Summary
With the NeutrAD ERC PoC project, we present the first disease-modifying Alzheimer’s Disease (AD) drugs that abrogate leukocyte-mediated neurotoxicity and represent a novel class of drugs in the treatment of AD.
AD is a neurological disorder characterized by progressive deterioration of cognitive function and leads to death within 3-9 years after diagnosis. AD is highly prevalent in elderly, and it is estimated that 35M patients suffer from the disease worldwide. As a result, AD has tremendous social and economic impact. This is aggravated by the lack of disease-modifying drugs, as current therapies only provide short-term symptomatic benefit. Hence, novel therapeutic approaches are of critical importance to resolve this urgent and growing health crisis.
Our novel anti-AD drug candidates use a neutrophil-targeted approach and unlock a novel avenue for the millions that suffer from AD. Growing evidence supports the role of inflammation in the development of neurodegeneration in AD. For example, our previous research has demonstrated a role for neutrophils in the induction of memory decline and neuropathological hallmarks of AD. Furthermore, our data shows that a highly activated and degranulating neutrophil phenotype induces neurotoxicity in an in vitro AD context. Preliminary results have also demonstrated that our novel drug candidates rescue neuronal death and have disease-modifying potential in AD-like mouse models.
In NeutrAD, we will explore the technical and commercial potential of our drug candidates as the first disease-modifying drugs against AD. Specifically, we will optimise and subsequently test the technical feasibility of our two drug candidates in AD-like in vitro and in vivo models. In parallel, we will explore the commercial opportunity of our novel AD drugs and analyse the IP position and strategy, as well as the market and (existing and emerging) competitors. Finally, we will consolidate the project outcomes in an investor-ready business plan.
AD is a neurological disorder characterized by progressive deterioration of cognitive function and leads to death within 3-9 years after diagnosis. AD is highly prevalent in elderly, and it is estimated that 35M patients suffer from the disease worldwide. As a result, AD has tremendous social and economic impact. This is aggravated by the lack of disease-modifying drugs, as current therapies only provide short-term symptomatic benefit. Hence, novel therapeutic approaches are of critical importance to resolve this urgent and growing health crisis.
Our novel anti-AD drug candidates use a neutrophil-targeted approach and unlock a novel avenue for the millions that suffer from AD. Growing evidence supports the role of inflammation in the development of neurodegeneration in AD. For example, our previous research has demonstrated a role for neutrophils in the induction of memory decline and neuropathological hallmarks of AD. Furthermore, our data shows that a highly activated and degranulating neutrophil phenotype induces neurotoxicity in an in vitro AD context. Preliminary results have also demonstrated that our novel drug candidates rescue neuronal death and have disease-modifying potential in AD-like mouse models.
In NeutrAD, we will explore the technical and commercial potential of our drug candidates as the first disease-modifying drugs against AD. Specifically, we will optimise and subsequently test the technical feasibility of our two drug candidates in AD-like in vitro and in vivo models. In parallel, we will explore the commercial opportunity of our novel AD drugs and analyse the IP position and strategy, as well as the market and (existing and emerging) competitors. Finally, we will consolidate the project outcomes in an investor-ready business plan.
Unfold all
/
Fold all
More information & hyperlinks
Web resources: | https://cordis.europa.eu/project/id/101069397 |
Start date: | 01-06-2022 |
End date: | 31-05-2024 |
Total budget - Public funding: | - 150 000,00 Euro |
Cordis data
Original description
With the NeutrAD ERC PoC project, we present the first disease-modifying Alzheimer’s Disease (AD) drugs that abrogate leukocyte-mediated neurotoxicity and represent a novel class of drugs in the treatment of AD.AD is a neurological disorder characterized by progressive deterioration of cognitive function and leads to death within 3-9 years after diagnosis. AD is highly prevalent in elderly, and it is estimated that 35M patients suffer from the disease worldwide. As a result, AD has tremendous social and economic impact. This is aggravated by the lack of disease-modifying drugs, as current therapies only provide short-term symptomatic benefit. Hence, novel therapeutic approaches are of critical importance to resolve this urgent and growing health crisis.
Our novel anti-AD drug candidates use a neutrophil-targeted approach and unlock a novel avenue for the millions that suffer from AD. Growing evidence supports the role of inflammation in the development of neurodegeneration in AD. For example, our previous research has demonstrated a role for neutrophils in the induction of memory decline and neuropathological hallmarks of AD. Furthermore, our data shows that a highly activated and degranulating neutrophil phenotype induces neurotoxicity in an in vitro AD context. Preliminary results have also demonstrated that our novel drug candidates rescue neuronal death and have disease-modifying potential in AD-like mouse models.
In NeutrAD, we will explore the technical and commercial potential of our drug candidates as the first disease-modifying drugs against AD. Specifically, we will optimise and subsequently test the technical feasibility of our two drug candidates in AD-like in vitro and in vivo models. In parallel, we will explore the commercial opportunity of our novel AD drugs and analyse the IP position and strategy, as well as the market and (existing and emerging) competitors. Finally, we will consolidate the project outcomes in an investor-ready business plan.
Status
SIGNEDCall topic
ERC-2022-POC1Update Date
09-02-2023
Images
No images available.
Geographical location(s)
Structured mapping