Notebook Artifact Registry

Computational analysis artifacts linked to analyses and knowledge graph entities

Filter by tag:All APOE4 Aging Allen Institute Alzheimer's CRISPR Circuit Analysis Cross-Age Analysis Epigenetics Gene Expression Immune Response Microglia Mouse Model Neural Dynamics Neurodegeneration Neuroinflammation Protein Propagation SEA-AD Senescent Cells Senolytics Structural Biology Tau Therapeutics []aging allen-brain allen-brain-atlas allen-institute alzheimers analysis artifact astrocytes auto biomarkers cell-atlas cell-types ci demo draft epigenetics forge-tools gene-editing gene-expression go hypotheses hypothesis-analysis kegg knowledge-gap lipid-rafts microglia neurodegeneration neuroinflammation neurons notebook pathway-enrichment reactome scanpy sea-ad seeded senescence showcase single-cell statistics stub tau template test transcriptomics tsne umap walkthrough

Sort:

🌟 Spotlight Notebooks

Gene Expression Changes in Aging Mouse Brain Predicting Neurodegenerative Vulnerability

Real Forge-powered analysis: PubMed search, STRING PPI, Reactome pathways, gene annotations for aging mouse brain transcriptomics.

showcase forge-tools transcriptomics neurodegeneration

📊 Gene expression changes in aging mouse brain predicting neurodegenerative vulnerability

Created: 2026-04-16

View Notebook →

Neuroinflammation and Microglial Priming in Early Alzheimer's Disease

Real Forge-powered analysis: PubMed search, STRING PPI, Reactome pathways, gene annotations for microglial priming in early AD.

showcase forge-tools neuroinflammation neurodegeneration

📊 Neuroinflammation and microglial priming in early Alzheimer's Disease

Created: 2026-04-16

View Notebook →

CRISPR-Based Therapeutic Approaches for Neurodegenerative Diseases

Real Forge-powered analysis: PubMed search, STRING PPI, Reactome pathways, gene annotations for CRISPR neurodegeneration therapy research.

showcase forge-tools gene-editing neurodegeneration

📊 CRISPR-based therapeutic approaches for neurodegenerative diseases

Created: 2026-04-16

View Notebook →

Mitochondrial Dysfunction as a Driver of Neurodegeneration

How does mitochondrial dysfunction drive neurodegeneration across AD, PD, and ALS? Characterize PINK1/Parkin mitophagy pathway, mtDNA damage, ETC complex activity, and ROS generati

[]

Created: 2026-04-13

View Notebook →

Tau Pathology Propagation in Tauopathies — Mechanistic Dissection

How does misfolded tau spread through the brain in tauopathies? Characterize prion-like propagation mechanisms, cell-to-cell transfer, and the role of MAPT mutations, ApoE genotype

[]

Created: 2026-04-13

View Notebook →

All Notebooks (11) (filtered by: draft)

Why have numerous phase 3 clinical trials failed despite advances in understanding AD pathobiology? - Analysis Notebook

CI-generated notebook stub for analysis SDA-2026-04-16-gap-pubmed-20260410-145418-c1527e7b. There's a clear disconnect between improved mechanistic understanding of AD and therapeutic success, with co

draft auto ci

📊 Why have numerous phase 3 clinical trials failed despite advances in understanding AD pathobiology? (neurodegeneration)

Created: 2026-04-17

Can P16INK4A expression reliably distinguish harmful from beneficial senescent microglia in neurodegeneration? — Analysis Notebook

CI-generated notebook stub for analysis SDA-2026-04-11-gap-debate-20260410-112619-9c3c13d2. The debate proposed P16INK4A-guided targeting but the Skeptic noted microglia exist in complex activation st

draft auto ci

📊 Can P16INK4A expression reliably distinguish harmful from beneficial senescent microglia in neurodegeneration? (neurodegeneration)

Created: 2026-04-12

What are the optimal timing windows for TREM2 agonism vs antagonism across disease progression stages? — Analysis Notebook

