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Springer Science and Business Media LLC

  1750-1326

 

 

Cơ quản chủ quản:  BioMed Central Ltd. , BMC

Lĩnh vực:
Cellular and Molecular NeuroscienceMolecular BiologyNeurology (clinical)

Các bài báo tiêu biểu

The SH-SY5Y cell line in Parkinson’s disease research: a systematic review
Tập 12 Số 1 - 2017
Helena Xicoy, Bé Wieringa, Gerard J. M. Martens
The release and trans-synaptic transmission of Tau via exosomes
- 2017
Yipeng Wang, Varun Balaji, Senthilvelrajan Kaniyappan, Lars Krüger, Stephan Irsen, Katharina Tepper, RamReddy Chandupatla, Walter Maetzler, Anja Schneider, Eckhard Mandelkow, Eva‐Maria Mandelkow
Oligomeric Aβ-induced synaptic dysfunction in Alzheimer’s disease
- 2014
Shichun Tu, Shu-ichi Okamoto, Stuart A. Lipton, Huaxi Xu
Alzheimer's disease: synaptic dysfunction and Aβ
- 2009
Ganesh M. Shankar, Dominic M. Walsh
HDAC6 as a target for neurodegenerative diseases: what makes it different from the other HDACs?
Tập 8 Số 1 - 2013
Cláudia A. Simões-Pires, Vincent Zwick, Alessandra Nurisso, Esther Schenker, Pierre Alain Carrupt, Muriel Cuendet
Abstract Histone deacetylase (HDAC) inhibitors have been demonstrated to be beneficial in animal models of neurodegenerative diseases. Such results were mainly associated with the epigenetic modulation caused by HDACs, especially those from class I, via chromatin deacetylation. However, other mechanisms may contribute to the neuroprotective effect of HDAC inhibitors, since each HDAC may present distinct specific functions within the neurodegenerative cascades. Such an example is HDAC6 for which the role in neurodegeneration has been partially elucidated so far. The strategy to be adopted in promising therapeutics targeting HDAC6 is still controversial. Specific inhibitors exert neuroprotection by increasing the acetylation levels of α-tubulin with subsequent improvement of the axonal transport, which is usually impaired in neurodegenerative disorders. On the other hand, an induction of HDAC6 would theoretically contribute to the degradation of protein aggregates which characterize various neurodegenerative disorders, including Alzheimer’s, Parkinson’s and Hutington’s diseases. This review describes the specific role of HDAC6 compared to the other HDACs in the context of neurodegeneration, by collecting in silico, in vitro and in vivo results regarding the inhibition and/or knockdown of HDAC6 and other HDACs. Moreover, structure, function, subcellular localization, as well as the level of HDAC6 expression within brain regions are reviewed and compared to the other HDAC isoforms. In various neurodegenerative diseases, the mechanisms underlying HDAC6 interaction with other proteins seem to be a promising approach in understanding the modulation of HDAC6 activity.
Blood–brain-barriers in aging and in Alzheimer’s disease
Tập 8 Số 1 - 2013
Fernanda Marques, João Carlos Sousa, Nuno Sousa, Joana Almeida Palha
Abstract The aging process correlates with a progressive failure in the normal cellular and organ functioning; these alterations are aggravated in Alzheimer’s disease (AD). In both aging and AD there is a general decrease in the capacity of the body to eliminate toxic compounds and, simultaneously, to supply the brain with relevant growth and nutritional factors. The barriers of the brain are targets of this age related dysfunction; both the endothelial cells of the blood–brain barrier and the choroid plexus epithelial cells of the blood-cerebrospinal fluid barrier decrease their secretory capacity towards the brain and their ability to remove toxic compounds from the brain. Additionally, during normal aging and in AD, the permeability of the brain barriers increase. As such, a greater contact of the brain parenchyma with the blood content alters the highly controlled neural environment, which impacts on neural function. Of interest, the brain barriers are more than mere obstacles to the passage of molecules and cells, and therefore active players in brain homeostasis, which is still to be further recognized and investigated in the context of health and disease. Herein, we provide a review on how the brain barriers change during aging and in AD and how these processes impact on brain function.
Alpha-synuclein and tau: teammates in neurodegeneration?
Tập 9 Số 1 - 2014
Simon Moussaud, Daryl Jones, Elisabeth L. Moussaud-Lamodière, Marion Delenclos, Owen A. Ross, Pamela J. McLean
Inoculation of α-synuclein preformed fibrils into the mouse gastrointestinal tract induces Lewy body-like aggregates in the brainstem via the vagus nerve
Tập 13 Số 1 - 2018
Norihito Uemura, Hisashi Yagi, Masanori Uemura, Yusuke Hatanaka, Hodaka Yamakado, Ryōsuke Takahashi
Differential effects of 24-hydroxycholesterol and 27-hydroxycholesterol on β-amyloid precursor protein levels and processing in human neuroblastoma SH-SY5Y cells
Tập 4 Số 1 - 2009
Jaya R.P. Prasanthi, Amber Huls, Sarah Thomasson, Alex J. Thompson, Eric Schommer, Othman Ghribi
Abstract Background Activation of the liver × receptors (LXRs) by exogenous ligands stimulates the degradation of β-amyloid 1–42 (Aβ42), a peptide that plays a central role in the pathogenesis of Alzheimer's disease (AD). The oxidized cholesterol products (oxysterols), 24-hydroxycholesterol (24-OHC) and 27-hydroxycholesterol (27-OHC), are endogenous activators of LXRs. However, the mechanisms by which these oxysterols may modulate Aβ42 levels are not well known. Results We determined the effect of 24-OHC and/or 27-OHC on Aβ generation in SH-SY5Y cells. We found that while 27-OHC increases levels of Aβ42, 24-OHC did not affect levels of this peptide. Increased Aβ42 levels with 27-OHC are associated with increased levels of β-amyloid precursor protein (APP) as well as β-secretase (BACE1), the enzyme that cleaves APP to yield Aβ. Unchanged Aβ42 levels with 24-OHC are associated with increased levels of sAPPα, suggesting that 24-OHC favors the processing of APP to the non-amyloidogenic pathway. Interestingly, 24-OHC, but not 27-OHC, increases levels of the ATP-binding cassette transporters, ABCA1 and ABCG1, which regulate cholesterol transport within and between cells. Conclusion These results suggest that cholesterol metabolites are linked to Aβ42 production. 24-OHC may favor the non-amyloidogenic pathway and 27-OHC may enhance production of Aβ42 by upregulating APP and BACE1. Regulation of 24-OHC: 27-OHC ratio could be an important strategy in controlling Aβ42 levels in AD.