Quantitative susceptibility mapping from basal ganglia and related structures: correlation with disease severity in progressive supranuclear palsy

Krishnan, Syam; George, Satheesh; Radhakrishnan, Vineeth; Raghavan, Sheelakumari; Thulaseedharan, Jissa Vinoda

doi:10.1007/s13760-023-02352-5

Cited by 2 publications

(2 citation statements)

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“…Accordingly, the correlations between susceptibility and flortaucipir uptake were shown to be significantly positive in the putamen, pallidum, subthalamic nucleus, RN, and the dentate nucleus of PSP patients, and it was suggested that susceptibility measures may mediate or explain the levels of flortaucipir uptake [87]. Furthermore, regional iron accumulation has been shown to correlate with atrophy as well as clinical severity in 13 and 51 PSP-affected brains, respectively [83,90,91], further supporting its involvement in disease pathology. Accordingly, iron deposition patterns have recently been compared in different PSP clinical subtypes for a possible stratification [86,87,92].…”

Section: Iron Dysregulation In Pspmentioning

confidence: 91%

“…The review by Lee et al [82] summarizes MRI observations of iron deposition in PSP subcortical regions, altogether demonstrating the clear involvement of subcortical iron deposition in PSP pathology. Further highlighting the prominent involvement in PSP pathology, comparative studies involving a total of 53 PSP patients consistently show the greatest levels of iron deposition in these regions of PSP-affected brains compared to other forms of Parkinsonism with subcortical iron dysregulation, including MSA and PD; these are discussed in the following sections [83][84][85]. Interestingly, these comparative studies identify the red nucleus (RN) iron MRI measures for effectively distinguishing PSP patients from those with MSA and PD.…”

Section: Iron Dysregulation In Pspmentioning

confidence: 93%

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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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