Alzheimer disease.
By R. Castellani, R. Rolston, Mark A. Smith. Disease-a-month : DM, 2010
2,961 citations recorded by the source corpus.
Subfields: Cognitive Neuroscience, Neurology, Rehabilitation
View Paper: https://www.semanticscholar.org/paper/1d54ed58f43755768a500c2893ed29cb506c1d4e
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In Cognitive Neuroscience
In Neurology
Citations in the corpus
- Mitochondrial dynamics in health and disease: mechanisms and potential targets (2023, background): “179 Mitochondria contribute signi fi cantly to the development of AD.”
- Comprehensive Review on Alzheimer’s Disease: Causes and Treatment (2020, background): “(4) Severe AD or late-stage, which involves the spread of the disease to the entire cortex area with a severe accumulation of neuritic plaques and neurofibrillary tangles, resulting in a progressive functional and cognitive impairment where the patients cannot recognize their family at all and may b”
- The amyloid hypothesis of Alzheimer's disease at 25 years (2016, background): “…how presenilin mediates intramembrane proteolysis (Qi-Takahara et al, 2005; Takami et al, 2009; Chavez-Gutierrez et al, 2012; Okochi et al, 2013; Fernandez et al, 2014): an initial endopeptidase cleavage of APP near the transmembrane/cytoplasmic interface of APP (the e-cleavage) is followed by…”
- Crossing the blood‐brain barrier with nanoparticles (2018, background): “According to these models, NPs may induce neurodegenerative amyloid diseases such as Alzheimer's disease.”
- APP mouse models for Alzheimer's disease preclinical studies (2017, neutral): “In 2015, of the ~ 47 million individuals with dementia worldwide (Prince et al , 2016), AD accounted for 50 – 70% of these cases (Winblad et al , 2016).”
- Oxidative Stress and Mitochondrial Dysfunction in Alzheimer’s Disease (2013, neutral): “…elderly populations and is characterized by selective neuronal death and two pathologic hallmarks, i.e., senile plaques formed by extracellular deposits of amyloid-β (A β ) peptides and neuro fi brillary tangles (NFTs) composed of intracellular aggregations of hyperphosphorylated tau protein [1].”
- Exercise, oxidative stress and hormesis. (2008, neutral): “This ROS mediated adaptation could play a significant role by which exercise decreases the incidence of ROS-associated diseases, including specific cardiovascular diseases, stroke, Alzheimer disease, and certain types of cancer (Perry et al., 2005; Radak et al., 2005; Mattson and Magnus, 2006; Matts”
- Impaired Balance of Mitochondria Fission and Fusion in Alzheimer Disease (2009, background): “…by neurofibrillary tangles, senile plaques, and progressive loss of neuronal cells in selective brain regions, Alzheimer’s disease (AD) is a fatal degenerative dementia with initial memory impairment that progresses to a total debilitating loss of mental and physical faculties (Smith, 1998).”