The Scientific Program - Alzheimer's Disease and Dementia

Friday April 05, 2019

Hall- CERVANTES

08:00-08:30

ALZHEIMER'S DISEASE FREE COMMUNICATIONS

Chairpersons: Nataliya Pryankova, Ukraine & Gabriel Vainstein, Israel

08:00-08:10

08:10-08:20

Use [18]f-fluoro- deoxyglucose positron emission tomography and other biomarkers to assess risk of clinical progression in patients with amnestic mild cognitive impairment: Maria Sagrario Manzano, Spain

Tau Protein in the Retina: Umur Kayabasi, Turkey

08:30-10:10

SESSION 17 | ALZHEIMER’S DISEASE (AD)

Chairpersons:

Nataliya Pryankova, Ukraine & Gabriel Vainstein, Israel

08:30-09:20

08:30-08:40

08:40-08:55

08:55-09:10

09:10-09:20

Is the evidence sufficient to recommend dietary interventions to reduce the risk of AD progression?

Capsule: Extensive epidemiologic evidence implicated modifiable metabolic and dietary factors in increasing the risk of dementia, including AD, and several interventions have shown promise in early trials. Definitive RCTs involving nutritional interventions to prevent the progression of cognitive decline in AD are eagerly awaited, but what do we need to do meanwhile?

Host: Yvonne Freund-Levi, Sweden

Yes: Aron Troen, Israel

No: Tobias Hartmann, Germany

Discussions and Rebuttals

09:20-10:10

Should cognitive disorders in older age be studied with FDG PET and amyloid PET or with MRI and CSF evaluation?

Capsule: The clinical evaluation alone will misclassify about 20% of patients with dementia and a larger proportion of those with mild cognitive impairment. For this reason, biomarkers are used to help separate AD from frontotemporal dementia, which are treated differently. For this purpose, is it better to use PET metabolic biomarkers or MRI and CSF evaluation?

09:20-09:30

Host: Maria Sagrario Manzano, Spain

09:30-09:45

Pro FDG and amyloid PET: Joseph Masdeu, USA

09:45-10:00

Pro MRI and CSF: Guillermo Garcia Ribas, Spain

10:00-10:10

Discussion and rebuttals

10:10-10:25

Coffee Break

10:25-12:05

SESSION 18 | RISK FACTORS FOR AD

Chairpersons:

Shira Knafo, Spain & Mee Young Park, South Korea  

10:25-11:15

There is no need to define dementia sub-types in older patients, as the majority have mixed pathologies anyway.

Capsule: Researchers who examined older adults' brains after death found that most had two or more pathologies. Amyloid and tau were the most common pathology but rarely occurred alone. So, if the majority of older patients have mixed dementia, it may not be worthwhile to attempt to make a firm clinical diagnosis?

10:25-10:35

Host: Pierre Krolak-Salmon, France

10:35-10:50

Pro: Pasquale Calabrese, Switzerland

10:50-11:05

Con: Michael Ewers, Germany

11:05-11:15

Discussion and rebuttals

11:15-12:05

Microglia activation should be a therapeutic target.

Capsule: Microglia activation and other innate immune responses seem to be associated with most neurodegenerative conditions, including AD.  Is microglia activation merely a non-specific response to AD pathology or should it be considered a potential therapeutic target?

11:15-11:25

Host: Robert Perneczky, Germany

11:25-11:40

Pro: Roger Bullock, UK

11:40-11:55

Con: Enrique Gabande, Spain

11:55-12:05

Discussion and rebuttals

13:15-14:15

Lunch Break

13:15-14:15

Meet the Expert- Alzheimer's disease (Rio Hortega)

AMBAR (Alzheimer´s Management By Albumin Replacement) Trial Results: Clinical and Biomarker Update

Laura Núñez, Spain

Javier Olazarán, Spain

14:15-15:45

SESSION 19 | MIXED DEMENTIA

Chairpersons:

Judith Aharon, Israel & Angel Martin Montes, Spain

14:15-14:55

Is APOE4 really toxic in AD?

