Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer's disease.

By G. Small, L. Ercoli, D. Silverman, Sung-Cheng Huang, S. Komo, Susan Y. Bookheimer, H. Lavretsky, K. Miller, P. Siddarth, N. Rasgon and 10 more. Proceedings of the National Academy of Sciences of the United States of America, 2000

761 citations recorded by the source corpus.

Subfields: Physiology, Psychiatry and Mental health, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/61c0f98270c133e30a71d39213626160435131ef

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Citations in the corpus

Ways toward an early diagnosis in Alzheimer's disease: The Alzheimer's Disease Neuroimaging Initiative (ADNI) (2005, neutral): “[73] Small GW, Ercoli LM, Silverman DH, et al.”
Functional connectivity hubs in the human brain (2011, neutral): “The females higher connectivity in DMN regions, which show metabolic decrements in Alzheimer’s disease (AD) (Small et al., 2000), could help explain why female AD-patients show greater impairments than male patients for the equivalent reduction in cerebral metabolic rate (Perneczky et al.”
Brain imaging in Alzheimer disease. (2012, background): “FDG hypometabolism is also predictive of the rate of memory decline in APOE 14 carriers with mild memory loss over 2 years (Small et al. 2000).”
Positron emission tomography in evaluation of dementia: Regional brain metabolism and long-term outcome. (2001, result): “The P1, P2, P3, and N1, N2, N3 designations refer to the patterns illustrated in the Figure, with the “+” sign indicating the presence of abnormal findings other than parietal/ temporal/frontal hypometabolism, which would be uncharacteristic of AD.”
Predictive Markers for AD in a Multi-Modality Framework: An Analysis of MCI Progression in the ADNI Population (2010, background): “, 1994) can be identified (in structural and functional images) in Mild Cognitive Impaired (MCI) and AD subjects, as well as at-risk individuals (Small et al., 2000; Querbes et al., 2009; Davatzikos et al., 2009).”
ApoE genotype accounts for the vast majority of AD risk and AD pathology. (2004, background): “In addition, in cognitively non-demented individuals, those withε4 show reduced brain metabolism and increased brain activation during recall [53].”
The Role of Apolipoprotein E in Alzheimer’s Disease (2009, neutral): “This suggests the possibility that an apoE-related decrease in brain metabolism may contribute to development of AD (Reiman et al., 1996; Reiman et al., 2004, 2005; Small et al., 2000).”
Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior. (2008, background): “Our work may provide an explanation for the observation that subtle brain dysfunction can be detected in certain individuals who are genetically at risk for AD but remain neurologically stable for many years before the expected onset of disease (Bookheimer et al. 2000; Small et al. 2000).”