Longitudinal CSF and MRI biomarkers improve the diagnosis of mild cognitive impairment

Leon, Mony J. de; DeSanti, Susan; Zinkowski, Raymond; Mehta, Pankaj; Praticò, Domenico; Segal, S.; Rusinek, Henry; Li, J.; Tsui, Wai; Louis, L.A. Saint; Clark, Christopher M.; Tarshish, Chaim; Li, Y.; Lair, Lindsey; Javier, Elizabeth; Rich, Kenneth; Lesbre, P; Mosconi, Lisa; Reisberg, Barry; Sadowski, Marcin; DeBernadis, J.F.; Kerkman, Daniel J.; Hampel, Harald; Wahlund, Lars‐Olof; Davies, Peter

doi:10.1016/j.neurobiolaging.2005.07.003

Cited by 229 publications

(198 citation statements)

References 37 publications

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“…In general, the effects were stron- ger in sample 2, but the relationship between the hippocampus and tau pathologic features was replicated across samples. The relationship between tau and hippocampal volume is well known, [11][12] but relationships between tau pathologic features and thickness in widespread cortical areas, to our knowledge, have not been reported previously. The discrepant findings across the 2 samples indicate that these effects are not very robust, however.…”

Section: Discussionmentioning

confidence: 73%

“…Thus, these data indicate that patients with pathologic CSF levels alone do not account for the group effect of a thinner cortex in MCI. It seems that tau-related pathologic features strike the hippocampus aggressively, as indicated by de Leon et al, 11 but cannot account for all cortical atrophy in MCI.…”

Section: Discussionmentioning

confidence: 96%

“…Correlations between CSF biomarkers and brain morphometry in the temporal areas have been found in MCI and AD. [10][11][12] Recent results indicate differences in thickness between patients with MCI and healthy controls outside the temporal brain areas (eg, in the frontal and parietal cortex.) 5 It has not been tested whether these changes can be explained by levels of CSF biomarkers in AD, only in frontotemporal dementia.…”

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confidence: 99%

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Morphometric Changes in the Episodic Memory Network and Tau Pathologic Features Correlate with Memory Performance in Patients with Mild Cognitive Impairment

Fjell¹,

Walhovd²,

Amlien³

et al. 2008

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE:Mild cognitive impairment (MCI) may affect several cognitive domains, including attention and reasoning, but is often first characterized by memory deficits. The purpose of this study was to ask these 2 questions: 1) Can levels of CSF tau proteins and amyloid beta 42 peptide explain thinning of the cerebral cortex in patients with MCI? 2) How are brain morphometry, CSF biomarkers, and apolipoprotein E (APOE) allelic variation related to episodic memory function in MCI?

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Section: Discussionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

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Morphometric Changes in the Episodic Memory Network and Tau Pathologic Features Correlate with Memory Performance in Patients with Mild Cognitive Impairment

Fjell¹,

Walhovd²,

Amlien³

et al. 2008

AJNR Am J Neuroradiol

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“…They concluded that a decline in episodic memory in older individuals may be caused by Aβ 1−42 -induced hippocampus atrophy, with Aβ 1−42 deposition as the primary event in this cascade [50]. In line with this explanation, longitudinal hippocampal volume losses in individuals with MCI appear to be closely associated with a decrease in CSF Aβ 1−42 levels and increasing hyperphosphorylated tau [51]. Moreover, our results correspond with a recent study from Petrie, in which correlations are shown between hypometabolism in FDG-PET: Lower Aβ is associated with hypometabolism, but only in the medial temporal lobe, and higher tau concentration is associated with hypometabolism in several brain regions [52].…”

Section: Discussionmentioning

confidence: 95%

Correlation between Cognitive Impairment and CSF Biomarkers in Amnesic MCI, non-Amnesic MCI, and Alzheimer's Disease

Haldenwanger

Eling

Kastrup

et al. 2010

JAD

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Abstract. Decreased delayed recall, decreased amyloid-β peptides (Aβ1−42), and increased tau protein concentration in cerebrospinal fluid (CSF) are generally regarded to be valid neuropsychological and biological markers for Alzheimer's disease (AD). Previous studies failed to demonstrate clear-cut correlations between neuropsychological impairment and CSF markers. In this study we test recent models of disease progression, that propose that changes in CSF biomarkers already reach a plateau in a preclinical phase, before cognitive decline begins, that is, even before MCI can be diagnosed. We recruited 73 patients with probable AD (n = 36) and mild cognitive impairment (MCI) (amnesic MCI = 25; non-amnesic MCI = 12). We used the CERAD-NP, a widely used neuropsychological battery with norms for different age and education groups, and additional neuropsychological tests for assessing the cognitive profile of these patient groups. We found a significant correlation between Aβ1−42 in the CSF and memory performance for amnesic MCI patients, but not for non-amnesic MCI and AD patients. All other correlations between cognitive tasks and Aβ1−42 were not significant. Tau protein concentration in the CSF was not correlated with any neuropsychological marker in any of the patients groups. We conclude that the decrease of Aβ1−42 in the CSF mirrors disease progression during the early stages up into AD and therefore is not restricted to the preclinical phase. The decrease of Aβ1−42 reaches a plateau only in the full blown demented syndrome and further functional disease progression is then related to neurodegeneration without further reduction of Aβ1−42 in the CSF.

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“…Regions of interest in the brain include substructures of the medial temporal lobe such as the hippocampus, amygdala and entorhinal cortex (Jack et al 1999;De Santi et al 2001;Hampel et al 2002;Chetelat and Baron 2003;de Leon et al 2006). Early AD is associated with neuronal loss and consequent changes in gray matter, which eventually leads to the atrophy of cortical gyri and widening of sulci.…”

Section: Introductionmentioning

confidence: 99%

T1ρ MRI of Alzheimer's disease

et al. 2008

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Alzheimer's disease (AD) is the most common form of dementia in the elderly. Classic symptoms of the disease include memory loss and confusion associated with the hallmark neuro-pathologic lesions of neurofibrillary tangles (NFT) and senile plaques (SP) and their sequelae, gray matter atrophy. Volumetric assessment methods measure tissue atrophy, which typically follows early biochemical changes. An alternate MRI contrast mechanism to visualize the early pathological changes is T 1ρ (or "T-1-rho"), the spin lattice relaxation time constant in the rotating frame, which determines the decay of the transverse magnetization in the presence of a "spin-lock" radio-frequency field. Macromolecular changes (in plaques and tangles) that accompany early AD are expected to alter bulk water T 1ρ relaxation times. In this work, we measure T 1ρ MRI on patients with clinically diagnosed AD, MCI and in age-matched ognitively normal control subjects in order to compare T 1ρ values with changes in brain volume in the same regions of the brain and demonstrate that T 1ρ can potentially constitute an important biomarker of AD.

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Longitudinal CSF and MRI biomarkers improve the diagnosis of mild cognitive impairment

Cited by 229 publications

References 37 publications

Morphometric Changes in the Episodic Memory Network and Tau Pathologic Features Correlate with Memory Performance in Patients with Mild Cognitive Impairment

Morphometric Changes in the Episodic Memory Network and Tau Pathologic Features Correlate with Memory Performance in Patients with Mild Cognitive Impairment

Correlation between Cognitive Impairment and CSF Biomarkers in Amnesic MCI, non-Amnesic MCI, and Alzheimer's Disease

T1ρ MRI of Alzheimer's disease

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