CONy 2020 Dementia Program
Section Heads:
*This program is subject to change
| Friday, March 27, 2020 | |
| 08:30-10:10 | PRECLINICAL AND EARLY ALZHEIMER’S DISEASE |
| 08:30-09:20 | Is subjective cognitive impairment itself a prelude to dementia? |
| Capsule: In a chronic medical condition, early diagnosis becomes an issue when treatment is available that can alter its course. Regarding AD, there is hope that novel disease-modifying drugs or prevention strategies will have the capacity of slowing down the neurodegeneration and the associated clinical decline. Such treatments may provide greatest benefit to patients at the stage of absent or minor cognitive impairment. This debate will focus on the central question if AD can (and should) be diagnosed in the stage of subjective cognitive deficits. | |
| 08:30-08:40 | Host: David Knopman, USA |
| 08:40-08:55 | Yes: Babak Tousi, USA |
| 08:55-09:10 | No: Panteleimon Giannakopoulos, Switzerland |
| 09:10-09:20 | Discussion and rebuttals |
| 09:20-10:10 | Is cognitive reserve a buzzword lacking scientific value? |
| Capsule: The concept of reserve was established to account for the observation that a given degree of neurodegenerative pathology may result in varying degrees of symptoms in different individuals. There is a large amount of evidence on epidemiological risk and protective factors for neurodegenerative diseases and de mentia, yet the biological mechanisms that underpin the protective effects of certain lifestyle and physiological variables remain poorly understood, limiting the development of more effective preventive and treatment strategies. This debate will focus on the important question, is reserve just another buzz word or is the phenomenon supported by enough scientific evidence. | |
| 09:20-09:30 | Host: Robert Perneczky, Germany |
| 09:30-09:45 | Yes: Panteleimon Giannakopoulos, Switzerland |
| 09:45-10:00 | No: Irena Rektorova, Czech Republic |
| 10:00-10:10 | Discussion and rebuttals |
| 10:10-10:25 | Coffee Break |
| 10:25-12:05 | PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE |
| 10:25-11:15 | The development in understanding AD has not made an impact on patient care. |
| Capsule: AD is characterized by cognitive deterioration, but non-cognitive behavioral symptoms are also frequent and often associated with more suffering than cognitive and functional decline. Treatment of those symptoms may be difficult and challenging, and there is insufficient evidence to support treatment decisions. Often a combination of different non-pharmacological approaches precedes drug treatment. This debate will focus on the question if the improved understanding of AD pathology has improved patient care and treatment, including non-cognitive symptoms. | |
| 10:25-10:35 | Host: Ruth Itzhaki, UK |
| 10:35-10:50 | Yes: Judith Aharon, Israel |
| 10:50-11:05 | No: Sagrario Manzano, Spain |
| 11:05-11:15 | Discussion and rebuttals |
| 11:15-12:05 | Vascular lesions contribute to AD pathology. |
| Capsule: Over several years, evidence has been accumulating that suggests vascular disease impacts on common causes of dementia, in particular Alzheimer’s disease. Modifiable vascular risk factors such as hypertension, diabetes, dyslipidaemia and adiposity are all linked to Alzheimer’s disease. However, it is unclear whether these factors contribute to or promote Alzheimer’s disease pathology and neurodegeneration. This debate will address whether vascular changes are just coincident with Alzheimer type of pathology or part and parcel of Alzheimer’s disease. | |
| 11:15-11:25 | Host: Nick Fox, UK |
| 11:25-11:40 | Yes: Rajesh Kalaria, UK |
| 11:40-11:55 | No: David Knopman, USA |
| 11:55-12:05 | Discussion and rebuttals |
| 12:15-13:15 | Industry Supported Symposium |
| 13:15-14:15 | Lunch Break |
| 13:15-14:15 | Meet the Expert |
| 14:15-15:45 | RISK AND PROTECTIVE FACTORS |
| 14:15-14:55 | Does aerobic exercise protect cognition? |
| Capsule: Lifestyle changes have been suggested for dementia prevention. Physical activity engagement has repeatedly been associated with preserved cognition and lower risk for cognitive decline and dementia among older adults. Whether physical activity is neuroprotective or if it mitigates enhanced risk for dementia via other risk factors is less well understood. This debate will discuss if physical activity protects cognitive function and whether we know enough about the phenomenon to design effective interventions. | |
| 14:15-14:25 | Host: Miia Kivipelto, Sweden/UK |
