ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2015
Altered expression of neurofilament 200 and amyloid-β peptide (1-40) in a rat model of chronic cerebral hypoperfusion.
Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Medical Histories of Control Subjects Influence the Biomarker Potential of Plasma Aβ in Alzheimer's Disease: a Meta-analysis.Journal of molecular neuroscience : MN · 2020Pooled it
- Arteriosclerosis in the heart-brain axis and Alzheimer's disease plasma markers in the Rotterdam Study.Journal of Alzheimer's disease : JAD · 2025Article
- Amyloid and tau pathology are associated with cerebral blood flow in a mixed sample of nondemented older adults with and without vascular risk factors for Alzheimer's disease.Neurobiology of aging · 2023Article
- Nicotinamide Improves Cognitive Function in Mice With Chronic Cerebral Hypoperfusion.Frontiers in neurology · 2021Article
- Progress of RAGE Molecular Imaging in Alzheimer's Disease.Frontiers in aging neuroscience · 2020Review
- Chronic Cerebral Hypoperfusion Promotes Amyloid-Beta Pathogenesis via Activating β/γ-Secretases.Neurochemical research · 2017Article
- Advances in clinical neurology through the journal "Neurological Sciences" (2015-2016).Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017Article
- Recombinant hNeuritin Promotes Structural and Functional Recovery of Sciatic Nerve Injury in Rats.Frontiers in neuroscience · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic cerebral hypoperfusion (CCH) is damaging to white matter in the brain. So far few studies have investigated long-term axonal damage following CCH. The aim of this study was to investigate the involvement of neurofilament 200 (NF200) and amyloid-β (1-40) [Aβ (1-40)] in the pathological mechanism for neuronal damage, and to quantify changes in their expression over time in a rat model of CCH. A rat model of CCH was established using partial bilateral ligation of the common carotid arteries. The extent of stenosis was verified by measuring the changes in cerebral blood flow after surgery. Histology was used to assess hippocampal neuronal pathology, and immunohistochemistry was used to quantify the expression of NF200 and Aβ (1-40) at 2, 4, and 12 weeks after surgery. The cerebral blood flow reduced to 33.89 ± 5.48 % at 2 weeks, 36.83 ± 4.63 % at 4 weeks and 51.44 ± 4.90 % at 12 weeks. Immunofluorescence staining of neuronal perikarya sections revealed a marked decrease in the population of surviving pyramidal cells in the hippocampal CA1 region, a significant up-regulation in the expression of Aβ (1-40), and a significant reduction in the expression of NF200 following CCH surgery. Moreover, this trend was increasingly obvious over time. Our data demonstrate that CCH leads to axonal damage over time. We also confirmed that the expression of Aβ (1-40) and NF200 may be useful biomarkers of axonal damage following CCH.
Indexed as
Identifiers
25452168What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.