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Record W2067396447 · doi:10.3389/fneur.2013.00194

The Cell and Molecular Biology of Neurodegenerative Diseases: An Overview

2013· article· en· W2067396447 on OpenAlexaff
Heather L. Montie, Thomas M. Durcan

Bibliographic record

VenueFrontiers in Neurology · 2013
Typearticle
Languageen
FieldNeuroscience
TopicNeurological diseases and metabolism
Canadian institutionsMontreal Neurological Institute and Hospital
Fundersnot available
KeywordsNeurodegenerationNeuroscienceMolecular cell biologyBiologyCognitive scienceMedicinePsychologyDiseasePathologyCell biology

Abstract

fetched live from OpenAlex

In this research topic, the primary focus is on understanding the cellular and molecular mechanisms in the pathogenesis of different neurodegenerative disorders.These include Alzheimer's disease (AD), Parkinson's disease (PD), and polyglutamine (polyQ) expansion diseases.To date, no cure exists for these disorders and it is paramount that research efforts continue to focus on understanding the molecular underpinnings behind these disorders.This will enable better symptom-directed therapeutics and perhaps even curative treatments to be developed.Throughout this topic, it becomes evident that there are common cellular pathways that are altered in these disorders, including protein, mitochondrial, and transcriptional homeostasis.In the case of AD, it has become widely accepted that AD is a synaptopathy, meaning that there is a loss or damage of synapses.This damage to synapses leads to altered neuronal circuitry.The neuronspecific, post-synaptic protein, Arc, has gained recent attention for its contribution in the regulation of memory consolidation.Kerrigan and Randall (1) discuss how alterations of Arc protein in the brains of AD patients and animal models of AD may be a clue as to how synaptic transmission is altered in AD, and how this cellular pathway may be of interest for therapeutic development.The next three reviews discuss the molecular events underlying PD and how the normal function of specific proteins associated with PD can help shed light on the causes of familial and sporadic PD.Lim and Zhang (2) outline a range of studies that implicate aberrations in mitochondrial function and protein homeostasis, with oxidative stress as the possible link between these two.A review from Dr. Edward A. Fon's group complements this discussion by focusing on the structure and function of Parkin, PINK1, and DJ-1 as they relate to PD (3).The second review from Dr. Fon's group digs even deeper into the role of Parkin and PINK1 in mitophagy in neurons.They discuss the importance of research initiatives to better define the roles of these two proteins in mitophagy and, in particular, within the context of a neuronal setting (4).The next five reviews focus on polyQ expansion diseases.Almeida et al. (5) provide a structural and functional view of trinucleotide repeats and encoded homopeptide expansions, emphasizing polyQ expansions and their role in inducing the self-assembly, aggregation, and functional alterations of the protein, leading to neuronal toxicity and cell death.These authors focus on ataxin-3 and huntingtin (Htt), the main protein implicated in Machado-Joseph Disease (MJD) and Huntington's disease (HD) respectively.

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)0.001
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: Not applicable · Consensus signal: none
GenreCandidate signal: Review · Consensus signal: Review
Teacher disagreement score0.004
Threshold uncertainty score0.012

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0020.001
Bibliometrics0.0030.003
Science and technology studies0.0010.001
Scholarly communication0.0020.004
Open science0.0010.001
Research integrity0.0020.003
Insufficient payload (model declined to judge)0.0040.003

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 head0.018
GPT teacher head0.269
Teacher spread0.250 · 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 designNot applicable
Domainnot available
GenreReview

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

Citations15
Published2013
Admission routes1
Has abstractyes

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