Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease
By R. Cutler, J. Kelly, K. Storie, W. A. Pedersen, Anita Tammara, K. Hatanpaa, J. Troncoso, Mark P. Mattson. 2004
1,098 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- Michal Levy
- A. Futerman
- Yusuf A. Hannun
- Mark P. Mattson
- Ron M. A. Heeren
- Juan Zhang
- Qiang Liu
- Liam A. McDonnell
In Physiology
- Mark P. Mattson
- A. Futerman
- Yusuf A. Hannun
- Michal Levy
- Juan Zhang
- Qiang Liu
- M. O’Banion
- Michael T. Heneka
Citations in the corpus
- Mammalian Ceramide Synthases (2010, background): “These changes are likely to be downstream to other pathological pathways that are altered in Alzheimer’s disease, although it should be noted that levels of C20 and C24ceramide were significantly elevated long before symptoms or a cellular Alzheimer phenotype emerged (69).”
- Calcium and neurodegeneration (2007, background): “degenerating neurons in tissue samples from patients with AD (Cutler et al., 2004) and even in the cerebrospinal fluid of AD patients (Lovell et al.”
- Imaging mass spectrometry. (2007, background): “…motives for recording the cholesterol and lipid images shown in Figure 14 is the increasing knowledge about the Mass Spectrometry Reviews DOI 10.1002/mas 631 role of these compounds in various clinical disorders, such as Alzheimer’s disease (Puglielli, Tanzi, & Kovacs, 2003; Cutler et al., 2004).”
- The complex life of simple sphingolipids (2004, background): “Recently, ceramide has been implicated in the cytotoxic responses to amyloid-β peptide, which suggests a role for this pathway in Alzheimer’s disease and neurodegeneration (Cutler et al, 2004).”
- Long-term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid β-42 and α-Synuclein in Children and Young Adults (2008, background): “Chronic oxidative stress is a major contributing factor in the pathogenesis of both Alzheimer’s and Parkinson’s diseases (Nunomura et al. 2006; Quilty et al. 2006).”
- Cholesterol metabolism and homeostasis in the brain (2015, positive): “The cholesterol level increases throughout the course of clinical disease, and more increase was observed when the disease progresses (Cutler et al., 2004;Xionget al., 2008).”
- Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders (2010, neutral): “Ceramides generated in response to membrane-associated oxidative stress are implicated in the dysfunction and death of cells in a range of disorders, including diabetes (428), emphysema (352), ischemic stroke (476), Alzheimer’s disease (141), and amyotrophic lateral sclerosis (142).”
- Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma. (2007, methodology): “Levels of lysine and histidine adducts of 4-hydroxynonenal and long-chain ceramides were measured by tandem mass spectrometry methods described previously [ 31 ].”
- Ageing and neuronal vulnerability (2006, background): “Increased ceramide production has been linked to neuronal death in AD, HIV dementia and AL”
- Long‐chain ceramide is elevated in presenilin 1 (PS1M146V) mouse brain and induces apoptosis in PS1 astrocytes (2008, background): “In particular, ceramide of C18 and C24 species has been reported to be elevated in tissues of human brain with severe AD (Cutler et al., 2004; Katsel et al., 2007).”
- Canonical Nlrp3 inflammasome links systemic low grade inflammation to functional decline in aging (2013, positive): “Many DAMPs are elevated during aging and thus could trigger Nlrp3 inflammasome activation to produce age-related inflammation (Ruggiero et al., 2006; Cutler et al., 2004).”