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

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

Tuesday, March 9, 2021
08:00 – 17:40
Pre-registration is required. To register, please click here.

For the third consecutive year 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.

New for AD/PD™ 2021: Guidelines for Abstract Submission for Early-Career Investigator Flash Presentations in the Common Features of Neurodegenerative Disease Pre-symposium.

  • Graduate students (PhD and/or MD) and postdoctoral fellows up to 5 years after post-terminal degree or clinical training. Please have your supervisor/mentor submit confirmation of your student/postdoc status when you submit your abstract.
  • Abstract Submission through the main abstract submission system, by clicking here
  • Abstract Submission Extended Deadline is Midnight CET on October 12, 2020.
  • When submitting an abstract for consideration for a flash presentation in this session, please read the detailed instructions inside the submission system.
  • The 3 abstract submission topics for this session will fall within the 3 sessions featured in the 2021 Symposium (senescence, resilience, neurovascular).
  • Up to 3 Flash Presenters will be chosen per session (total of 9).
  • Applications will be reviewed by the pre-symposium Co-Chairs.
  • Submissions that do not become Flash Presentations in this session will be considered for presentation in the main meeting, following a review by ADPD committee and providing the presenter registers to the main meeting.
  • Notification and Invitation for Flash Presentations shall be sent by November 20, 2020

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

NOVEL TREATMENT MODELS ATTACKING SENESCENCE IN ALZHEIMER’S DISEASE

Darren Baker (USA)

08:50 – 09:10

CELLULAR SENESCENCE IN THE EYE – FOCUS ON RETINA

Dorota Skowronska-Krawczyk (USA)

09:10 – 09:30

SYSTEMS PHARMACOLOGY, SENESCENCE AND AGING: LESSONS FROM AMD

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

FUNCTIONAL RESILIENCE OF RETINAL GANGLION CELLS DURING MITOCHONDRIAL DYSFUNCTION 

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

BLOOD-BRAIN BARRIER-ASSOCIATED PERICYTES AND LRP1-DEPENDENT APOLIPOPROTEIN E ISOFORM-SPECIFIC BETA-AMYLOID CLEARANCE MECHANISMS

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)
Cheryl Wellington (Canada)

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