis

Hase

Polvikoski

Ihara

et al. 2019

Neuropathology Appl Neurobio

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2019) Neuropathology and Applied Neurobiology 45, 681-697 Carotid artery disease in post-stroke survivors and effects of enriched environment on stroke pathology in a mouse model of carotid artery stenosisAims: Carotid artery disease (CAD) is an important risk factor for stroke. We first evaluated CAD and stroke pathology in elderly post-stroke survivors. To simulate CAD, we assessed long-term consequences of bilateral common carotid artery stenosis (BCAS) in mice and exposed them to environmental enrichment (EE). Methods: Histopathological methods were used to determine degrees of CAD (% area stenosis), brain infarct types, sizes and distribution in post-stroke survivors and BCAS mice. Adult male C57BL/6J mice after BCAS or sham surgery were randomly assigned to standard housing (Std) or limited (3 h) or full-time (Full) exposure to EE per day for 12 weeks. Results: High frequencies of moderate carotid artery stenosis (51-75%) were evident in post-stroke survivors whereas those with severe CAD (>75% stenosis) exhibited greater numbers of cortical rather than subcortical infarcts and, were at higher risk of developing dementia. BCAS in mice reduced cerebral blood flow by 52% (P < 0.01) and thickened carotid artery walls, regardless of EE duration. Remarkably, the total and cortical infarcts declined by >50% in BCAS mice exposed to EE compared with BCAS-Std (P < 0.01). Frontal lobe and cortical strokes were associated with worsening working memory tested in a radial maze paradigm. Proteomic analysis revealed EE, both BCAS-3 h and BCAS-Full attenuated coagulation cascade factors including fibrinogen and von Willebrand factor, markers of blood-brain barrier damage. Conclusion: Small cortical and subcortical infarcts were evident in both poststroke survivors with CAD and BCAS mice. Experimental evidence suggested that moderate exposure to EE is sufficient to reduce subsequent stroke lesions.

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Section: Methodsmentioning

confidence: 99%

Carotid artery disease in post‐stroke survivors and effects of enriched environment on stroke pathology in a mouse model of carotid artery stenosis

Hase

Polvikoski

Ihara

et al. 2019

Neuropathology Appl Neurobio

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“…Последние исследования показывают значительный вклад нейровоспаления в развитие психических и нейродегенеративных заболеваний, таких как болезнь Альцгеймера, Паркинсона, деменции и многих других [1][2][3][4][5][6]. При тяжелых соматических заболеваниях нередко развиваются различные психические расстройства: астенические, неврозоподобные состояния, депрессии, психозы.…”

Section: оригинальные статьи § введениеunclassified

Dynamics of brain CD68+ and stabilin-1+ macrophage infiltration in patients with myocardial infarction

et al. 2019

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Te aim of the study was to evaluate the temporal dynamics of brain CD68+ and stabilin-1+ macrophage infltration in patients with fatal myocardial infarction (MI) type 1.Materials and Methods. Te study included 31 patients with fatal MI type I. Te control group comprised 10 patients of 18–40 age group who died from injuries incompatible with life. Patients with MI were divided into two groups. Group 1 comprised patients who died during the frst 72 hours of MI, group 2 comprised patients who died on days 4‒28. Macrophage infltration in the brain was assessed by immunohistochemical analysis. We used CD68 as a marker for the cells of the macrophage lineage and stabilin-1 as an M2-like macrophage biomarker.Results. In group 1 the number of brain CD68+ macrophages was signifcantly higher than in the control group. In group 2 the intensity of brain CD68+ cells infltration was lower than in group 1 and higher than in the control group. Tere was a small amount of stabilin-1+ macrophages in the brain of healthy people, as well as of patients who died from MI. Tere were no signifcant diﬀerences in the number of stabilin-1+ cells between group 1 and group 2. Correlation analysis revealed the presence of positive correlation between the number of CD68 + macrophages in the infarct, peri-infarct, and non-infarct areas of the myocardium and the number of CD68+ macrophages in the brain in patients with MI. Tere were not correlations between the number of CD68 + and stabilin-1+ cells and the presence of diabetes mellitus, history of stroke, history of MI, and pre-infarction angina.Conclusion. Te number of brain CD68+ macrophages signifcantly increased during the frst three days of MI. Te number of brain stabilin-1+ macrophages did not increase and did not diﬀer from the control values. We observed a positive correlation between the number of CD68+ macrophages in the brain and myocardium.

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“…MBP is implicated in auto-immune responses within the human CNS, and is thought to be a target for T cell activity in multiple sclerosis and other demyelinating or degenerative disorders. Its reduction over an extended period is usually associated with glial inflammation activation and proliferation, leading to reactive astrocytosis [48,49].…”

Section: Consistent With the Upregulation Of Proteins Related To Neurmentioning

confidence: 99%

Proteomic Analysis of Mouse Brain Subjected to Spaceflight

Mao¹,

Sandberg²,

Gridley³

et al. 2018

Preprint

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There is evidence that spaceflight poses acute and late risks on the central nervous system. To explore possible mechanisms, the proteomic changes following spaceflight in mouse brain were characterized. Space Shuttle Atlantis (STS-135) was launched at the Kennedy Space Center on a 13-day mission. Within 3–5 hours after landing, brain tissue was collected to evaluate protein expression profiles using quantitative proteomic analysis. Our results showed that there were 26 proteins that were significantly altered after spaceflight in the grey and/or white matter. While there was no overlap between the white and grey matter in terms of individual proteins, there was overlap in terms of function, synaptic plasticity, vesical activity, protein/organelle transport, and metabolism. Our data demonstrate that exposure to the spaceflight environment induces significant changes in protein expression related to neuronal structure and metabolic function. This might lead to a significant impact on brain structural and functional integrity that could affect the outcome of space missions.

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Brain ureido degenerative protein modifications are associated with neuroinflammation and proteinopathy in Alzheimer’s disease with cerebrovascular disease

Cited by 40 publications

References 81 publications

Carotid artery disease in post‐stroke survivors and effects of enriched environment on stroke pathology in a mouse model of carotid artery stenosis

Carotid artery disease in post‐stroke survivors and effects of enriched environment on stroke pathology in a mouse model of carotid artery stenosis

Dynamics of brain CD68+ and stabilin-1+ macrophage infiltration in patients with myocardial infarction

Proteomic Analysis of Mouse Brain Subjected to Spaceflight

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