Capsule: The ε4 allele of apolipoprotein E (APOE) is the major genetic risk factor for AD. Many studies suggest that the differential effects of APOE isoforms on Aβ aggregation and clearance play the major role in AD pathogenesis. Inconsistent results among studies have made it difficult to define whether the APOE ε4 allele represents a gain of toxic function, a loss of neuroprotective function, or both.

14:15-14:25

Host: David Knopman, USA

14:25-14:35

Pro: Danny Michaelson, Israel

14:35-14:45

Con: Illiya Lefterov, USA

14:45-14:55

Discussion and rebuttals

14:55-15:45

Vascular risk factors in AD - real or fake?

Capsule: Aging is associated with a large increase in the prevalence and incidence of degenerative and vascular dementia. Several vascular risk factors have been found to be associated with vascular dementia but also AD. Vascular risk factors and their treatments are a promising avenue of research for prevention of dementia, but do they really affect AD?

14:55-15:05

Host: Maria Sagrario Manzano, Spain

15:05-15:20

Real: Jan Kassubek, Germany

15:20-15:35

Fake: Giancarlo Logroscino, Italy

15:35-15:45

Discussion and rebuttals

15:45-16:00

Coffee Break

16:00-17:40

SESSION 20 | DEMENTIA CAUSES

Chairpersons:

Nina Sofilkanych, Ukraine & Ascensión Zea-Sevilla, Spain

16:00-16:50

The recent reduction of dementia incidence can be ascribed mainly to better management of hypertension, dyslipidemia and diabetes.

Capsule: The prevalence of dementia is expected to soar as the average life expectancy increases, but recent epidemiological results suggest that the age-specific incidence of dementia is declining. We are going to discuss these results: is prevention possible?

16:00-16:10

Host: Michael Ewers, Germany

16:10-16:25

Yes: Milica G. Kramberger, Slovenia

16:25-16:40

No: Roger Bullock, UK

16:40-16:50

Discussion and rebuttals

16:50-17:40

Have we got it all wrong? Amyloid cascade is not the key etiological factor in AD.

Capsule: The dominant hypothesis of AD etiology which has been built around one casual factor only, ß-amyloid (Aß), remains unproven. No conclusive evidence has been presented that Aß pathology represents the first biomarker of the disease and the first sign of sporadic AD onset. Treatments aiming to reduce Aß formation have proven to be toxic or worsen cognition. Immunization with anti Aß antibodies has not yet demonstrated a clinical effect. Should we discard the amyloid hypothesis?

16:50-17:00

Host: Ruth Itzhaki, UK

17:00-17:15

Pro: Ezio Giacobini, Switzerland

17:15-17:30

Con: Eugen Tarnow, USA

17:30-17:40

Discussion and rebuttals

17:40-19:20

SESSION 21 | AD: CAUSE AND THERAPY

Chairpersons:

Mun Seong Choi, South Korea & Latchezar Traykov, Bulgaria

17:40-18:30

Is herpes virus infection a risk factor for AD?

Capsule: Herpes simplex virus type 1 (HSV1), when present in the brain of carriers of APOE4, has been implicated as a major factor in AD. It is proposed that virus is normally latent in many elderly brains but reactivates periodically. Implicating HSV1 further in AD is the discovery that HSV1 DNA is specifically localized in amyloid plaques in AD. Can we implicate HSV in AD pathogenesis?

17:40-17:50

Host: David Knopman, USA

17:50-18:05

Yes: Ruth Itzhaki, UK

18:05-18:20

No: Israel Steiner, Israel

18:20-18:30

Discussion and rebuttals

18:30-19:20

Is non-invasive brain stimulation (NIBS) useful for improvement of cognition in  MCI subjects?

Capsule: NIBS techniques include repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS). While these have been mostly used to treat pharmaco-resistant depression, mild cognitive impairment has also been reported to improve. However, the question remains: Is NIBS really useful for modulation of cognition in MCI?

18:30-18:40

Host: Jack de la Torre, USA

18:40-18:55

Yes: Irena Rektorova, Czech Republic

18:55-19:10

No: Friedhelm Hummel, Switzerland

19:10-19:20

Discussion and rebuttals