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Printable Handouts
Navigable Slide Index
- Introduction
- Advances in technology
- Alzheimer: senile plaques
- Ancient history: Mendelian disease
- AD/FTDP-17: Pathways to neurodegeneration
- Summary so far
- IGAP Alzheimer analysis 74,000 subjects
- Examples of risk loci for Alzheimer’s disease (AD)
- Cholesterol metabolism in the aetiology of AD
- TREM2 loss of function mutations
- Corroborating evidence
- TREM2 mutations in AD
- Lipomembranous polycystic osteodysplasia
- TREM2 expression during plaque development
- Whole genome databases of gene expression
- Plaque and amyloid pathology-associated genes
- Network analysis of altered gene expression
- Abi3 & Plcg2: same ‘immune’ module as Trem2
- Lipid metabolism in the aetiology of Alzheimer’s
- Risk factors in the innate immune system
- More evidence for innate immune cell involvement
- Apolipoprotein E (ApoE)
- ABCA7 is primarily a phospholipid transporter
- Phospholipids are TREM2 ligands
- Amyloid precursor protein (APP)
- Amyloid clearance by ApoE and Microglia
- Pathogenesis length explains drug trial failure
- Alzheimer, markers and disease
- Tangle pathology potentiation
- Tangle imaging in the human brain
- Summary of amyloid pathology
- Therapeutic intervention: what and when?
- Early identification of disease onset
- ROC curves for pathologic AD using PRS
- Possible presymptomatic diagnostic path
- The future
Topics Covered
- Advances in technology
- Alzheimer: senile plaques
- Examples of risk loci for Alzheimer’s disease (AD)
- TREM2 mutations in AD
- Genomic analysis of Alzheimer’s disease
- Plaque and amyloid pathology
- Lipid metabolism in the aetiology of AD
- Risk factors expressed in the innate immune system
- Implications for therapy
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Hardy, J. (2017, October 31). Alzheimer's disease: where are we up to? [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 14, 2024, from https://doi.org/10.69645/DKDG4319.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. John Hardy, Consultant: Eisai Speaker's Bureau: Eli Lily Grant/Research Support (Principal Investiqator): MRC/Wellcome Trust
Alzheimer's disease: where are we up to?
Other Talks in the Series: Periodic Reports: Advances in Clinical Interventions and Research Platforms
Transcript
Please wait while the transcript is being prepared...
0:00
My name is John Hardy,
and I'm a professor at the UCL Institute of Neurology in London.
And my group works on the genetic analysis of Alzheimer's disease.
And this has been an area in which there has been a lot of work over the last five years.
And the power of genetic analysis has increased over this period, too.
So, we're now making a lot of findings in this disease area.
However, the utility of genetic analysis is becoming questioned,
because we have not yet developed therapies for the disease.
And so, the promise of genetic analysis has been that,
by understanding the genes for the disease,
we would be able to develop therapies.
And so far, that has not been the case.
And in this lecture,
I'm both going to talk about the genetic analysis and the findings that have been made,
and also discuss why there have been problems in getting to therapies.
So by the end of the lecture,
I hope you have an understanding of where genetic analysis is,
and how I hope that things will move in the future.
1:15
So, we live in a time where because of the power of genetic analysis,
we have many many genes for diseases in general;
not just Alzheimer's disease,
but in all diseases for which there has been extensive genetic analysis,
we're now finding many genes for those diseases.
And our intention is to map these genes into pathways for disease,
and to use this understanding of pathways to develop therapeutics.