Alzheimer's
Definition
Alzheimer's disease is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and behavioral changes. It is the most common cause of dementia, affecting millions worldwide. The disease involves the accumulation of amyloid-beta plaques and tau protein tangles in the brain, leading to neuronal death and synaptic dysfunction. Key pathological features include oxidative stress, neuroinflammation, mitochondrial dysfunction, and disrupted neurotransmitter systems, particularly cholinergic signaling. Genetic risk factors include APOE4 variants, while mutations in APP, PSEN1, and PSEN2 genes cause early-onset familial forms. Understanding the complex molecular networks underlying Alzheimer's is crucial for developing effective therapeutics and biomarkers.
Visualize Alzheimer's in Nodes Bio
Researchers can use Nodes Bio to map complex molecular interactions in Alzheimer's pathology, visualizing relationships between amyloid-beta processing pathways, tau phosphorylation cascades, and inflammatory signaling networks. Network analysis reveals key hub proteins, identifies potential drug targets, and explores how genetic variants influence disease progression through multi-omics integration of genomic, proteomic, and transcriptomic data.
Visualization Ideas:
- Amyloid-beta processing pathway network with APP, BACE1, and gamma-secretase interactions
- Tau phosphorylation cascade showing kinases and phosphatases involved in neurofibrillary tangle formation
- Multi-omics integration network connecting genetic risk variants, gene expression changes, and protein-protein interactions in Alzheimer's brain tissue
Example Use Case
A pharmaceutical research team investigating novel Alzheimer's therapeutics uses network analysis to identify druggable targets. They integrate protein-protein interaction data with gene expression profiles from patient brain tissue, revealing that neuroinflammatory pathways centered around microglia activation strongly correlate with disease severity. By visualizing the network connections between TREM2, complement cascade proteins, and amyloid-beta clearance mechanisms, they identify a previously overlooked kinase as a potential therapeutic intervention point that could modulate both inflammation and protein aggregation simultaneously.