Common Features of Neurodegenerative Diseases: Exploring the Brain-Eye Connection and Beyond

Illustration showing the connection between the eye and the brain
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.
Tuesday, March 9, 2021 - 8:00 am

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.

The abstract submission deadline for the Early-Career Investigator Flash Presentations is September 21, 2020, using the portal accessible by the “Submit Abstract” button below. Learn more about the Flash Presentations, and the pre-conference symposium agenda and speakers.

This is a full day satellite workshop to AD/PD™ 2021, the 15th International Conference on Alzheimer’s & Parkinson’s Diseases.

Co-Organizers:

  • 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)

AD-PD 2021 Official Logo and Banner


Workshop Topics

(On mobile devices, swipe left to see all of the table columns.)

The following table lists times, topics, and speakers.

TimeTopics

08:00 – 08:10

 

WELCOME AND INTRODUCTION
G. Bu, A. Di Polo, T. Golde and D. Bovenkamp

08:10 – 08:30

.

WORKSHOP GENERAL DISCUSSION PRIMER
G. Bu, A. Di Polo and T. Golde

WHAT IS CELLULAR SENESCENCE AND WHAT IS ITS IMPACT IN NEURODEGENERATIVE DISEASES OF THE BRAIN AND EYE?
Chair: T. Golde, USA

Section 1 Summary:
Many age-related neurodegenerative diseases, like Alzheimer’s, Parkinson’s, macular degeneration and glaucoma, share pathogenic elements that accumulate over time at the genetic, molecular, and cellular levels, including an increase in cellular senescence. When cells of the brain and retina senesce, they transition into a permanent, irreversible state of cell cycle arrest that can reduce the function and regenerative potential of these terminally differentiated tissues as well as increase a senescent pro-inflammatory phenotype. Reducing cellular senescence could be a promising approach to prevent the loss of cells and the alteration of their function. The speakers in this section will define the phenotype and pathology of senescent cells in dementia and blinding diseases, and outline the genetics, mechanisms, systems pharmacology, and potential treatment methods

08:30 – 08:50

 

DEFINED SECRETORY PHENOTYPE OF SENESCENCE
TBA

08:50 – 09:10

 

CELLULAR SENESCENCE IN GLAUCOMA AND AMD
TBA

09:10 – 09:30

 

MULTIDIMENSIONAL SYSTEMS BIOLOGY ANALYSIS OF CELLULAR SENESCENCE IN AGING AND DISEASE
TBA

09:30 – 09:50

 

SENESCENCE-ASSOCIATED SECRETORY PHENOTYPE AND PATHOLOGICAL ANGIOGENESIS IN RETINOPATHY
TBA

09:50 – 10:30

 

SECTION 1 DISCUSSION / Q&A

10:30 – 10:50

 

Lightning Round: x3 Flash Presentations

10:50 – 11:00

 

COFFEE BREAK
 

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.

11:10 – 11:30

 

APOE2 AND RARE PROTECTIVE VARIANTS AGAINST ALZHEIMER’S DISEASE: HOW DO THEY DO IT?
G. Bu, USA

11:30 – 11:50

 

ASSESSMENT OF DEMOGRAPHIC, GENETIC, AND IMAGING VARIABLES ASSOCIATED WITH BRAIN RESILIENCE AND COGNITIVE RESILIENCE TO PATHOLOGICAL TAU IN PATIENTS WITH ALZHEIMER DISEASE
TBA

11:50 – 12:10

 

CELLULAR RESILIENCE AND SELECTIVE VULNERABILITY IN VISION NEURONS
TBA

12:10 – 12:30

 

OXIDATIVE STRESS AND RESILIENCE IN THE RETINA
TBA

12:30 – 13:10

 

SECTION II DISCUSSION / Q&A

13:10 – 13:30

 

Lightning Round: x3 Flash Presentations

13:30 – 14:30

 

LUNCH BREAK
 

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?
Chair: A. Di Polo, Canada

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.

14:30 – 14:50

 

INTERPERICYTE TUNNELLING NANOTUBES: PHYSIOLOGICAL AND PATHOLOGICAL IMPLICATIONS OF A NEW COMMUNICATION CONDUIT REQUIRED FOR NEUROVASCULAR COUPLING

A. Di Polo, Canada

14:50 – 15:10

 

AMYLOID Β OLIGOMERS CONSTRICT HUMAN CAPILLARIES IN ALZHEIMER’S DISEASE VIA SIGNALING TO PERICYTES.
TBA

15:10 – 15:30

 

OCULAR GLYMPHATIC CLEARANCE SYSTEM THAT REMOVES Β-AMYLOID FROM THE RODENT EYE
TBA

15:30 – 15:50

 

BIOENGINEERED VASCULAR MODELS FOR DEMENTIA (INVOLVING ENDOTHELIA, SMOOTH MUSCLE, AND ASTROCYTES)
TBA

15:50 – 16:30

 

SECTION 3 DISCUSSION / Q&A

16:30 – 16:50

 

Lightning Round: x3 Flash Presentations

16:50 – 17:30

 

GENERAL DISCUSSION ALL SECTIONS/ALL SPEAKERS

17:30 – 17:40

 

CLOSING REMARKS
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