CI-generated notebook stub for analysis SDA-2026-04-11-gap-debate-20260410-112636-141592ba. The debate highlighted that TREM2 therapeutic targeting remains contested across disease stages, but no clea

draft auto ci

📊 What are the optimal timing windows for TREM2 agonism vs antagonism across disease progression stages? (neurodegeneration)

Created: 2026-04-12

How can CRISPR systems achieve persistent therapeutic effects while avoiding chronic immune responses to Cas proteins in the CNS? — Analysis Notebook

CI-generated notebook stub for analysis SDA-2026-04-11-gap-debate-20260410-112625-c44578b5. The debate highlighted that long-term CRISPR expression triggers immune responses, but epigenetic therapies

draft auto ci

📊 How can CRISPR systems achieve persistent therapeutic effects while avoiding chronic immune responses to Cas proteins in the CNS? (gene therapy)

Created: 2026-04-12

Which neural cell types exhibit the most pronounced gene expression alterations in neurodegeneration? — Analysis Notebook

CI-generated notebook stub for analysis SDA-2026-04-11-gap-debate-20260410-112336-ccdef571. The debate generated therapeutic hypotheses targeting different cell types but never resolved the fundamenta

draft auto ci

📊 Which neural cell types exhibit the most pronounced gene expression alterations in neurodegeneration? (neurodegeneration)

Created: 2026-04-12

Does SYK activation provide neuroprotection or exacerbate neuroinflammation in established Alzheimer's disease? — Analysis Notebook

CI-generated notebook stub for analysis SDA-2026-04-11-gap-debate-20260410-111113-052488a8. The debate revealed fundamental uncertainty about whether enhancing TYROBP-SYK signaling would be beneficial

draft auto ci

📊 Does SYK activation provide neuroprotection or exacerbate neuroinflammation in established Alzheimer's disease? (neurodegeneration)

Created: 2026-04-11

How do disease-associated mutations in G3BP1 or its binding partners alter stress granule dynamics? — Analysis Notebook

CI-generated notebook stub for analysis SDA-2026-04-06-gap-pubmed-20260406-041428-e14e6524. The study establishes G3BP1's role as a tunable switch for stress granule assembly, but doesn't address how

draft auto ci

📊 How do disease-associated mutations in G3BP1 or its binding partners alter stress granule dynamics? (neurodegeneration)

Created: 2026-04-06

APOE4-driven lipid metabolism dysregulation in astrocytes and its role in AD — Analysis Notebook

CI-generated notebook stub for analysis SDA-2026-04-04-gap-apoe4-lipid-metabolism. APOE4 is the strongest genetic risk factor for late-onset AD. How APOE4 specifically disrupts lipid homeostasis in as

draft auto ci

📊 APOE4-driven lipid metabolism dysregulation in astrocytes and its role in AD (neuroscience)

Created: 2026-04-05

epigenetic reprogramming aging neurons — Analysis Notebook

CI-generated notebook stub for analysis SDA-2026-04-04-gap-20260404-060512. epigenetic reprogramming aging neurons

draft auto ci

📊 epigenetic reprogramming aging neurons (neurodegeneration)

Created: 2026-04-05

Investigate prion-like spreading of tau pathology through connected brain regions — Analysis Notebook

CI-generated notebook stub for analysis SDA-2026-04-04-gap-20260404-052358. Investigate prion-like spreading of tau pathology through connected brain regions

draft auto ci

📊 Investigate prion-like spreading of tau pathology through connected brain regions (neurodegeneration)

Created: 2026-04-05

What are the mechanisms by which gut microbiome dysbiosis influences Parkinson's disease pathogenesis through the gut-brain axis? — Analysis Notebook

Computational analysis notebook for 'What are the mechanisms by which gut microbiome dysbiosis influences Parkinson's disease pathogenesis through the gut-brain axis?'. Domain: neurodegeneration. Rese

draft artifact notebook

📊 What are the mechanisms by which gut microbiome dysbiosis influences Parkinson's disease pathogenesis through the gut-brain axis? (neurodegeneration)

Created: 2026-04-04