Abstract
Research utilizing magnetic resonance imaging (MRI) has been crucial to the understanding of the neuropathological mechanisms behind and clinical identification of Alzheimer’s disease (AD) and mild cognitive impairment (MCI). MRI modalities show patterns of brain damage that discriminate AD from other brain illnesses and brain abnormalities that are associated with risk of conversion to AD from MCI and other behavioural outcomes. This review discusses the application of various MRI techniques to and their clinical usefulness in AD and MCI. MRI modalities covered include structural MRI, diffusion tensor imaging (DTI), arterial spin labelling (ASL), magnetic resonance spectroscopy (MRS), and functional MRI (fMRI). There is much evidence supporting the validity of MRI as a biomarker for these disorders; however, only traditional structural imaging is currently recommended for routine use in clinical settings. Future research is needed to warrant the inclusion for more advanced MRI methodology in forthcoming revisions to diagnostic criteria for AD and MCI.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common cause of dementia
Data used in preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database
AD is a devastating illness that leads to cognitive impairment and functional deterioration
Summary
Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common cause of dementia. Notable hypoperfusion is present in the posterior cingulate, precuneus, and, occipital, temporal, parietal cortical areas in AD and MCI, and in frontal and orbitofrontal cortex, and the hippocampus in AD. AD patients demonstrate greater CBF declines in cortex found in temporal, parietal, frontal, and orbitofrontal areas, in addition to the thalamus and middle temporal structures including the hippocampus and amygdala when compared to those with MCI [41,42,43]. Compared to MCI patients, AD patients showed decreased CBF in temporal, parietal, frontal orbitofrontal cortex and temporal regions such as hippocampus, amygdala, and thalamus. MI/Cr ratios are increased for AD patients lead to variable transit times for its delivery This might result in artificial changes in signal intensity, which a clinician might mistake as a disease-related abnormality in CBF. Unexplained variability in this signal might result from hemodynamic factors that are not controlled for [78]
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