scholarly journals Ultrasonic force microscopy for nanomechanical characterization of early and late-stage amyloid-β peptide aggregation

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Claire Tinker-Mill ◽  
Jennifer Mayes ◽  
David Allsop ◽  
Oleg V. Kolosov
Keyword(s):  
Late Stage ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
Peptide Aggregation ◽  
Force Microscopy

Direct electrochemical and AFM detection of amyloid-β peptide aggregation on basal plane HOPG

Nanoscale ◽  
2014 ◽  
Vol 6 (14) ◽  
pp. 7853-7857 ◽  
Author(s):  
Paula Lopes ◽  
Meng Xu ◽  
Min Zhang ◽  
Ting Zhou ◽  
Yanlian Yang ◽  
...  
Keyword(s):  
Basal Plane ◽  
Amyloid Β ◽  
Electrochemical Characterization ◽  
Amyloid Peptide ◽  
Amyloid Β Peptide ◽  
Peptide Aggregation ◽  
Β Amyloid ◽  
Β Amyloid Peptide ◽  
First Time

AFM and electrochemical characterization of β-amyloid peptide aggregation was for the first time performed on the same substrate thus enabling advanced screening of amyloidosis progression.

Modulation of amyloid β peptide aggregation by hydrophilic polymers

2019 ◽  
Vol 21 (37) ◽  
pp. 20999-21006
Author(s):  
Zhanna Evgrafova ◽  
Bruno Voigt ◽  
Andreas H. Roos ◽  
Gerd Hause ◽  
Dariush Hinderberger ◽  
...  
Keyword(s):  
Amyloid Β ◽  
Hydrophilic Polymers ◽  
Amyloid Β Peptide ◽  
Peptide Aggregation ◽  
Amyloidogenic Protein

Careful balance of hydrophilicity of precisely engineered polymers alters aggregation of the amyloidogenic protein Aβ1–40.

scholarly journals Tip60 protects against amyloid-β peptide-induced transcriptomic alterations via different modes of action in early versus late stages of neurodegenerative progression

2020 ◽  
Author(s):  
Haolin Zhang ◽  
Bhanu Chandra Karisetty ◽  
Akanksha Bhatnagar ◽  
Ellen M. Armour ◽  
Mariah Beaver ◽  
...  
Keyword(s):  
Cell Death ◽  
Cognitive Deficits ◽  
Late Stage ◽  
Neurodegenerative Disorder ◽  
Amyloid Β ◽  
Neuronal Cell ◽  
Amyloid Β Peptide ◽  
Histone Deacetylase 2 ◽  
Age Related ◽  
Late Stages

ABSTRACTAlzheimer’s disease (AD) is an age-related neurodegenerative disorder hallmarked by amyloid-β (Aβ) plaque accumulation, neuronal cell death, and cognitive deficits that worsen during disease progression. Histone acetylation dysregulation, caused by an imbalance between reduced histone acetyltransferases (HAT) Tip60 and increased histone deacetylase 2 (HDAC2) levels, can directly contribute to AD pathology. However, whether such AD-associated neuroepigenetic alterations occur in response to Aβ peptide production and can be protected against by increasing Tip60 levels over the course of neurodegenerative progression remains unknown. Here we profile Tip60 HAT/HDAC2 dynamics and transcriptome-wide changes across early and late stage AD pathology in the Drosophila brain produced solely by human amyloid-β42. We show that early Aβ42 induction leads to disruption of Tip60 HAT/HDAC2 balance during early neurodegenerative stages preceding Aβ plaque accumulation that persists into late AD stages. Correlative transcriptome-wide studies reveal alterations in biological processes we classified as transient (early-stage only), late-onset (late-stage only), and constant (both). Increasing Tip60 HAT levels in the Aβ42 fly brain protects against AD functional pathologies that include Aβ plaque accumulation, neural cell death, cognitive deficits, and shorter life-span. Strikingly, Tip60 protects against Aβ42-induced transcriptomic alterations via distinct mechanisms during early and late stages of neurodegeneration. Our findings reveal distinct modes of neuroepigenetic gene changes and Tip60 neuroprotection in early versus late stages in AD that can serve as early biomarkers for AD, and support the therapeutic potential of Tip60 over the course of AD progression.

scholarly journals Inhibition of metal-induced amyloid β-peptide aggregation by a blood–brain barrier permeable silica–cyclen nanochelator

RSC Advances ◽  
2019 ◽  
Vol 9 (25) ◽  
pp. 14126-14131 ◽  
Author(s):  
Jinzhuan Wang ◽  
Kun Wang ◽  
Zhenzhu Zhu ◽  
Yafeng He ◽  
Changli Zhang ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Amyloid Β ◽  
Brain Barrier ◽  
Amyloid Β Peptide ◽  
Peptide Aggregation ◽  
Blood Brain

A BBB-passable nanoscale silica–cyclen chelator effectively reduces the metal-induced Aβ aggregates and related ROS, thereby decreasing the neurotoxicity of Aβ.

Quenched hydrogen/deuterium exchange NMR characterization of amyloid-β peptide aggregates formed in the presence of Cu2+or Zn2+

FEBS Journal ◽  
2009 ◽  
Vol 276 (15) ◽  
pp. 4051-4060 ◽  
Author(s):  
Anders Olofsson ◽  
Malin Lindhagen-Persson ◽  
Monika Vestling ◽  
A. Elisabeth Sauer-Eriksson ◽  
Anders Öhman
Keyword(s):  
Amyloid Β ◽  
Deuterium Exchange ◽  
Amyloid Β Peptide ◽  
Hydrogen Deuterium Exchange ◽  
Nmr Characterization ◽  
Hydrogen Deuterium
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