AATF protects neural cells against oxidative damage induced by amyloid β-peptide

2004 ◽  
Vol 16 (1) ◽  
pp. 150-157 ◽  
Author(s):  
Jun Xie ◽  
Qing Guo
Keyword(s):  
Oxidative Damage ◽  
Amyloid Β ◽  
Neural Cells ◽  
Amyloid Β Peptide

Metal-Catalyzed Oxidative Damage and Oligomerization of the Amyloid-β Peptide of Alzheimer′s Disease

ChemInform ◽  
2004 ◽  
Vol 35 (33) ◽  
Author(s):  
Feda E. A. Ali ◽  
Kevin J. Barnham ◽  
Colin J. Barrow ◽  
Frances Separovic
Keyword(s):  
Oxidative Damage ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
Metal Catalyzed

Potential of medicinal plants as neuroprotective and therapeutic properties against amyloid-β-related toxicity, and glutamate-induced excitotoxicity in human neural cells

2021 ◽  
Vol 19 ◽  
Author(s):  
Devina Lobine ◽  
Nabeelah Sadeer ◽  
Sharmeen Jugreet ◽  
Shanoo Suroowan ◽  
Bibi Sumera Keenoo ◽  
...  
Keyword(s):  
Plant Species ◽  
Neuronal Cell Death ◽  
Amyloid Β ◽  
Neuronal Cell ◽  
Neural Cells ◽  
Amyloid Β Peptide ◽  
Limited Effectiveness ◽  
Baseline Information ◽  
Approved Drugs ◽  
Pharmacologically Active

: Alzheimer’s disease (AD) and Parkinson disease (PD) are notorious neurodegenerative diseases amongst the general population. Being age-associated diseases, the prevalence of AD and PD is forecasted to rapidly escalate with the progressive aging population of the world. These diseases are complex and multifactorial. Among the different events, amyloid β peptide (Aβ) induced toxicity is a well‐established pathway of neuronal cell death which plays a vital function in AD. Glutamate, the major excitatory transmitter, acts a neurotoxin when present in excess at the synapses; this latter mechanism is termed as excitotoxicity. It is hypothesised that glutamate-induced excitotoxicity contributes to the pathogenesis of AD and PD. No cure for AD and PD is currently available and the currently approved drugs available to treat these diseases have limited effectiveness and pose adverse effects. Indeed, plants have been a major source for the discovery of novel pharmacologically active compounds for distinct pathological conditions. Diverse plant species employed for brain related disorders in the traditional medicine are being explored to determine them scientific rationale behind their uses. Herein, we present a comprehensive review of plants and their constituents have shown promise in reversing the (i) amyloid-β -related toxicity in AD models and (ii) glutamate-induced excitotoxicity in AD and PD models. This review summarizes information with regard to the phytochemistry, biological and cellular activities as well as clinical trials of several plant species in view to provide adequate scientific baseline information that could be used in drug development process, thereby providing effective leads for AD and PD.

Metal-Catalyzed Oxidative Damage and Oligomerization of the Amyloid-β Peptide of Alzheimer’s Disease

2004 ◽  
Vol 57 (6) ◽  
pp. 511 ◽  
Author(s):  
Feda E. A. Ali ◽  
Kevin J. Barnham ◽  
Colin J. Barrow ◽  
Frances Separovic
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oxidative Damage ◽  
Conformational Changes ◽  
Senile Plaque ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
Zinc Ions ◽  
Amino Acid Peptide

The most common form of dementia in old age is Alzheimer’s disease (AD). The presence in the brain of senile plaque is the major pathological marker of AD. The plaques are primarily composed of aggregated amyloid-β peptide (Aβ). Aβ is a 40–42 amino acid peptide that is a proteolytic product derived from the β-amyloid precursor protein. The function of Aβ and the exact mechanism of Aβ aggregation and neurotoxicity are unclear. However, metal coordination by Aβ plays an important role in inducing aggregation and the generation of reactive oxygen species, which appears to be at least partially responsible for Aβ neurotoxicity. In this review we examine the role of copper and zinc ions in Aβ neurotoxicity, especially with regards to the generation of free radicals. We discuss the role of copper or zinc ions in oxidative damage and Aβ conformational changes and the relationship of these metals to AD.

Protein kinase C iota protects neural cells against apoptosis induced by amyloid β-peptide

2000 ◽  
Vol 82 (1-2) ◽  
pp. 107-113 ◽  
Author(s):  
Jun Xie ◽  
Qing Guo ◽  
Haiyan Zhu ◽  
Marie W Wooten ◽  
Mark P Mattson
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Amyloid Β ◽  
Neural Cells ◽  
Amyloid Β Peptide ◽  
Kinase C ◽  
Protein Kinase C Iota

scholarly journals Amyloid precursor protein and amyloid β-peptide bind to ATP synthase and regulate its activity at the surface of neural cells

2007 ◽  
Vol 13 (10) ◽  
pp. 953-969 ◽  
Author(s):  
C Schmidt ◽  
E Lepsverdize ◽  
S L Chi ◽  
A M Das ◽  
S V Pizzo ◽  
...  
Keyword(s):  
Amyloid Precursor Protein ◽  
Atp Synthase ◽  
Amyloid Β ◽  
Precursor Protein ◽  
Neural Cells ◽  
Amyloid Β Peptide

Evidence of oxidative damage in Alzheimer's disease brain: central role for amyloid β-peptide

2001 ◽  
Vol 7 (12) ◽  
pp. 548-554 ◽  
Author(s):  
D.Allan Butterfield ◽  
Jennifer Drake ◽  
Chava Pocernich ◽  
Alessandra Castegna
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oxidative Damage ◽  
Amyloid Β ◽  
Amyloid Β Peptide
Sign in / Sign up

Export Citation Format

Share Document