ArticleCell stress & chaperones2013
Dynamics of endogenous Hsp70 synthesis in the brain of olfactory bulbectomized mice.
Article in Cell stress & chaperones, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
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- Heat shock proteins: Biological functions, pathological roles, and therapeutic opportunities.MedComm · 2022Review
- Impact of Heat Shock Proteins in Neurodegeneration: Possible Therapeutical Targets.Annals of neurosciences · 2022Review
- Mesenchymal stem cells as a potential therapeutic tool to cure cognitive impairment caused by neuroinflammation.World journal of stem cells · 2021Review
- Heat stress aggravates oxidative stress, apoptosis, and endoplasmic reticulum stress in the cerebellum of male C57 mice.Molecular biology reports · 2021Article
- Heat shock proteins: a history of study in Russia.Cell stress & chaperones · 2021Review
- Review
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- Ablation of olfactory bulb glutamatergic neurons induces depressive-like behaviors and sleep disturbances in mice.Psychopharmacology · 2020Article
- Immunization Against Specific Fragments of Neurotrophin p75 Receptor Protects Forebrain Cholinergic Neurons in the Olfactory Bulbectomized Mice.Journal of Alzheimer's disease : JAD · 2016Article
- Olfactory Deprivation Hastens Alzheimer-Like Pathologies in a Human Tau-Overexpressed Mouse Model via Activation of cdk5.Molecular neurobiology · 2016Article
- The brain compensatory mechanisms and Alzheimer's disease progression: a new protective strategy.Neural regeneration research · 2015Article
- The Y-Box Binding Protein 1 Suppresses Alzheimer's Disease Progression in Two Animal Models.PloS one · 2015Article
- The importance of the cellular stress response in the pathogenesis and treatment of type 2 diabetes.Cell stress & chaperones · 2014Article
Corrections and comments
- Erratum issuedMedvedinskaya, Natalia [corrected to Medvinskaya, Natalia]
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous epidemiological studies have established acute brain injury as one of the major risk factors for the Alzheimer's disease (AD). However, the lack of animal models of AD-like degeneration triggered by a defined injury hampered the development of adequate therapies. Here we report that the surgical damage of the olfactory bulbs triggers the development of several pathologies, including amyloid-β accumulation and strong decrease of neuron density in the cortex and hippocampus as well as significant disturbance of spatial memory. Characteristically, these harmful consequences of the olfactory bulbectomy (OBX) have a peculiar dynamics in time with maximal manifestation in periods of 1-1.5 months and 8 months after the surgery and, hence, exhibit biphasic pattern with almost complete recovery period taking place at 5-6 months after the operation. The quantitative determination of endogenous inducible form of Hsp70 in different brain areas of OBX mice demonstrated characteristic fluctuations of Hsp70 levels depending on the time after the operation and age of mice. Interestingly, maximal induction of Hsp70 synthesis in the hippocampus exhibits clear-cut coincidence with the recovery period in OBX animals. The observed correlation enables to suggest curing effect of Hsp70 synthesis at an earlier period of pathology development and establishes it as a possible therapeutic agent for secondary grave consequences of brain injury, such as AD-like degeneration, for which neuroprotective therapy is urgently needed.
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