Related Experiment Video
Updated: Jul 20, 2026

09:22
In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
Published on: January 2, 2015
A longitudinal model for tau aggregation in Alzheimer's disease based on structural connectivity
Fan Yang1,2, Samadrita Roy Chowdhury1,2, Heidi I L Jacobs2
1Department of Electrical and Computer Engineering, University of Massachusetts Lowell, Lowell, MA, USA.
Summary
This study introduces a network diffusion model to track tau spread in Alzheimer's disease (AD). The model uses brain connectivity to predict tau buildup, offering insights into disease progression.
Area of Science:
- Neuroscience
- Medical Imaging
- Computational Biology
Background:
- Tau tangles are key Alzheimer's disease (AD) markers, correlating with cognitive decline.
- Tau spread in the brain follows neural connections, not just physical proximity.
Purpose of the Study:
- To develop and validate a network diffusion model for tau aggregation in the aging brain.
- To identify mechanisms of tau buildup using neuroimaging data and network analysis.
Main Methods:
- Utilized longitudinal tau Positron Emission Tomography (PET) and structural connectivity Diffusion Tensor Imaging (DTI).
- Employed graph Laplacians as diffusion kernels and sparse source localization for model fitting.
- Validated the parametric model on an independent cohort to predict future tau buildup.
Main Results:
- Identified distinct propagative and generative patterns of tau buildup at a population level.
- Successfully predicted future tau accumulation with high accuracy.
- The model quantifies network-based tau spread and identifies seeding regions.
Conclusions:
- The network diffusion model accurately captures tau spread mechanisms in the aging brain.
- This approach provides a macroscopic view of tau pathology progression in Alzheimer's disease.
- The model successfully differentiates between network-driven spread and regional seeding.
Related Concept Videos
Alzheimer's Disease: Overview
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Dementia l: Introduction
Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...