| 14:25-14:35 | Yes: Catherine Robb, UK |
| 14:35-14:45 | No: Naji Tabet, UK |
| 14:45-14:55 | Discussion and rebuttals |
| 14:55-15:45 | Is deafness a causative risk factor to dementia? |
| Capsule: Hearing loss is associated with increased risk for dementia is this association causative? Other data suggest that there may be a causal link between deafness and cognitive decline but hearing loss may merely be an early symptom of neurodegenerative changes. | |
| 14:55-15:05 | Host: Gill Livingston, UK |
| 15:05-15:20 | Yes: Sergi Costafreda, UK |
| 15:20-15:35 | No: Lev Kruglov, Russia |
| 15:35-15:45 | Discussion and rebuttals |
| 15:45-16:00 | Coffee Break |
| 16:00-17:30 | NEW DEFINITIONS AND APPROACHES |
| 16:00-16:45 | Is the new NIA-AA research definition of AD helpful? |
| Capsule: There is ample evidence that AD (co-)pathology is the most prevalent pathological change in older individuals with dementia. However, relationship is weaker in the eldest elderly. The assumption of clear-cut dementia subtypes is put into question by biomarker and neuropathological research suggesting that a substantial proportion of clinically ‘pure’ AD cases have mixed pathology at autopsy and that amyloid-β (Aβ) is commonly found in cognitively normal older adults. This debate will focus on the key question whether Aβ is a central characteristic of AD or merely an age-related phenomenon and how this is reflected by the new research diagnostic criteria, which require evidence of Aβ pathology to diagnose AD. | |
| 16:00-16:10 | Host: Edson Amaro, Brazil |
| 16:10-16:25 | Yes: Paul Edison, UK |
| 16:25-16:40 | No: Mee Park, South Korea |
| 16:40-16:45 | Discussion and rebuttals (5 min) |
| 16:45-17:30 | Will big data help us to find cure for dementia? |
| Capsule: In recent years there has been a surge towards big data approaches in AD, following a general trend in other disciplines in medicine and beyond. However, not everyone is convinced and the debate on the merits of big data for identifying effective treatments for AD is in full swing. That big collections might generally be useful is not the issue. It was suggested that we can let the data speak for itself. But what does the amassed data actually explain about the underlying pathophysiology and how can it help us identify new drug targets? This debate will focus on the promise of big data initiatives for finding a cure for AD. | |
| 16:45-16:55 | Host: Stefano Sensi, Italy |
| 16:55-17:10 | Yes: John Gallacher, UK |
| 17:10-17:25 | No: Eugen Tarnow, USA |
| 17:25-17:30 | Discussion and rebuttals (5 min) |
| 17:30-19:00 | FRONTOTEMPORAL DEMENTIA |
| 17:30-18:15 | The term Frontotemporal Dementia (FTD) is no longer of value |
| Capsule: FTD is the second most common cause of young-onset dementia, which includes several distinct, heterogeneous sub-syndromes. FTD is characterized by progressive deficits in behavior, language, and executive function, but individual symptoms vary considerably. Typically, prefrontal and temporal brain regions are affected preferentially, but the underlying pathology is also heterogeneous. Over the last decades, the nomenclature of this group of disorders has undergone several iterations. This debate focusses on the question whether the term FTD is still relevant or if it should be replaced. | |
| 17:30-17:40 | Host: Janine Diehl-Schmid, Germany |
| 17:40-17:55 | Yes: Eugen Tarnow, USA |
| 17:55-18:10 | No: James Rowe, UK |
| 18:10-18:15 | Discussion and rebuttals (5 min) |
| 18:15-19:00 | All patients with a diagnosis of FTD should have genetic testing |
| Capsule: Approximately 40 percent of affected individuals with FTD have a family history that includes at least one other relative diagnosed with a neurodegenerative disorder. Three genes account for the majority of mutation-associated hereditary FTD cases, including C9orf72, GRN and MAPT. Mutations in other genes have also been described but are much rarer than the three mentioned above. Furthermore, a very small percentage of people with sporadic FTD have a mutation in a known FTD gene. Meanwhile, an estimated 10-15% of people with familial FTD have a similar mutation. This debate focuses on the question if this knowledge about the genetics of FTD is reason enough to perform genetic testing (and counselling) in all patients diagnosed with the disease. | |
| 18:15-18:25 | Host: John Hardy, UK |
| 18:25-18:40 | Yes: Lea Grinberg, Brazil/USA |
| 18:40-18:55 | No: |
| 18:55-19:00 | Discussion and rebuttals |