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Alzheimers

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by

Funbi Olowlafe

on 26 May 2014

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Transcript of Alzheimers

Tau Tangles & Amyloid Plaques
Neuropathology:
Genetics
Sporadic vs Familial
Tau Tangles
Amyloid Precursor Protein (APP)
Proteolysis
Beta Amyloid (Aβ) peptides
Degradation
Aβ accumulation
AD
Aβ peptides
GSK-3
Hyperphosphorylated Tau
Phosphorylation
Activation
Apoptosis
In vivo models
In vitro models
Advantages
Disadvantages
Identify heterogeneity
Non invasive tissue sampling
Drugs Screening
Difficult to stimulate ageing
Disrupts the interconnected nature between various cell types found in the brain
The Future of iPSC?
Non-neuronal cell involvement
When degeneration = pathology
When degeneration is conducive to drugs
Universality of drugs
Regeneration
What is Ageing?
Why do we Age?
Ageing
IGF Signaling Pathway
Relationship between IGF, Insulin and AD
Morris Water Maze
AAP23 Mice Model
Telomere shortening
Therapeutic targets
IGF
ROS & ApoE
WE CAN'T STOP AGEING!
APP
Tau
Neurotrophins and Growth Factors
Oxidative capacity
Metabolism
Physical Activity and APP
TgCRND8 mice
Improved water maze performance
Tau pathology
BDNF Protein
IGF-1
Conclusion
1.5 Million
AD increasing
Who is susceptible?
Age
Men
Women
Sex
Lifestyle
Blacks
Hispanics
Depression
Exercise
Diabetes
High blood pressure
Education
Physical activity and Tau
Heterogeneity
Phenotypes manifest in months not years
Genetics
Lifestyle
Advantages
Disadvantages
Neuropathological hallmarks
Isolated pathological components
Little neurodegeneration
The End
Behavioural alternations
Learning and memory impairement
Aberrant network connections
Genes involved in sporadic AD
Heterogeneity
Are there good experimental models for Alzheimer's Disease
?
Alzheimer's is multifactorial
No cure available yet
Multiple therapeutic targets developed
Ageing is inevitable
Exercise!
But...
Full transcript