For the third consecutive AD/PD bi-annual conference, this workshop will provide participants with an understanding of the common and distinct features of neurodegenerative diseases, which include not only those affecting the brain, such as Alzheimer’s disease, Parkinson’s disease, dementia with Lewy bodies, vascular dementia, frontotemporal dementia, and mixed dementia; but also the ocular diseases including age-related macular degeneration, glaucoma, diabetic retinopathy, and inherited retinal degenerative diseases.
This is a full day satellite workshop to AD/PD™ 2021, the 15th International Conference on Alzheimer’s & Parkinson’s Diseases.
- Diane Bovenkamp, PhD (BrightFocus Foundation)
- Guojun Bu, PhD (Mayo Clinic, Jacksonville, Florida)
- Adriana Di Polo, PhD (University of Montreal, Montreal, Canada)
- Todd E. Golde, MD, PhD (University of Florida in Gainesville, Florida)
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10:00 – 10:10
|WELCOME AND INTRODUCTION|
D. Bovenkamp welcome
G. Bu, A. Di Polo, T. Golde opening comments
10:10 – 10:30
WORKSHOP GENERAL DISCUSSION PRIMER
WHAT IS CELLULAR SENESCENCE AND WHAT IS ITS IMPACT IN NEURODEGENERATIVE DISEASES OF THE BRAIN AND EYE?
Section 1 Summary:
10:30 – 10:50
NOVEL TREATMENT MODELS ATTACKING SENESCENCE IN ALZHEIMER’S DISEASE
10:50 – 11:10
CELLULAR SENESCENCE IN THE EYE – FOCUS ON RETINA
11:10 – 11:30
AGEING, SENESCENCE AND NEURODEGENERATIVE DISEASES
11:30 – 11:50
|SENESCENCE-ASSOCIATED SECRETORY PHENOTYPE AND PATHOLOGICAL ANGIOGENESIS IN RETINOPATHY|
Mike Sapieha, Canada
HOW DOES RESILIENCE, FROM GENETICS TO ENVIRONMENTAL, AT THE CELLULAR, SYSTEMS, OR POPULATION LEVELS, PLAY A ROLE IN REDUCING RISK FOR NEURODEGENERATIVE DISEASE?
Chair: G. Bu, USA
|Section 2 Summary:|
Why do some people escape disease? Resilience occurs when risk factors or pathology are present, but that person doesn’t succumb to clinically detectable disease. At the cellular level, differential expression of genes, proteins and/or epigenetic markers makes one vulnerable or resistant to different eye or brain diseases. At the organismal level, how does one define that a tissue has pathology and how is that related to the ‘tipping point’ to develop cognitive or visual issues? At the population level, what are the origins of racial/ethnic, sex-based, environmental and other differences that can lead to one group being more resilient or at-risk than another? It’s more important than ever, when assessing resilience, to pursue a cross-disease, multi-organ, multi-cell type, and systemic approach.
|11:50 – 12:10||ASSESSMENT OF DEMOGRAPHIC, GENETIC, AND IMAGING VARIABLES ASSOCIATED WITH BRAIN RESILIENCE AND COGNITIVE RESILIENCE TO PATHOLOGICAL TAU IN PATIENTS WITH ALZHEIMER DISEASE|
Rik Ossenkoppele ,The Netherlands
|12:10 – 12:30|
RESISTANCE, RESILIENCE, RESERVE AND COMPENSATION
|12:30 – 12:50||APOE2 AND RARE PROTECTIVE VARIANTS AGAINST ALZHEIMER’S DISEASE: HOW DO THEY DO IT?|
G. Bu, USA
|12:50 – 13:10|
FUNCTIONAL RESILIENCE OF RETINAL GANGLION CELLS DURING MITOCHONDRIAL OXIDANT GENERATION
WHY ARE THE VASCULAR COMPONENTS AND BLOOD-BRAIN/BLOOD-RETINA BARRIERS OF THE BRAIN AND EYE IMPORTANT CONTRIBUTORS TO THE TIPPING POINT BETWEEN HEALTH AND DISEASE?
Section 3 Summary
Despite recent advances in our understanding of the pathology of cognitive and retinal degenerative diseases, the actual triggers that lead to neurodegeneration are not currently known. One of the ‘tipping points’ for the onset and progression of pathology can be dysfunction of the microvasculature, dysregulation of neurovascular coupling, and alteration of the blood-brain/blood-retinal barriers. Alzheimer’s, glaucoma, and macular degeneration all feature vascular abnormalities, but the full extent to which these factors contribute to the development of disease is not well understood. This session will explore the molecular and cellular mechanisms that could be exploited to better understand the role of microvascular components in the pathophysiology, risk assessment, diagnostic and novel therapeutic targets for brain and eye diseases.
|13:10 – 13:30||BIOENGINEERED VASCULAR MODELS FOR DEMENTIA (INVOLVING ENDOTHELIA, SMOOTH MUSCLE, AND ASTROCYTES)|
Cheryl Wellington, Canada
|13:30 – 13:50||INTERPERICYTE TUNNELLING NANOTUBES: A NEW CONDUIT ESSENTIAL FOR NEUROVASCULAR COUPLING|
Luis Alarcon Martinez, Australia
|13:50 – 14:10||ISCHEMIA-INDUCED CEREBROVASCULAR DYSREGULATION CONTRIBUTES TO ALZHEIMER’S DISEASE|
Anusha Mishra, USA
|14:10 – 14:30||BLOOD-BRAIN BARRIER-ASSOCIATED PERICYTES AND LRP1-DEPENDENT APOLIPOPROTEIN E ISOFORM-SPECIFIC BETA-AMYLOID CLEARANCE MECHANISMS|
Berislav Zlokovic, USA
|14:30 – 14:50||NEW DYNAMIC ASPECTS OF NEUROVASCULAR COUPLING IN THE HUMAN RETINA, CHOROID AND OPTIC NERVE RELEVANT TO BRAIN NEURO-DEGENERATIONS|
Randy Kardon, USA
|14:50 – 15:20||Break|
|15:20– 15:50||LIVE DISCUSSION / Q&A: WHAT IS CELLULAR SENESCENCE AND WHAT IS ITS IMPACT IN NEURODEGENERATIVE DISEASES OF THE BRAIN AND EYE?|
|15:50 – 16:20||LIVE DISCUSSION / Q&A:HOW DOES RESILIENCE, FROM GENETICS TO ENVIRONMENTAL, AT THE CELLULAR, SYSTEMS, OR POPULATION LEVELS, PLAY A ROLE IN REDUCING RISK FOR NEURODEGENERATIVE DISEASE?|
|16:20 – 16:50||LIVE DISCUSSION / Q&A:WHY ARE THE VASCULAR COMPONENTS AND BLOOD-BRAIN/BLOOD-RETINA BARRIERS OF THE BRAIN AND EYE IMPORTANT CONTRIBUTORS TO THE TIPPING POINT BETWEEN HEALTH AND DISEASE?|
|16:50 – 17:20||LIVE GENERAL DISCUSSION: ALL FACULTY|
|17:20 – 17:30||LIVE CLOSING REMARKS|
This content was last updated on: February 23, 2021