Christoffer G. Alexandersen

Rise-and-fall dynamics reveal a molecular and cellular vulnerability axis in prion-like α-synuclein propagation

The paper analyzes longitudinal histopathology data to show that α-synuclein pathology follows rise-and-fall dynamics, revealing a vulnerability axis linked to energy metabolism and monoaminergic neurons.

Neuronal activity and amyloid-beta cause tau seeding in the entorhinal cortex in Alzheimer's disease

The paper uses a computational model to show neuronal activity and amyloid-beta drive tau seeding in the entorhinal cortex, linking these factors to early Alzheimer's disease pathology.

The fluctuations of alpha power: bimodalities, connectivity, and neural mass models

This study examines dynamic alpha power fluctuations, their relationship with functional connectivity, and the ability of a neural mass model to replicate these patterns using MRI and MEG data.

A mean-field to capture asynchronous irregular dynamics of conductance-based networks of adaptive quadratic integrate-and-fire neuron models

The paper adapts a mean-field model to quadratic integrate-and-fire neuron models with adaptation and conductance-based synapses, validating it against a spiking network model.

Neuronal activity induces symmetry breaking in neurodegenerative disease spreading

The paper studies how neuronal activity influences the spread of toxic proteins in neurodegenerative diseases through a multi-timescale model of spreading on adaptive networks.

Pseudo-craniotomy of a whole-brain model reveals tumor-induced alterations to neuronal dynamics in glioma patients

The paper uses a whole-brain model to show glioma patients have altered neuronal dynamics compared to healthy controls, with changes in interregional coupling and excitability.

A mechanistic model explains oscillatory slowing and neuronal hyperactivity in Alzheimer's disease

This paper models the spread of amyloid-β and tau in the human brain to explain Alzheimer's disease-related neuronal hyperactivation, frequency slowing, and hypoactivation.