Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's dementia

By Eric M. Reiman, Kewei Chen, G. Alexander, R. Caselli, D. Bandy, D. Osborne, A. Saunders, John Hardy. Proceedings of the National Academy of Sciences of the United States of America, 2003

977 citations recorded by the source corpus.

Subfields: Neurology, Physiology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/eb994dc7b585b491e0b2814b9c41734a99570732

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Neurology

1. Randy L. Buckner
2. Ronald C. Petersen
3. Yaakov Stern
4. William E. Klunk
5. John C. Morris
6. Reisa A. Sperling
7. William J. Jagust
8. Clifford R. Jack Jr.

In Physiology

1. Randy L. Buckner
2. Clifford R. Jack Jr.
3. John C. Morris
4. Reisa A. Sperling
5. Ronald C. Petersen
6. Yaakov Stern
7. William J. Jagust
8. David S. Knopman

In Psychiatry and Mental health

1. Randy L. Buckner
2. John C. Morris
3. Clifford R. Jack Jr.
4. Ronald C. Petersen
5. Reisa A. Sperling
6. Abraham Z. Snyder
7. David S. Knopman
8. Yaakov Stern

Citations in the corpus

• Ways toward an early diagnosis in Alzheimer's disease: The Alzheimer's Disease Neuroimaging Initiative (ADNI) (2005, neutral): “[72] Reiman EM, Chen K, Alexander GE, et al.”
• Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade (2010, neutral): “105 , 106 No consensus exists on the interpretation of these observations at this point.”
• Toward defining the preclinical stages of Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease (2011, background): “Note that in this biomarker model, brain Aβ accumulation is necessary but not sufficient to produce the clinical symptoms of MCI and dementia, (2) biomarkers of synaptic dysfunction, including FDG and functional MRI (fMRI), may demonstrate abnormalities very early, particularly in APOE gene ε4 allel”
• Fibrillar amyloid-β burden in cognitively normal people at 3 levels of genetic risk for Alzheimer's disease (2009, background): “of putative genetic and nongenetic AD risk factors (particularly risk factors thought to contribute to A pathology) (20, 21, 23), and as an endpoint for evaluating putative A -modifying treatments in prevention trials (24), without statistical correction for multiple comparisons.”
• Neurodegenerative diseases target large-scale human brain networks (2009, background): “, 2001) or risk factor allele (Reiman et al., 2004) may destabilize network connectivity and function in young adulthood or even childhood (Shaw et al.”
• BRAIN FUEL METABOLISM, AGING AND ALZHEIMER’S DISEASE (2010, background): “3), which is equivalent to the early cortical glucose deficit in those genetically at risk AD [131].”
• Mitochondrial bioenergetic deficit precedes Alzheimer's pathology in female mouse model of Alzheimer's disease (2009, background): “In this report, we demonstrated that the female 3xTg-AD mouse brain recapitulates multiple indicators of mitochondrial dysfunction found in the human AD patients, including decreased mitochondrial bioenergetics, increased oxidative stress, and increased mitochondrial amyloid load in the 3xTg-AD mous”
• Introduction to Revised Criteria for the Diagnosis of Alzheimer’s Disease: National Institute on Aging and the Alzheimer Association Workgroups (2011, background): “[23] Neary D.”