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Hybrid PET/MRI Imaging of Alzheimer's Disease Based on 18F-AV-1451
Published on: April 18, 2025
MRI of the 'Alzheimer syndrome'
1Department of Radiology, Bichat-Claude-Bernard University Hospital, APHP, 46, rue Henri-Huchard, 75877 Paris cedex 18, France. marie-cecile.henry-feugeas@bch.ap-hop-paris.fr
Abstract:
Interest in the identification of cognitive decline in its earliest manifestations and the heterogeneity of clinically diagnosed Alzheimer's disease (AD) explain the growing number of neuroimaging studies of AD. Alzheimer-type lesions are associated with loss of neurons, and magnetic resonance imaging (MRI) can detect predominantly left atrophic changes in the entorhinal cortex, amygdala and anterior hippocampus several years before the onset of clinical symptoms. Cerebrovascular disease can mimic AD in the elderly whereas MR markers of subcortical vascular disease-leukoaraiosis, lacunar infarcts, microbleeds, ventricular enlargement, cortical and hippocampal atrophy-appear to be structural changes associated with vascular-related cognitive impairment. Furthermore, analysis of prodromal forms of late-onset dementia of Alzheimer's type (DAT) differentiates amnesic single-domain mild cognitive impairment, which shows MR patterns similar to those observed in early-onset DAT, from other predementia patterns without atrophy at the earliest sites of AD pathology. Mesiotemporal atrophy on MRI predicts late-onset DAT, but the current rating scales or measurements of mesiotemporal atrophy do not differentiate anteromesial temporal atrophy that is highly suggestive of AD from predominantly hippocampal atrophy, suggestive of non-AD damage and, usually, vascular disease. The other, most common MRI predictors of late-onset DAT may be considered indirect markers of arterial senescence whereas brain atrophy is diffusely milder and MR markers of small-vessel disease more frequent in late-onset, compared with early-onset, DAT. Thus, MRI suggests an overestimation of AD pathology while underestimating 'arteriosclerotic brain degeneration' in the clinical picture of 'Alzheimer syndrome'.
Insights
Magnetic resonance imaging (MRI) can detect early Alzheimer's disease (AD) changes, but differentiating AD from vascular cognitive impairment is challenging. MRI findings may overestimate AD pathology and underestimate vascular disease in
Area of Science:
- Neuroimaging
- Neurology
- Radiology
Background:
- Growing interest in early cognitive decline and Alzheimer's disease (AD) heterogeneity fuels neuroimaging research.
- Magnetic resonance imaging (MRI) detects early atrophic changes in AD, preceding clinical symptoms.
- Cerebrovascular disease can mimic AD, presenting similar imaging markers.
Purpose of the Study:
- To investigate the utility of MRI in differentiating early Alzheimer's disease (AD) from vascular cognitive impairment.
- To analyze MRI patterns in prodromal forms of late-onset dementia of Alzheimer's type (DAT).
- To assess the accuracy of current MRI measurements in distinguishing AD-specific atrophy from other forms of brain degeneration.
Main Methods:
- Review of neuroimaging studies focusing on Alzheimer's disease (AD) and cerebrovascular disease.
- Analysis of MRI markers, including atrophy patterns (mesiotemporal, hippocampal) and signs of subcortical vascular disease.
- Differentiation of imaging patterns in amnesic single-domain mild cognitive impairment and other predementia states.
Main Results:
- MRI can detect early brain atrophy suggestive of Alzheimer's disease (AD) years before symptom onset.
- Subcortical vascular disease markers on MRI are associated with vascular-related cognitive impairment.
- Current MRI methods struggle to differentiate AD-specific anteromesial temporal atrophy from hippocampal atrophy linked to vascular disease.
Conclusions:
- MRI findings in late-onset dementia may overestimate Alzheimer's disease (AD) pathology.
- MRI may underestimate 'arteriosclerotic brain degeneration' in cases clinically presenting as 'Alzheimer syndrome'.
- Refined MRI analysis is needed to accurately distinguish AD from vascular contributions to cognitive decline.
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