Results 71 to 80 of about 7,479 (177)
iTRAQ-Based Analysis of Progerin Expression Reveals Mitochondrial Dysfunction, Reactive Oxygen Species Accumulation and Altered Proteostasis [PDF]
, 2015 [Abstract] Introduction. Nuclear accumulation of a mutant form of the nuclear protein Lamin-A, called Progerin (PG) or Lamin AΔ50, occurs in Hutchinson-Gilford Progeria Syndrome (HGPS) or Progeria, an accelerated aging disease. One of the main symptoms
Arufe, M.C. +10 more
core +3 more sources
Informing Dose for Pediatric Rare Diseases—A Survey of Recent Orphan Drugs Approvals
Clinical and Translational Science, Volume 19, Issue 2, February 2026.ABSTRACT Collectively, pediatric rare diseases affect millions of children worldwide. Yet, treatment options are limited. Dose selection presents unique challenges in pediatric rare disease drug development. Traditional dose‐finding approaches are impractical for these populations, and conventional pediatric dosing methods like exposure matching face ...
Elimika Pfuma Fletcher +6 more
wiley +1 more source
Trends in PediatricsHutchinson-Gilford Progeria Syndrome (HGPS) is a rare genetic condition characterized by premature aging resulting from an autosomal mutation in the LMNA gene.
Nelson Carlos Reis-Filho +6 more
doaj +1 more source
Emerging Therapeutic Strategies in Anti‐Aging Medicine: A Comprehensive Review
Medicine Bulletin, Volume 2, Issue 1, Page 94-123, January 2026.ABSTRACT Aging is orchestrated by interconnected hallmarks such as genomic instability, mitochondrial dysfunction, cellular senescence, and disrupted intercellular communication, which collectively drive chronic disease progression. Recent advances have expanded therapeutic opportunities to include pharmacological agents, gene and epigenome editing ...
Yundong Peng +8 more
wiley +1 more source
Promising Results With NAD Supplementation in Rare Diseases With Premature Aging and DNA Damage
Aging Cell, Volume 25, Issue 1, January 2026.Increased DNA damage leads to increased parylation, causing mitochondrial dysfunction. This happens when DNA repair is defective, for example in known diseases and DNA repair capacity varies between individuals, some being at higher risk for hyperparylation.
Vilhelm A. Bohr
wiley +1 more source
Model of human aging: Recent findings on Werner’s and Hutchinson-Gilford progeria syndromes
Clinical Interventions in Aging, 2008 Shian-ling Ding1, Chen-Yang Shen2,3,41Department of Nursing, Kang-Ning Junior College of Medical Care and Management, Taipei, Taiwan; 2Institute of Biomedical Sciences, and 3Life Science Library, Academia Sinica, Taipei, Taiwan; 4Graduate Institute of ...
Shian-ling Ding, Chen-Yang Shen
doaj
Mouse models of ageing and their relevance to disease [PDF]
, 2016 Ageing is a process that gradually increases the organism’s vulnerability to death. It affects different biological pathways, and the underlying cellular mechanisms are complex.
Dogan, Soner +5 more
core +2 more sources
Aging Cell, Volume 25, Issue 1, January 2026.P62‐TIF‐IA–mediated regulation of senescence and ageing. In healthy tissue, p62 facilitates TIF‐IA turnover. Upon senescence induction, ATM activation increases TIF‐IA phosphorylation at S44, reducing its p62 binding and causing TIF‐IA accumulation.
Hazel C. Thoms +17 more
wiley +1 more source
The epidemiology of premature aging and associated comorbidities
Clinical Interventions in Aging, 2013 Fabio Coppedè Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy Abstract: Hutchinson–Gilford Progeria Syndrome and Werner syndrome, also known as childhood- and adulthood ...
Coppedè F
doaj
Structure and stability of the lamin A tail domain and HGPS mutant [PDF]
, 2011 Hutchinson–Gilford progeria syndrome (HGPS) is a premature aging syndrome caused by the expression and accumulation of a mutant form of lamin A, Δ50 lamin A.
Buehler, Markus J +3 more
core +1 more source