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Record W2753483016

Determination of the Sub-cellular Mechanisms Underlying Neurodegeneration in Parkinson's Disease

2013· dissertation· en· W2753483016 on OpenAlexvenueno aff
C. J. Yong-Kee

Bibliographic record

VenueLibrary and Archives Canada (Government of Canada) · 2013
Typedissertation
Languageen
FieldNeuroscience
TopicGenetic Neurodegenerative Diseases
Canadian institutionsnot available
Fundersnot available
KeywordsNeurodegenerationParkinson's diseaseNeuroscienceDiseaseMedicineBiologyPathology
DOInot available

Abstract

fetched live from OpenAlex

Parkinson’s disease (PD) is the second most common neurodegenerative disease affecting approximately 1.8% of the population over 65 years of age. It is characterized by three cardinal symptoms: bradykinesia, muscle rigidity and resting tremor. Symptoms are presented following 50% loss of dopaminergic neurons within the substantia nigra pars compacta (SNc). Neurodegeneration is associated with reactive oxygen species (ROS) production, protein aggregation, mitochondrial dysfunction, ubiquitin-proteasome system (UPS) inhibition and lysosomal malfunction; however it is unclear if a single mechanism or multiple mechanisms lead to disease onset. The primary aim of the studies described in this thesis was to elucidate the interactions between various pathological mechanisms underlying PD pathology. An examination of organelle function during exposure of SH-SY5Y neuroblastoma to a variety of toxins which mimic purported pathological processes in PD reveal mitochondrial membrane potential becomes depolarized, not only following mitochondrial impairment, but also after the UPS and lysosome are inhibited. Given that mitochondrial dysfunction appeared to be central to PD pathology, mitochondrial dysfunction was studied in more detail. Mitochondrial fission and fusion maintains mitochondrial integrity, which is critical to neuronal health. Thus, we examined mitochondrial dynamics in a common genetic variant linked with familial PD, known as leucine-rich repeat kinase 2 (LRRK2). Upon the expression of wild-type and mutant LRRK2, mitochondrial fusion was inhibited causing fragmentation of mitochondria. This inhibition of fusion may be the initial step leading to mitochondrial dysfunction, since inhibition of fusion occurs prior to the induction of cell stress. The findings that mitochondrial dysfunction appears to be central to PD pathology, suggest that mitochondria may be an excellent therapeutic target for PD. Thus, the potential neuroprotective function of a regulator of mitochondrial function, known as SIRT3 was examined. In SH-SY5Y cells, over-expression of SIRT3 protected neurons from degeneration associated with LRRK2 over-expression. The studies described in this thesis provide evidence that multiple sub-cellular mechanisms converge to inhibit mitochondrial function. Furthermore, mitochondrial dynamics which regulate mitochondrial function could be a key mediator in the pathology associated with PD. The work herein suggests therapies which target the mitochondria are likely to be successful in the treatment of PD.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Other · Consensus signal: none
Teacher disagreement score0.000
Threshold uncertainty score0.002

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.009
GPT teacher head0.175
Teacher spread0.166 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreOther

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2013
Admission routes1
Has abstractyes

Explore more

Same venueLibrary and Archives Canada (Government of Canada)→Same topicGenetic Neurodegenerative Diseases→French-language works237,207→