Glial connexin expression and function in the context of Alzheimer's disease.
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TL;DR: Recent data that suggest glial Cx channels participate in the neurodegenerative process of Alzheimer's disease are summarized and discussed.
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About: This article is published in Biochimica et Biophysica Acta. The article was published on 01 Aug 2012. and is currently open access. The article focuses on the topics: Gliosis & Neuroglia.
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Citations
Connexins and pannexins in Alzheimer's disease
TL;DR: Validation of the molecular mechanisms by which connexin and pannexin membrane channels influence neurodegeneration particularly in Alzheimer's disease could lead to new and alternative therapeutic strategies targeting these channels.
Differential alteration of hippocampal function and plasticity in females and males of the APPxPS1 mouse model of Alzheimer's disease.
TL;DR: It is reported that spatial memory is strongly affected in APPxPS1 females while remarkably spared in males, at all ages tested, and sex-dependent hippocampal alterations may provide causal explanation to APPx PS1 females' memory deficits.
Connexins Control Glial Inflammation in Various Neurological Diseases
Ryo Yamasaki
TL;DR: The fundamental roles of Cxs and their clinical implications in various neurological dysfunctions, including hereditary diseases, ischemic brain disorders, degenerative conditions, demyelinating disorders, and psychiatric illnesses are explored.
Turning microglia neuroprotective: Towards connexin43-specific therapy of Alzheimer’s disease
Yixun Su,Jin Li,Wei Zhang,Shi Tao,Li Wang,Mi Zhou,Yong Tang,Hui Chen,Alexei Verkhratsky,Zhengbao Zha,Jianqin Niu,Chenju Yi +11 more
- 08 Aug 2024
TL;DR: Researchers identified connexin 43 as a therapeutic target for Alzheimer's disease, as it controls microglial reactivity and influences β-amyloid pathology. A novel small molecule peptide, TAT-CX43@LNPs, selectively blocks Cx43 hemichannels, delaying and rescuing neuropathology and cognitive impairment in AD mice.
Gap junctions and hemichannels: communicating cell death in neurodevelopment and disease.
TL;DR: With the ever-increasing understanding of connexins in the brain, therapeutic strategies could be developed to target these membrane channels in various neurological disorders.
References
Alzheimer's Disease: Genes, Proteins, and Therapy
TL;DR: Evidence that the presenilin proteins, mutations in which cause the most aggressive form of inherited AD, lead to altered intramembranous cleavage of the beta-amyloid precursor protein by the protease called gamma-secretase has spurred progress toward novel therapeutics and provided discrete biochemical targets for drug screening and development.
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Inflammation and Alzheimer's disease.
Haruhiko Akiyama,Steven W. Barger,Scott R. Barnum,B Bradt,Jürgen Bauer,Greg M. Cole,Neil R. Cooper,Piet Eikelenboom,Mark R. Emmerling,Bernd L. Fiebich,Caleb E. Finch,Sally A. Frautschy,W. S. T. Griffin,Harald Hampel,Michael Hüll,Gary E. Landreth,Lih-Fen Lue,Robert E. Mrak,Ian R. A. Mackenzie,Patrick L. McGeer,M K O'Banion,Joel S. Pachter,Giulio Maria Pasinetti,C Plata-Salaman,Joseph G. Rogers,Russell E. Rydel,Yueyang Shen,Wolfgang J. Streit,Ronald Strohmeyer,I Tooyoma,F L van Muiswinkel,R. Veerhuis,David G. Walker,Scott D. Webster,Beatrice Hauss–Wegrzyniak,Gary L. Wenk,Tony Wyss-Coray +36 more
TL;DR: By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.
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TL;DR: Extracellular ATP regulates microglial branch dynamics in the intact brain, and its release from the damaged tissue and surrounding astrocytes mediates a rapid microglia response towards injury.
Molecular dissection of reactive astrogliosis and glial scar formation.
TL;DR: Developments in the signaling mechanisms that regulate specific aspects of reactive astrogliosis are reviewed and the potential to identify novel therapeutic molecular targets for diverse neurological disorders is highlighted.
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Glial and neuronal control of brain blood flow.
David Attwell,Alastair M. Buchan,Serge Charpak,Martin Lauritzen,Brian A. MacVicar,Eric A. Newman +5 more
TL;DR: It is now recognized that neurotransmitter-mediated signalling has a key role in regulating cerebral blood flow, that much of this control is mediated by astrocytes, that oxygen modulates blood flow regulation, and that blood flow may be controlled by capillaries as well as by arterioles.