Multimodal comparisons of QSM and PET in neurodegeneration and aging

Cogswell, Petrice M; Fan, Audrey P.

doi:10.1016/j.neuroimage.2023.120068

Cited by 15 publications

(13 citation statements)

References 151 publications

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“…Consistent reports of correlations between QSM measures of iron and tau pathology in AD patients strongly support the relationship between the two phenomena in disease pathology [25]. Although the degree of off-target binding of tau PET SUVR needs to be evaluated further [25], a number of in vitro and in vivo studies support the pathogenic role of iron in tau pathology. In this section, we will focus on studies which used three-repeat (3R) tau or mixed four-repeat (4R)/3R tau, and AD mouse models, for a more specific relevance to AD.…”

Section: Iron Accumulation Promotes Tau Pathologymentioning

confidence: 78%

“…Subcortical regions, most consistently in the caudate nucleus and the putamen, are observed with higher iron burden, which are reported to be more closely associated with disease progression defined by advanced cognitive impairment and duration of disease [18,20,23,24]. This may explain the inconsistency in subcortical iron examinations in AD [25].…”

Section: Iron Dysregulation In Admentioning

confidence: 99%

“…An extensive number of recent research works demonstrate a strong association between pathological iron and cognitive decline [25]. Evaluating Aβ-CSF-positive cognitively unimpaired versus impaired AD patients, quantitative susceptibility mapping (QSM) values of the cortical and inferior temporal gyrus (ITG), as well as their tau-SUVR uptake levels were found to be increased, with a negative correlation between the QSM signal in the ITG and global cognition, as quantified by the mini-mental state examination (MMSE) [19].…”

Section: Iron Dysregulation In Admentioning

confidence: 99%

“…In imaging studies focusing on aging or AD, negative correlations between Aβ pathology and iron levels are also reported [23,25,28,70]. Whether such observations represent inhibitory mechanisms between each other remains unknown, and no experimental evidence yet supports this hypothesis.…”

Section: Hypothesis 3: Iron Accumulation Protects From or Hinders The...mentioning

confidence: 99%

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The Irony of Iron: The Element with Diverse Influence on Neurodegenerative Diseases

Lee,

Kovacs

2024

IJMS

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Iron accumulation in the brain is a common feature of many neurodegenerative diseases. Its involvement spans across the main proteinopathies involving tau, amyloid-beta, alpha-synuclein, and TDP-43. Accumulating evidence supports the contribution of iron in disease pathologies, but the delineation of its pathogenic role is yet challenged by the complex involvement of iron in multiple neurotoxicity mechanisms and evidence supporting a reciprocal influence between accumulation of iron and protein pathology. Here, we review the major proteinopathy-specific observations supporting four distinct hypotheses: (1) iron deposition is a consequence of protein pathology; (2) iron promotes protein pathology; (3) iron protects from or hinders protein pathology; and (4) deposition of iron and protein pathology contribute parallelly to pathogenesis. Iron is an essential element for physiological brain function, requiring a fine balance of its levels. Understanding of disease-related iron accumulation at a more intricate and systemic level is critical for advancements in iron chelation therapies.

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Section: Iron Accumulation Promotes Tau Pathologymentioning

confidence: 78%

Section: Iron Dysregulation In Admentioning

confidence: 99%

Section: Iron Dysregulation In Admentioning

confidence: 99%

Section: Hypothesis 3: Iron Accumulation Protects From or Hinders The...mentioning

confidence: 99%

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The Irony of Iron: The Element with Diverse Influence on Neurodegenerative Diseases

Lee,

Kovacs

2024

IJMS

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“…Furthermore, QSM is a versatile method for visualising changes in the brain (Betts et al, 2016), such as those that opccur in ageing, especially when paired with R2* measures. QSM provides indices of demyelination, tissue mineralisation, changes in oxygen extraction fraction (or OEF; see sections 5 & 6 for more) and vascular changes (Betts et al, 2016;Cogswell & Fan, 2023).…”

Section: Quantitative Susceptibility Mappingmentioning

confidence: 99%

Linking the Meso and Macroscale Determinants of Cerebral Ageing

Paolo¹,

Deery²,

Jamadar³

2023

Preprint

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Neuroimaging methods provide a non-invasive means to understand how the brain changes over the course of a typical lifespan in-vivo. Macroscale neuroimaging studies of “healthy” human ageing rarely consider small-scale (microscale) biological processes that underlie age-related changes to the tissues, processes and functions of the brain. By considering these microscale changes, we stand to better understand the underlying causes and processes that give rise to age-related cerebral changes captured by these images. This review addresses the gap by describing the known and putative connections between neuroimaging studies of ageing and molecular biology. The connections are described in relation to structural, inflammatory, vascular, and metabolic brain changes with age. We summarise the cerebral changes, how they can be visualised with neuroimaging methods and the microscale biological processes that underlie the visible macroscale changes.

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