Project acronym GEM
Project Generalised Entropy Models for Spatial Choices
Researcher (PI) Mogens FOSGERAU
Host Institution (HI) KOBENHAVNS UNIVERSITET
Call Details Advanced Grant (AdG), SH2, ERC-2016-ADG
Summary This project will create a new category of models that can be used for describing a wide range of spatial choice problems in the social sciences. Spatial settings often have a very large number of choice alternatives. Discrete choice models are used extensively to make counterfactual predictions based on observations of individual choices. Despite forty years of research, current spatial choice models still have two major generic short-comings that seriously limit their ability to make counterfactual predictions. The new category of models will address these two short-comings.
The first issue is that substitution patterns between choice alternatives are very complex. The new models will allow substitution patterns to be specified in a general and transparent way. The second issue is that so-called endogeneity issues are pervasive, which violates the underlying statistical assumptions of common models and leads to inconsistent results. The new models will enable endogeneity issues to be dealt with in a simple way.
The new models rely on a concept of generalised entropy and are related via duality to classical discrete choice models. A generalised entropy model, or just GEM, will be specified in terms of a transformation from choice probabilities to utilities. This idea is completely new. It is the exact opposite of classical discrete choice models and makes available a whole universe of new models. Early results suggest that GEM will enable the short-comings of the standard models to be overcome.
The project develops GEM in three prototypical spatial contexts: equilibrium sorting of households, travel demand modelling, and network route choice.
Classical discrete choice models are extensively used for policy analysis and planning. Replacing these by GEM will therefore influence a multitude of decisions across a range of sectors of great societal importance with environmental, economic and welfare consequences that reach far into the future.
Summary
This project will create a new category of models that can be used for describing a wide range of spatial choice problems in the social sciences. Spatial settings often have a very large number of choice alternatives. Discrete choice models are used extensively to make counterfactual predictions based on observations of individual choices. Despite forty years of research, current spatial choice models still have two major generic short-comings that seriously limit their ability to make counterfactual predictions. The new category of models will address these two short-comings.
The first issue is that substitution patterns between choice alternatives are very complex. The new models will allow substitution patterns to be specified in a general and transparent way. The second issue is that so-called endogeneity issues are pervasive, which violates the underlying statistical assumptions of common models and leads to inconsistent results. The new models will enable endogeneity issues to be dealt with in a simple way.
The new models rely on a concept of generalised entropy and are related via duality to classical discrete choice models. A generalised entropy model, or just GEM, will be specified in terms of a transformation from choice probabilities to utilities. This idea is completely new. It is the exact opposite of classical discrete choice models and makes available a whole universe of new models. Early results suggest that GEM will enable the short-comings of the standard models to be overcome.
The project develops GEM in three prototypical spatial contexts: equilibrium sorting of households, travel demand modelling, and network route choice.
Classical discrete choice models are extensively used for policy analysis and planning. Replacing these by GEM will therefore influence a multitude of decisions across a range of sectors of great societal importance with environmental, economic and welfare consequences that reach far into the future.
Max ERC Funding
2 500 000 €
Duration
Start date: 2017-09-01, End date: 2022-08-31
Project acronym GlymphEye
Project The Ocular Glymphatic System
Researcher (PI) Maiken Nedergaard
Host Institution (HI) KOBENHAVNS UNIVERSITET
Call Details Advanced Grant (AdG), LS5, ERC-2016-ADG
Summary The glymphatic system is a highly organized brain-wide mechanism by which fluid wastes are removed from the brain that was recently described by my team. The glymphatic system clears 65% of amyloid-beta from the normal adult brain. A rapidly evolving literature has shown that the major neurodegenerative diseases of the eye, macular degeneration and glaucoma, may also result from the toxicity of uncleared protein wastes, including amyloid-beta. Yet the eye, like the brain, has no traditional lymphatic vessels. In this application, I propose that two of the most significant causes of human visual loss, macular degeneration and glaucoma – previously thought of as both intractable and unrelated – are instead mechanistically allied disorders that not only share a common causal pathway, but may both be therapeutically modified by targeting dysregulation of the glymphatic pathway. As such, this proposal seeks to link the biology of a fundamentally new pathway for both metabolic substrate and waste transport in the adult brain, to diseases of the eye that have long been resistant to either understanding or treatment.
The objectives: WP1: Define the cellular mechanisms that drive ocular glymphatic transport of Amyloid-beta using an ex vivo preparation of the optic nerve. WP2: Use magnetic resonance imaging (MRI) to establish the existence of ocular glymphatic transport in live animals. WP3: Determine whether the ocular glymphatic system, like the brain lymphatic system, is critically regulated by the sleep-wake cycle. WP4: Test the hypothesis that age-dependent macular degeneration is caused by a suppression of ocular glymphatic transport, with secondary accumulation of toxic protein products in and subjacent to the retinal pigment epithelium? WP5: Define the impact of increased intraocular pressure on glymphatic export of amyloid-beta, and test the hypothesis that the decrease in ocular glymphatic transport contributes to degeneration of retinal ganglion cells in glaucoma.
Summary
The glymphatic system is a highly organized brain-wide mechanism by which fluid wastes are removed from the brain that was recently described by my team. The glymphatic system clears 65% of amyloid-beta from the normal adult brain. A rapidly evolving literature has shown that the major neurodegenerative diseases of the eye, macular degeneration and glaucoma, may also result from the toxicity of uncleared protein wastes, including amyloid-beta. Yet the eye, like the brain, has no traditional lymphatic vessels. In this application, I propose that two of the most significant causes of human visual loss, macular degeneration and glaucoma – previously thought of as both intractable and unrelated – are instead mechanistically allied disorders that not only share a common causal pathway, but may both be therapeutically modified by targeting dysregulation of the glymphatic pathway. As such, this proposal seeks to link the biology of a fundamentally new pathway for both metabolic substrate and waste transport in the adult brain, to diseases of the eye that have long been resistant to either understanding or treatment.
The objectives: WP1: Define the cellular mechanisms that drive ocular glymphatic transport of Amyloid-beta using an ex vivo preparation of the optic nerve. WP2: Use magnetic resonance imaging (MRI) to establish the existence of ocular glymphatic transport in live animals. WP3: Determine whether the ocular glymphatic system, like the brain lymphatic system, is critically regulated by the sleep-wake cycle. WP4: Test the hypothesis that age-dependent macular degeneration is caused by a suppression of ocular glymphatic transport, with secondary accumulation of toxic protein products in and subjacent to the retinal pigment epithelium? WP5: Define the impact of increased intraocular pressure on glymphatic export of amyloid-beta, and test the hypothesis that the decrease in ocular glymphatic transport contributes to degeneration of retinal ganglion cells in glaucoma.
Max ERC Funding
2 176 250 €
Duration
Start date: 2017-09-01, End date: 2022-08-31
