Results 101 to 110 of about 252,333 (374)
The amyloid hypothesis of Alzheimer's disease at 25 years
Despite continuing debate about the amyloid β‐protein (or Aβ hypothesis, new lines of evidence from laboratories and clinics worldwide support the concept that an imbalance between production and clearance of Aβ42 and related Aβ peptides is a very early,
D. Selkoe, J. Hardy
semanticscholar +1 more source
Solving the Amyloid Paradox: Unveiling the Complex Pathogenicity of Amyloid Fibrils
This review addresses the gap between strong evidence for the involvement of amyloid fibrils in neurodegeneration and the failure of anti‐amyloid therapies, a phenomenon herein termed the “amyloid paradox.” To address this paradox, we provide a comprehensive summary of the current understanding of fibrils' pathogenic properties and mechanisms ...
Maksim I. Sulatsky+3 more
wiley +1 more source
Premenopausal bilateral oophorectomy and Alzheimer's disease imaging biomarkers later in life
Abstract INTRODUCTION Premenopausal bilateral oophorectomy (PBO) before the age of 46 years is associated with an increased risk of dementia. We investigated the long‐term effects of PBO performed before age 50 years on amyloid beta (Aβ), tau, and neurodegeneration imaging biomarkers of Alzheimer's disease (AD).
Kejal Kantarci+13 more
wiley +1 more source
Bleeding is increased in amyloid precursor protein knockout mouse
Background Amyloid precursor protein (APP) is highly expressed in platelets. APP is the precursor to amyloid beta (Aβ) peptides that accumulate in cerebral amyloid angiopathy and plaques in Alzheimer disease.
Nima Mazinani+5 more
doaj +1 more source
Amyloid Precursor Protein Trafficking, Processing, and Function*
Intracellular trafficking and proteolytic processing of amyloid precursor protein (APP) have been the focus of numerous investigations over the past two decades.
G. Thinakaran, E. Koo
semanticscholar +1 more source
Possible roles of amyloid intracellular domain of amyloid precursor protein
Amyloid precursor protein (APP), which is critically involved in the pathogenesis of Alzheimer's disease (AD), is cleaved by gamma/epsilon-secretase activity and results in the generation of different lengths of the APP Intracellular C-terminal Domain (AICD).
Yoo-Hun Suh, Keun-A Chang
openaire +4 more sources
Autosomal Recessive Cerebellar Ataxias: Translating Genes to Therapies
Autosomal recessive cerebellar ataxias are disabling neurodegenerative genetic conditions affecting balance and coordination. Advancements in genomic testing have improved diagnosis, leading to a new focus on the development of targeted precision therapeutics addressing cellular, biochemical, and genetic disease mechanisms with a resulting emphasis on ...
Brent L. Fogel+10 more
wiley +1 more source
Neurobiological pathways to Alzheimer's disease: Amyloid-beta, TAU protein or both?
Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline, including memory loss, behavioral and psychological symptoms and personality changes.
Vanessa de Jesus R. de Paula+3 more
doaj +1 more source
Atomic-resolution structures of prion AGAAAAGA amyloid fibrils [PDF]
To the best of the author's knowledge, there is little structural data available on the AGAAAAGA palindrome in the hydrophobic region (113-120) of prion proteins due to the unstable, noncrystalline and insoluble nature of the amyloid fibril, although many experimental studies have shown that this region has amyloid fibril forming properties and plays ...
arxiv
Even though the idea that amyloid β peptide accumulation is the primary event in the pathogenesis of Alzheimer's disease has become the leading hypothesis, the causal link between aberrant amyloid precursor protein processing and tau alterations in this ...
Elena M. Ribé+18 more
doaj