Cortical phase changes in Alzheimer's disease at 7T MRI: A novel imaging marker

Rooden, Sanneke van; Versluis, Mieke; Liem, Michael; Milles, Julien; Maier, Andrea B.; Oleksik, Anna M.; Webb, Andrew; Buchem, Mark A. van; Grond, Jeroen van der

doi:10.1016/j.jalz.2013.02.002

Cited by 47 publications

(39 citation statements)

References 52 publications

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“…21,22 However, a reduction of T 2 * can also be caused by an elevation of brain iron, and has been used to map such changes in diseases where iron levels rise, such as cortical tissue in Alzheimer's disease (AD). 23 Lithium has attracted considerable interest as a therapeutic candidate in AD research. In neuronal cultures, lithium is reported to decrease tau phosphorylation 24,25,26,27 and to inhibit A generation.…”

Section: Introductionmentioning

confidence: 99%

Lithium suppression of tau induces brain iron accumulation and neurodegeneration

et al. 2016

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Lithium is a first-line therapy for bipolar affective disorder. However, various adverse effects, including a Parkinson-like hand tremor, often limit its use. The understanding of the neurobiological basis of these side effects is still very limited. Nigral iron elevation is also a feature of Parkinsonian degeneration that may be related to soluble tau reduction. We found that magnetic resonance imaging T 2 relaxation time changes in subjects commenced on lithium therapy were consistent with iron elevation. In mice, lithium treatment lowers brain tau levels and increases nigral and cortical iron elevation that is closely associated with neurodegeneration, cognitive loss and parkinsonian features. In neuronal cultures lithium attenuates iron efflux by lowering tau protein that traffics amyloid precursor protein to facilitate iron efflux. Thus, tauand amyloid protein precursor-knockout mice were protected against lithium-induced iron elevation and neurotoxicity. These findings challenge the appropriateness of lithium as a potential treatment for disorders where brain iron is elevated (for example, Alzheimer's disease), and may explain lithium-associated motor symptoms in susceptible patients.

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Section: Introductionmentioning

confidence: 99%

Lithium suppression of tau induces brain iron accumulation and neurodegeneration

et al. 2016

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“…The PADRE technique may be beneficial not only in detecting small epileptogenic lesions such as cavernous malformations, hemosiderin, and calcification in cortical regions [38,39], but also in facilitating the detection of cortical lesions in multiple sclerosis [5] and Alzheimer's disease [40], as well as the identification and characterization of focal cortical dysplasia [39]. Other applications include precise positioning of striate cortex and optic radiation, as well as evaluation and diagnosis of their involvement in diseases, especially in the planning of a neurosurgical resection approach for mass lesions [21,41].…”

Section: Discussionmentioning

confidence: 99%

Characterizing the contrast of white matter and grey matter in high-resolution phase difference enhanced imaging of human brain at 3.0 T

et al. 2014

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• Phase difference enhanced (PADRE) imaging can yield diverse contrasts between tissues • The PADRE technique utilizes the inherent variety of magnetic susceptibilities • PADRE MR imaging provides better visualization of certain cerebral anatomy in vivo • PADRE imaging is able to delineate the stria of Gennari in the primary visual cortex • PADRE imaging is able to identify the two optic radiation layers.

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“…Technical improvement of MR technology has led to the development of scanners operating at ultra-high magnetic fields, from 7T up to 11.7T, with the potential for higher image resolution with finer definition of anatomical details; this is expected to increase the accuracy of quantification of brain atrophy, and to improve spectra definition and quantification in MRS (Balchandani and Naidich, 2015). Moreover, a potential new biomarker for AD is the increased cortical phase shift demonstrated in AD subjects on T2*-weighted images obtained with a 7T scanner, a parameter sensitive to iron content that may reflect amyloid pathology (van Rooden et al, 2014). F]FDG-6-phosphate is not further metabolized by the isomerase enzyme; instead, in relation to aerobic glycolysis, it accumulates in the cells of the nervous system.…”

Section: Magnetic Resonance Spectroscopymentioning

confidence: 99%

Magnetic resonance imaging and positron emission tomography in the diagnosis of neurodegenerative dementias

Sole¹,

Malaspina²,

A³

2016

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SummaryNeuroimaging, both with magnetic resonance imaging (MRI) and positron emission tomography (PET), has gained a pivotal role in the diagnosis of primary neurodegenerative diseases. These two techniques are used as biomarkers of both pathology and progression of Alzheimer's disease (AD) and to differentiate AD from other neurodegenerative diseases. MRI is able to identify structural changes including patterns of atrophy characterizing neurodegenerative diseases, and to distinguish these from other causes of cognitive impairment, e.g. infarcts, space-occupying lesions and hydrocephalus. PET is widely used to identify regional patterns of glucose utilization, since distinct patterns of distribution of cerebral glucose metabolism are related to different subtypes of neurodegenerative dementia. The use of PET in mild cognitive impairment, though controversial, is deemed helpful for predicting conversion to dementia and the dementia clinical subtype. Recently, new radiopharmaceuticals for the in vivo imaging of amyloid burden have been licensed and more tracers are being developed for the assessment of tauopathies and inflammatory processes, which may underlie the onset of the amyloid cascade. At present, the cerebral amyloid burden, imaged with PET, may help to exclude the presence of AD as well as forecast its possible onset. Finally PET imaging may be particularly useful in ongoing clinical trials for the development of dementia treatments. In the near future, the use of the above methods, in accordance with specific guidelines, along with the use of effective treatments will likely lead to more timely and successful treatment of neurodegenerative dementias.

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Cortical phase changes in Alzheimer's disease at 7T MRI: A novel imaging marker

Cited by 47 publications

References 52 publications

Lithium suppression of tau induces brain iron accumulation and neurodegeneration

Lithium suppression of tau induces brain iron accumulation and neurodegeneration

Characterizing the contrast of white matter and grey matter in high-resolution phase difference enhanced imaging of human brain at 3.0 T

Magnetic resonance imaging and positron emission tomography in the diagnosis of neurodegenerative dementias

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