Increased hippocampal activation in mild cognitive impairment compared to normal aging and AD
By Bradford C. Dickerson, David H. Salat, Douglas N. Greve, E. Chua, Erin Rand-Giovannetti, Dorene M. Rentz, Lars Bertram, K. Mullin, Rudolph E. Tanzi, Deborah Blacker and 2 more. Neurology, 2005
886 citations recorded by the source corpus.
Subfields: Cognitive Neuroscience, Physiology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/cb82d1b6baf9378bc705a7a4e79e5291fc750338
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cognitive Neuroscience
- Bruce Fischl
- Randy L. Buckner
- Olaf Sporns
- Douglas N. Greve
- David H. Salat
- H. Rosas
- John C. Morris
- Philip Scheltens
In Physiology
- L. Mucke
- J. Palop
- Randy L. Buckner
- D. Selkoe
- Reisa A. Sperling
- Bradley T. Hyman
- Jeannie Chin
- Marilyn S. Albert
In Psychiatry and Mental health
- Randy L. Buckner
- John C. Morris
- Bruce Fischl
- David H. Salat
- Douglas N. Greve
- Reisa A. Sperling
- Philip Scheltens
- Cornelis J. Stam
Citations in the corpus
- Brain imaging in Alzheimer disease. (2012, background): “Interestingly, several fMRI studies have reported evidence of increased MTL activity in at-risk subjects, particularly among very mild MCI subjects (Dickerson et al. 2004, 2005; Celone et al. 2006; Hamalainen et al. 2006; Heun et al. 2007; Kircher et al. 2007; Lenzi et al. 2009), and cognitively…”
- High-resolution structural and functional MRI of hippocampal CA3 and dentate gyrus in patients with amnestic mild cognitive impairment (2010, background): “Previous studies of MCI patients have noted elevated BOLD fMRI signals in the hippocampus and parahippocampal gyrus during a variety of memory tasks (Celone et al., 2006; Dickerson et al., 2005; Hamalainen et al., 2007; Johnson et al., 2006), as noted above, although none of the studies localized th”
- Activity Dependent Degeneration Explains Hub Vulnerability in Alzheimer's Disease (2012, background): “Excessive hippocampal activity is related to cortical thinning in nondemented elderly persons, is present in MCI patients, and is related to neurodegeneration in AD [49,65,66].”
- Amyloid deposition is associated with impaired default network function in older persons without dementia (2009, positive): “This finding is consonant with our previous studies and those of other groups reporting hippocampal hyperactivation in very mild MCI subjects (Celone et al., 2006; Dickerson et al., 2005; Kircher et al., 2007; Miller et al., 2007) and in subjects at genetic risk for AD (Bondi et al.”
- Detection of cortical thickness correlates of cognitive performance: Reliability across MRI scan sessions, scanners, and field strengths (2008, background): “, 2000b), others demonstrate its importance in delayed recall (Rodrigue and Raz, 2004; Dickerson et al., 2005).”
- Critical role of soluble amyloid-β for early hippocampal hyperactivity in a mouse model of Alzheimer’s disease (2012, background): “In humans with AD, there is also evidence for early functional magnetic resonance (fMRI) hyperactivation of the hippocampus, which is followed by hypoactivity at later disease stages (36, 37).”
- Impairment and compensation coexist in amnestic MCI default mode network (2010, positive): “Because MCI patients are a heterogeneous population, inconsistencies have been observed in MTL activation during memory tasks (Machulda et al., 2003; Dickerson et al., 2004, 2005). tivity in the left lateral PFC (x=−42, y=17, z=51, t=5.45), dorsal MPFC (x=−4, 38, z=−1, t=5.05) was observed in aMCI…”
- A network dysfunction perspective on neurodegenerative diseases (2006, background): “Radiological imaging studies in patients with MCI have identified hyperactivation of hippocampal and neocortical regions that become hypoactive and atrophic with the progression to A”
- The Cortical Signature of Alzheimer's Disease: Regionally Specific Cortical Thinning Relates to Symptom Severity in Very Mild to Mild AD Dementia and is Detectable in Asymptomatic Amyloid-Positive Individuals (2008, background): “…that described above (details have been previously published as cited below), with 39 participants in Sample 2 (Atri et al. 2005), 41 participants in Sample 3 (Wright, Dickerson, et al. 2007; Wright, Feczko, et al. 2007), and 40 participants in Sample 4 (Dickerson et al. 2005; Celone et al. 2006).”