scholarly journals Abca7 deletion does not affect adult neurogenesis in the mouse

2016 ◽  
Vol 36 (2) ◽  
Author(s):  
Hongyun Li ◽  
Tim Karl ◽  
Brett Garner
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Adult Neurogenesis ◽  
Abc Transporters ◽  
Atp Binding ◽  
Wild Type ◽  
Atp Binding Cassette Transporter ◽  
The Brain ◽  
Deficient Mice ◽  
Atp Binding Cassette

ATP-binding cassette transporter A7 (ABCA7) is expressed in the brain and linked with Alzheimer's disease. Since other ABC transporters regulate adult neurogenesis, we assessed neurogenesis in wild-type (WT) and Abca7 deficient mice. Abca7 deletion did not affect adult neurogenesis in the mouse.

Increased ATP-Binding Cassette Transporter A1 Expression in Alzheimer's Disease Hippocampal Neurons

2010 ◽  
Vol 21 (1) ◽  
pp. 193-205 ◽  
Author(s):  
Woojin Scott Kim ◽  
Surabhi Bhatia ◽  
David A. Elliott ◽  
Lotta Agholme ◽  
Katarina Kågedal ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hippocampal Neurons ◽  
Atp Binding ◽  
Atp Binding Cassette Transporter ◽  
Atp Binding Cassette

P3-053: ATP-binding cassette transporter A7 (ABCA7) effects on amyloid processing and relevance to Alzheimer's disease

2012 ◽  
Vol 8 (4S_Part_13) ◽  
pp. P473-P473 ◽  
Author(s):  
Kanayo Satoh ◽  
Sumiko Abe-Dohmae ◽  
Shinji Yokoyama ◽  
Peter St. George-Hyslop ◽  
Paul Fraser
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Atp Binding ◽  
Atp Binding Cassette Transporter ◽  
Atp Binding Cassette

Association of ATP-binding cassette transporter variants with the risk of Alzheimer’s disease

2013 ◽  
Vol 14 (5) ◽  
pp. 485-494 ◽  
Author(s):  
Ingolf Cascorbi ◽  
Charlotte Flüh ◽  
Cornelia Remmler ◽  
Sierk Haenisch ◽  
Frank Faltraco ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Atp Binding ◽  
Atp Binding Cassette Transporter ◽  
Atp Binding Cassette

Meta-analysis on association between the ATP-binding cassette transporter A1 gene (ABCA1) and Alzheimer's disease

Gene ◽  
2012 ◽  
Vol 510 (2) ◽  
pp. 147-153 ◽  
Author(s):  
Mei Jiang ◽  
Lei Lv ◽  
Hairong Wang ◽  
Xuelian Yang ◽  
Haifeng Ji ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Meta Analysis ◽  
Atp Binding ◽  
Atp Binding Cassette Transporter ◽  
Atp Binding Cassette

scholarly journals The Function and Expression of ATP-Binding Cassette Transporters Proteins in the Alzheimer's Disease

2021 ◽  
Author(s):  
Asli Aykac ◽  
Ahmet Özer Sehirli
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Choroid Plexus ◽  
Abc Transporters ◽  
Amyloid Β ◽  
Neuronal Cell ◽  
Tau Proteins ◽  
Atp Binding ◽  
Aβ Peptide ◽  
Atp Binding Cassette

AbstractDespite many years of research, radical treatment of Alzheimer's disease (AD) has still not been found. Amyloid-β (Aβ) peptide is known to play an important role in the pathogenesis of this disease. AD is characterized by three main changes occurring in the central nervous system: (1) Aβ plaque accumulation that prevents synaptic communication, (2) the accumulation of hyperphosphorylated tau proteins that inhibit the transport of molecules inside neurons, and (3) neuronal cell loss of the limbic system. Mechanisms leading to Aβ accumulation in AD are excessive Aβ production as a result of mutations in amyloid precursor protein or genes, and impairment of clearance of Aβ due to changes in Aβ aggregation properties and/or Aβ removal processes. Human ATP-binding cassette (ABC) transporters are expressed in astrocyte, microglia, neuron, brain capillary endothelial cell, choroid plexus, choroid plexus epithelial cell, and ventricular ependymal cell. ABC transporters have essential detoxification and neuroprotective roles in the brain. The expression and functional changes in ABC transporters contribute to the accumulation of Aβ peptide. In conclusion, the review was aimed to summarize and highlight accumulated evidence in the literature focusing on the changing functions of human ABC transporter members, in AD pathogenesis and progression.

