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Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes
TLDR
A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented. Expand
Iron accumulation in Alzheimer disease is a source of redox-generated free radicals.
TLDR
It is found, using a modified histochemical technique that relies on the formation of mixed valence iron complexes, that redox-active iron is associated with the senile plaques and neurofibrillary tangles-the pathological hallmark lesions of Alzheimer disease. Expand
Oxidative Damage Is the Earliest Event in Alzheimer Disease
TLDR
The observations indicate that increased oxidative damage is an early event in AD that decreases with disease progression and lesion formation and suggest that AD is associated with compensatory changes that reduce damage from reactive oxygen. Expand
Mitochondrial Abnormalities in Alzheimer's Disease
TLDR
Morphometric analysis showed that mitochondria are significantly reduced in Alzheimer's disease, and the relationship shown here between the site and extent of mitochondrial abnormalities and oxidative damage suggests an intimate and early association between these features in dementia. Expand
Impaired Balance of Mitochondrial Fission and Fusion in Alzheimer's Disease
TLDR
DLP1 overexpression, likely through repopulation of neuronal processes with mitochondria, prevented ADDL-induced synaptic loss, suggesting that abnormal mitochondrial dynamics plays an important role in ADDL -induced synaptic abnormalities. Expand
Oxidative stress in Alzheimer's disease.
TLDR
Determining which of the proposed sources of free radicals, which include mitochondrial dysfunction, amyloid-beta-mediated processes, transition metal accumulation and genetic factors like apolipoprotein E and presenilins, is responsible for redox imbalance will lead to a better understanding of Alzheimer's disease pathogenesis and novel therapeutic approaches. Expand
Widespread Peroxynitrite-Mediated Damage in Alzheimer’s Disease
TLDR
There is strong evidence that peroxynitrite is involved in oxidative damage of Alzheimer’s disease, and the widespread occurrence of nitrotyrosine in neurons suggests that oxidative damage is not restricted to long-lived polymers such as NFTs, but instead reflects a generalized oxidative stress that is important in disease pathogenesis. Expand
RNA Oxidation Is a Prominent Feature of Vulnerable Neurons in Alzheimer’s Disease
TLDR
Surprisingly, the oxidized nucleoside was associated predominantly with RNA because immunoreaction was diminished greatly by preincubation in RNase but only slightly by DNase, the first evidence of increased RNA oxidation restricted to vulnerable neurons in AD. Expand
Parkinson's disease is associated with oxidative damage to cytoplasmic DNA and RNA in substantia nigra neurons.
TLDR
Results suggest that oxidative damage to cytoplasmic nucleic acid is selectively increased in midbrain, especially the SN, of PD patients and much less so in MSA-P and DLB patients. Expand
LRRK2 regulates mitochondrial dynamics and function through direct interaction with DLP1.
TLDR
It is demonstrated that wild-type LRRK2 expression caused mitochondrial fragmentation along with increased mitochondrial dynamin-like protein (DLP1), a fission protein, which was further exacerbated by expression of PD-associated mutants (R1441C or G2019S) in both SH-SY5Y and differentiated primary cortical neurons. Expand
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