Abstract
Alzheimer’s disease (AD) affects several important molecules in brain metabolism. The resulting neurochemical changes can be quantified non-invasively in localized brain regions using in vivo single-voxel proton magnetic resonance spectroscopy (SV 1H MRS). Although the often heralded diagnostic potential of MRS in AD largely remains unfulfilled, more recent use of high magnetic fields has led to significantly improved signal-to-noise ratios and spectral resolutions, thereby allowing clinical applications with increased measurement reliability. The present article provides a comprehensive review of SV 1H MRS studies on AD at high magnetic fields (3.0 Tesla and above). This review suggests that patterned regional differences and longitudinal alterations in several neurometabolites are associated with clinically established AD. Changes in multiple metabolites are identifiable even at early stages of AD development. By combining information of neurochemicals in different brain regions revealing either pathological or compensatory changes, high field MRS can be evaluated in AD diagnosis and in the detection of treatment effects. To achieve this, standardization of data acquisition and analytical approaches is needed.
Highlights
Alzheimer’s disease (AD), the most common cause of dementia in late life [1], is characterized by an insidious onset and progressive neurodegeneration [2]
This study showed that neurochemical changes in the aging brain might be reflected by sI, in addition to NAA and mI, even though the latter were more reliably quantifiable [108]
The development of high-field single-voxel 1H MRS technology has enabled in vivo measurement of brain metabolites that cannot be reliably quantified at lower magnetic fields
Summary
Alzheimer’s disease (AD), the most common cause of dementia in late life [1], is characterized by an insidious onset and progressive neurodegeneration [2]. The hallmark accumulation of extracellular amyloid plaques and intracellular neurofibrillary tangles typically start in the entorhinal cortex and the medial temporal lobe (MTL) and extend gradually to the entire neocortex [2]. AD treatments are symptomatic and administered only when the disease is established. There is a strong belief that real progress will require early administration of disease modifying interventions – given perhaps even before clinical symptoms [5,6,7].
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