ATP-binding cassette transporters and neurodegenerative diseases

2021 ◽  
Author(s):  
Jared S. Katzeff ◽  
Woojin Scott Kim
Keyword(s):  
Neurodegenerative Diseases ◽  
Abc Transporters ◽  
Brain Diseases ◽  
Atp Binding ◽  
Future Directions ◽  
Diverse Range ◽  
The Brain ◽  
Lateral Sclerosis ◽  
Atp Binding Cassette

Abstract ATP-binding cassette (ABC) transporters are one of the largest groups of transporter families in humans. ABC transporters mediate the translocation of a diverse range of substrates across cellular membranes, including amino acids, nucleosides, lipids, sugars and xenobiotics. Neurodegenerative diseases are a group of brain diseases that detrimentally affect neurons and other brain cells and are usually associated with deposits of pathogenic proteins in the brain. Major neurodegenerative diseases include Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. ABC transporters are highly expressed in the brain and have been implicated in a number of pathological processes underlying neurodegenerative diseases. This review outlines the current understanding of the role of ABC transporters in neurodegenerative diseases, focusing on some of the most important pathways, and also suggests future directions for research in this field.

scholarly journals ATP Binding Cassette Transporter A1 is Involved in Extracellular Secretion of Acetylated APE1/Ref-1

2019 ◽  
Vol 20 (13) ◽  
pp. 3178 ◽  
Author(s):  
Yu Ran Lee ◽  
Hee Kyoung Joo ◽  
Eun Ok Lee ◽  
Hyun Sil Cho ◽  
Sunga Choi ◽  
...  
Keyword(s):  
Abc Transporter ◽  
Abc Transporters ◽  
Secretory Pathway ◽  
Trichostatin A ◽  
Atp Binding ◽  
Terminal Protein ◽  
Secretion Signal ◽  
Extracellular Secretion ◽  
Atp Binding Cassette Transporter ◽  
Atp Binding Cassette

Acetylation of nuclear apurinic/apyrimidinic endonuclease-1/redox factor-1 (APE1/Ref-1) is associated with its extracellular secretion, despite the lack of an N-terminal protein secretion signal. In this study, we investigated plasma membrane targeting and translocation of APE1/Ref-1 in HEK293T cells with enhanced acetylation. While APE1/Ref-1 targeting was not affected by inhibition of the endoplasmic reticulum/Golgi-dependent secretion, its secretion was reduced by inhibitors of ATP-binding cassette (ABC) transporters, and siRNA-mediated down-regulation of ABC transporter A1. The association between APE1/Ref-1 and ABCA1 transporter was confirmed by proximal ligation assay and immunoprecipitation experiments. An APE1/Ref-1 construct with mutated acetylation sites (K6/K7R) showed reduced co-localization with ABC transporter A1. Exposure of trichostatin A (TSA) induced the acetylation of APE1/Ref-1, which translocated into membrane fraction. Taken together, acetylation of APE1/Ref-1 is considered to be necessary for its extracellular targeting via non-classical secretory pathway using the ABCA1 transporter.

scholarly journals Arginase Inhibition Supports Survival and Differentiation of Neuronal Precursors in Adult Alzheimer’s Disease Mice

2020 ◽  
Vol 21 (3) ◽  
pp. 1133 ◽  
Author(s):  
Baruh Polis ◽  
Kolluru D. Srikanth ◽  
Vyacheslav Gurevich ◽  
Naamah Bloch ◽  
Hava Gil-Henn ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Adult Neurogenesis ◽  
Progenitor Cell ◽  
Molecular Mechanisms ◽  
Neuronal Cell ◽  
Cell Number ◽  
Wild Type ◽  
Newborn Neuron

Adult neurogenesis is a complex physiological process, which plays a central role in maintaining cognitive functions, and consists of progenitor cell proliferation, newborn cell migration, and cell maturation. Adult neurogenesis is susceptible to alterations under various physiological and pathological conditions. A substantial decay of neurogenesis has been documented in Alzheimer’s disease (AD) patients and animal AD models; however, several treatment strategies can halt any further decline and even induce neurogenesis. Our previous results indicated a potential effect of arginase inhibition, with norvaline, on various aspects of neurogenesis in triple-transgenic mice. To better evaluate this effect, we chronically administered an arginase inhibitor, norvaline, to triple-transgenic and wild-type mice, and applied an advanced immunohistochemistry approach with several biomarkers and bright-field microscopy. Remarkably, we evidenced a significant reduction in the density of neuronal progenitors, which demonstrate a different phenotype in the hippocampi of triple-transgenic mice as compared to wild-type animals. However, norvaline showed no significant effect upon the progenitor cell number and constitution. We demonstrated that norvaline treatment leads to an escalation of the polysialylated neuronal cell adhesion molecule immunopositivity, which suggests an improvement in the newborn neuron survival rate. Additionally, we identified a significant increase in the hippocampal microtubule-associated protein 2 stain intensity. We also explore the molecular mechanisms underlying the effects of norvaline on adult mice neurogenesis and provide insights into their machinery.

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