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Search for "neurodegeneration" in Full Text gives 9 result(s) in Beilstein Journal of Organic Chemistry.
Multicomponent reactions driving the discovery and optimization of agents targeting central nervous system pathologies
Beilstein J. Org. Chem. 2024, 20, 3151–3173, doi:10.3762/bjoc.20.261
- caused by several biological causes, such as uncontrolled inflammation, neurodegeneration, and aberrant neurogenesis. Levetiracetam is the first member of a new class of anti-epileptic drugs, which selectively accumulates rapidly firing neurons and inhibits their activity. This drug binds to SV2A, a
Effects of the aldehyde-derived ring substituent on the properties of two new bioinspired trimethoxybenzoylhydrazones: methyl vs nitro groups
Beilstein J. Org. Chem. 2023, 19, 1713–1727, doi:10.3762/bjoc.19.125
- thus less side-effects in therapy [23]. In this sense, we have reported dicopper(II) complexes from different N-acylhydrazonic binucleating ligands with potent antiproliferative activity against a panel of cancer cell lines [24][25][26]. On the field of neurodegeneration, our research group was the
- display a role in neurodegeneration [38]. A comparative study between these two N-acylhydrazones is interesting, especially considering that they possess different substituents at the same position in the phenol ring: the electron-donating methyl group (hdz-CH3) and the electron-withdrawing nitro group
Crystal structure of the inclusion complex of cholesterol in β-cyclodextrin and molecular dynamics studies
Beilstein J. Org. Chem. 2018, 14, 838–848, doi:10.3762/bjoc.14.69
- clinical symptoms, such as progressive neurodegeneration and hepatosplenomegaly, often resulting in fatality at an early age [2]. As the cholesterol exchange between tissues at the whole body level and fundamental insights into the physiology of cholesterol trafficking are already known, the development of
A chemoselective and continuous synthesis of m-sulfamoylbenzamide analogues
Beilstein J. Org. Chem. 2017, 13, 303–312, doi:10.3762/bjoc.13.33
- ) aggregation [14], which is a major cause of neurodegeneration in Huntington’s disease. Although there are numerous reports available on the study of these analogues, an automated, chemoselective alternative to the synthesis is not yet available. The most common synthetic approach starts from m-(chlorosulfonyl
Synthesis of multi-lactose-appended β-cyclodextrin and its cholesterol-lowering effects in Niemann–Pick type C disease-like HepG2 cells
Beilstein J. Org. Chem. 2017, 13, 10–18, doi:10.3762/bjoc.13.2
- Niemann–Pick type C (NPC) disease, characterized by intracellular accumulation of unesterified cholesterol and other lipids owing to defects in two proteins NPC1 and NPC2, causes neurodegeneration and other fatal neurovisceral symptoms. Currently, treatment of NPC involves the use of 2-hydroxypropyl-β
- children, results in severe hepatosplenomegaly and neurodegeneration [3][6]. Hence, the sequestration of cholesterol is an important factor in the development of the NPC disease. Cyclodextrins (CDs) are cyclic glucose oligosaccharides used by the pharmaceutical industry to enhance solubility, stability
Interactions between cyclodextrins and cellular components: Towards greener medical applications?
Beilstein J. Org. Chem. 2016, 12, 2644–2662, doi:10.3762/bjoc.12.261
Cholesterol lowering effects of mono-lactose-appended β-cyclodextrin in Niemann–Pick type C disease-like HepG2 cells
Beilstein J. Org. Chem. 2015, 11, 2079–2086, doi:10.3762/bjoc.11.224
- disease (NPC) is one of inherited lysosomal storage disorders, emerges the accumulation of unesterified cholesterol in endolysosomes. NPC was caused by mutations in either the NPC1 or the NPC2 gene, and usually develops severe neurodegeneration, hepatosplenomegaly and failure to thrive childhood [1][2][3
Recent progress in the discovery of small molecules for the treatment of amyotrophic lateral sclerosis (ALS)
Beilstein J. Org. Chem. 2013, 9, 717–732, doi:10.3762/bjoc.9.82
- preclinical characterization of lead compounds that may ultimately provide novel drugs to treat patients suffering from ALS. Keywords: amyotrophic lateral sclerosis (ALS); copper/zinc (Cu-Zn) superoxide dismutase 1 (SOD1); glutamate toxicity; neurodegeneration; oxidative stress; Introduction Amyotrophic
- (thiosemicarbazonato)copper complexes (Cu(II)(btsc)s; Figure 9), reduced stress-induced kinase activity and prevented TDP-43 aggregation [38]. Cu(II)(btsc)s have previously been demonstrated to have neuroprotective effects in mouse models of neurodegeneration [47] and elicited similar results in cells overexpressing
Hydrophobic analogues of rhodamine B and rhodamine 101: potent fluorescent probes of mitochondria in living C. elegans
Beilstein J. Org. Chem. 2012, 8, 2156–2165, doi:10.3762/bjoc.8.243
- Mitochondria undergo dynamic fusion and fission events that affect the structure and function of these critical energy-producing cellular organelles. Defects in these dynamic processes have been implicated in a wide range of human diseases including ischemia, neurodegeneration, metabolic disease, and cancer
- , including ischemia, neurodegeneration, metabolic disease, and cancer [19][20]. In vivo, the pharmacokinetics of some rhodamines have been evaluated [21][22][23], and some have been used for imaging of mitochondria in the optically transparent model organism C. elegans (nematode worm) [24][25]. However
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