The role of protein phosphorylation modifications mediated by iron metabolism regulatory networks in the pathogenesis of Alzheimer’s disease DOI Creative Commons

Fei-Xiang Liu,

Yang Su, K. Shi

et al.

Frontiers in Aging Neuroscience, Journal Year: 2025, Volume and Issue: 17

Published: Feb. 25, 2025

Alzheimer's disease (AD) is a severe neurodegenerative characterized mainly by the formation of amyloid beta (Aβ) plaques and abnormal phosphorylation tau. In recent years, an imbalance in iron homeostasis has been recognized to play key role pathological process AD. Abnormal accumulation can activate various kinases such as glycogen synthase kinase-3β, cyclin-dependent kinase 5, mitogen-activated protein kinase, leading tau precursor protein, accelerating Aβ neurofibrillary tangles. addition, iron-mediated oxidative stress not only triggers neuronal damage, but also exacerbates dysfunction altering N-methyl-D-aspartate receptors γ-aminobutyric acid type A receptors. Iron affects status tyrosine hydroxylase, rate-limiting enzyme for dopamine synthesis, interfering with signaling pathway. On other hand, transport metabolism brain regulating transferrin, further disrupting homeostasis. Therapeutic strategies targeting show promise reducing accumulation, inhibiting stress, proteins. This article reviews molecular mechanisms modifications mediated AD, discusses potential interventions that regulate related pathways, providing new theoretical basis treatment

Language: Английский

The role of protein phosphorylation modifications mediated by iron metabolism regulatory networks in the pathogenesis of Alzheimer’s disease DOI Creative Commons

Fei-Xiang Liu,

Yang Su, K. Shi

et al.

Frontiers in Aging Neuroscience, Journal Year: 2025, Volume and Issue: 17

Published: Feb. 25, 2025

Alzheimer's disease (AD) is a severe neurodegenerative characterized mainly by the formation of amyloid beta (Aβ) plaques and abnormal phosphorylation tau. In recent years, an imbalance in iron homeostasis has been recognized to play key role pathological process AD. Abnormal accumulation can activate various kinases such as glycogen synthase kinase-3β, cyclin-dependent kinase 5, mitogen-activated protein kinase, leading tau precursor protein, accelerating Aβ neurofibrillary tangles. addition, iron-mediated oxidative stress not only triggers neuronal damage, but also exacerbates dysfunction altering N-methyl-D-aspartate receptors γ-aminobutyric acid type A receptors. Iron affects status tyrosine hydroxylase, rate-limiting enzyme for dopamine synthesis, interfering with signaling pathway. On other hand, transport metabolism brain regulating transferrin, further disrupting homeostasis. Therapeutic strategies targeting show promise reducing accumulation, inhibiting stress, proteins. This article reviews molecular mechanisms modifications mediated AD, discusses potential interventions that regulate related pathways, providing new theoretical basis treatment

Language: Английский

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