The Diseases Dashboard provides a comprehensive overview of neurodegenerative disease coverage in NeuroWiki. This page serves as a central navigation hub for finding disease information by category, progression stage, and research focus. [1]
| Metric | Value | [2]
|--------|-------|
| Total Disease Pages | 373 |
| Alzheimer's Related | ~40 |
| Parkinson's Related | ~25 |
| FTD Variants | ~15 |
| ALS Variants | ~10 |
| Rank | Disease | Severity | Key Mechanism |
|---|---|---|---|
| 1 | ALS | Very High | Motor neuron degeneration |
| 2 | FTD | High | Frontotemporal atrophy |
| 3 | Parkinson's | Moderate-High | Dopaminergic loss |
| 4 | Alzheimer's | Moderate | Amyloid/tau pathology |
NeuroWiki documents the major molecular and cellular pathways implicated in neurodegenerative diseases. These pathways form the mechanistic basis for understanding disease progression and identifying therapeutic targets.
Amyloid Processing Pathway: The amyloid precursor protein (APP) is cleaved by beta-secretase (BACE1) and gamma-secretase to produce amyloid-beta peptides. Aggregated amyloid-beta forms plaques that disrupt synaptic function and trigger neuroinflammation. See Amyloid Cascade Hypothesis for detailed mechanism.
Tau Pathology Pathway: Hyperphosphorylated tau protein dissociates from microtubules and forms neurofibrillary tangles (NFTs). This disrupts axonal transport and leads to neuronal death. The tau propagation model describes how pathological tau spreads between connected neurons. See Tau Pathogenesis.
Alpha-Synuclein Aggregation: Native alpha-synuclein misfolds and forms oligomers, then fibrils, and eventually Lewy bodies. This process is implicated in Parkinson's disease and dementia with Lewy bodies. The spreading hypothesis suggests prion-like transmission between cells. See Alpha-Synuclein Pathology.
Neuroinflammation Cascade: Activated microglia release pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) that create a chronic inflammatory environment. This neuroinflammation accelerates neuronal loss and exacerbates protein aggregation. See Neuroinflammation Mechanisms.
Mitochondrial Dysfunction: Impaired mitochondrial function leads to reduced ATP production, increased reactive oxygen species (ROS), and apoptosis activation. Mitochondrial DNA mutations accumulate in neurons with age. See Mitochondrial Pathways.
Current research in neurodegenerative diseases focuses on several key areas that NeuroWiki tracks comprehensively:
Genetic Risk Factors: Genome-wide association studies (GWAS) have identified numerous risk loci for AD and PD. Key genes include APOE, TREM2, and CLU for Alzheimer's, and LRRK2, GBA, and SNCA for Parkinson's. NeuroWiki maintains detailed gene-disease association pages.
Biomarker Development: Researchers are developing fluid biomarkers (Aβ42, tau, α-synuclein) and imaging biomarkers (PET tracers, MRI) for early diagnosis and disease monitoring. The Biomarkers section tracks these advances.
Therapeutic Strategies: Drug development focuses on disease-modifying therapies targeting amyloid, tau, α-synuclein, and neuroinflammation. The Treatments section documents clinical trials and approved therapies.
NeuroWiki ranks diseases by various severity metrics to help prioritize research and treatment efforts:
| Rank | Disease | Key Features |
|---|---|---|
| 1 | Alzheimer's Disease | Most prevalent, progressive cognitive decline |
| 2 | Parkinson's Disease | Motor symptoms, Lewy body pathology |
| 3 | ALS | Rapid progression, motor neuron degeneration |
| 4 | Frontotemporal Dementia | Behavioral variant, language deficits |
| 5 | Huntington's Disease | Genetic, movement and cognitive decline |