A Patient With Suspicious Oxygen Desaturations at Sleep Onset

Wagner, Mary H.; Raza, Wajiha; Esteves, Arnaldo Reyes; Ryals, Scott; Berry, Richard B.

doi:10.5664/jcsm.7294

Cited by 1 publication

(2 citation statements)

References 2 publications

(4 reference statements)

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“…Interestingly, phospho-Tau levels were decreased in SNpc and cortical samples. Previous in vitro studies showed that microtubule disassembly induced by mitochondrial dysfunction impairs autophagy and decreases lysosomal activation leading to SNCA aggregation and neurodegeneration 17 . Herein, we observed an increase in LC3II levels and a decrease in Cathepsin D (CatD) levels ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…We showed in PD cellular models that mitochondrial dysfunction triggers abnormal microtubule protein posttranslational modifications (PTMs), namely tubulin and tau acetylation and tau phosphorylation 10 , 17 , 18 . Additionally, it is well accepted that mitochondrial pools are dysfunctional in PD brain, namely in SNpc 19 and also in peripheral cells 20 , 21 .…”

Section: Resultsmentioning

confidence: 99%

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Differential protein expression in diverse brain areas of Parkinson’s and Alzheimer’s disease patients

Esteves

Cardoso

2020

Sci Rep

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Many hypotheses have been postulated to define the etiology of sporadic Parkinson's and Alzheimer's disorders (PD and AD) but there is no consensus on what causes these devastating age-related diseases. Braak staging of both pathologies helped researchers to better understand the progression and to identify their prodromal and symptomatic phases. Indeed, it is well accepted that Lewy body pathology and neurofibrillary tangles appearance correlates with disease progression and severity of symptoms in PD and AD, respectively. Additionally, several studies in PD and AD models try to disclose which cellular mechanisms are defaulted and trigger the neurodegenerative process that culminates with neuronal death causing PD and AD classical symptomatology. Herein, we determined expression levels of proteins involved in microtubule assembly, autophagic-lysosomal pathway and unfolded protein response in the cortex, hippocampus and SNpc of PD and AD patients, vascular dementia patients and aged-match controls. The differential expression allowed us to determine which pathways are determinant to synaptic dysfunction and to establish a time line for disease progression. Our results allow us to challenge the hypothesis that both PD and AD pathologies are caused by α-synuclein or Aβ pathology propagation throughout the brain in a prion-like manner.

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Section: Resultsmentioning

confidence: 99%