Biography:

Oliveira is a Research Fellow Nurse working for the Institute of Mental Health, University of Nottingham. She is currently leading a national UK survey on dementia risk reduction funded by the Alzheimer Research UK and editing a book on this topic. Dr Oliveira completed her PhD in 2016, in which she developed and validated an age- and dementia-specific quality of life scale for use with older family carers – the DQoL-OC.

Abstract:

Individuals’ lifestyle contributes to the risk of dementia and lack of physical exercises, lack of social interaction, poor diet, smoking and alcohol consumption are among the major risk factors. Researchers have developed interventions aimed at promoting mental and physical fitness via increased cognitive and physical activity and improving diet and health, but too little is known about possible benefits or levels of uptake. Implementation of life style changes depends on individual attitudes and little is known about what and how much older people are prepared to change in order to prevent dementia. If the factors associated with better attitudes towards change of life style can be predicted, more accurate interventions tailored to these specific issues can be developed in order to reduce the risk of dementia. This presentation will show preliminary data from a national UK survey that involved aproximately 4,000 people aged 50+ without dementia. The study aimed to assess people’s willingness to change their lifestyle to potentially reduce their risk of future dementia, as well as understand more about factors that might predict willingness to change. Sociodemographic and current lifestyle information was collected. Motivation to change lifestyle was assesed using the MCLHB-DRR scale and non-validated questions based on the current lifestyle profile (e.g. if the individual smoked, it was asked how much he/she would be willing to stop smoking). The data suggests important differences in gender and age in relation to motivation to change lifestyle. These will be discussed in detail in this presentation.

*This research was funded by the Alzheimer’s Research UK Midland (2016-2017)

Biography:

Jagdish Singh is Professor and Chair of the Department of Pharmaceutical Sciences at NDSU College of Pharmacy, North Dakota and a Fellow of American Association of Pharmaceutical Scientists (AAPS) and Fellow, Association of Biotechnology and Pharmacy. His efforts focus on the mechanistic studies for developing and testing novel delivery technologies to deliver biotechnologically derived molecules (e.g., peptide, protein, and gene). He has published over 150 peer-reviewed papers and 270 abstracts. 

Abstract:

Neuro-degenerative diseases have become the most common cause of dementia among the elderly. There were 36 million people living with dementia worldwide in 2010, increasing to 66 million by 2030 and 115 million by 2050. In 2010, the global cost of dementia was $604 billion. This is 1% of global GDP and it is likely that these costs will increase in proportion to the number of people with dementia. Gene therapy has been identified to possess a broad potential for the treatment of numerous neurological diseases, including Alzheimer’s disease (AD). AD is a progressive neurodegenerative disease and the most common form of dementia caused by accumulation of toxic amyloid-β (Aβ) peptides in the brain, in which the development of effective therapies have been desired. However, the major challenge in the field of gene therapy is the design of safe vectors that can cross the blood brain barrier (BBB). It has been found that the transferrin receptors are present on the surface of brain endothelial cells. The liposomes, lipid based nanoparticles, can be surface modified with transferrin (Tf) protein for targeting the brain endothelial receptors and conjugated to cell penetrating peptide (CPP) for improving their internalization into brain by overcoming receptor saturation. In order to deliver gene/drug across the BBB, we conjugated the liposomes with two ligands (1) a receptor targeting protein (Tf) and (2) a CPP. Thus, we designed near-neutral, PEGylated liposomal nanoparticles encapsulating gene and drug and modifying the surface with Tf and CPP. Findings of in vitro characterization and in vivo bio-distribution will be discussed. 

Biography:

Si Ching Lim has a special interest in dementia care particularly in patients with behavioural and psychological symptoms of dementia. She is currently In-charge of a 20 bedded dementia ward in a teaching hospital in Singapore and is responsible in developing the ward and training the staff in managing elderly with delirium and dementia with challenging behaviour. She is also an Adjunct Assistant Professor at National University of Singapore and Dukes Graduate Medical School.

Abstract:

Dementia is becoming an expensive disease worldwide and its prevalence is on the rise, particularly in the developing countries. Eating disorders are common among the different types of dementia at various stages of the disease process. In the early stages, cognitive deficits cause them to eat very frequently, having forgotten they had just eaten. At the late stages, metabolic rate gets down regulated as the disease cause increasingly severe atrophy and physical activities reduce. The patients develop anorexia and together with functional dysphagia, nutritional intake and adequacy becomes a big concern for the caregivers. In addition, they have difficulties using the cutlery, recognizing food and are easily distracted by changes in the environment. The presence of behavioural problems also interferes with meal times and nutritional intake. There are ways to manipulate and increase the nutritional values of their intake at the late stages and explore the pros and cons of tube feeding for the elderly with severe dementia, the ethical consideration of tube feeding, etc.

Biography:

Markku Kurkinen completed his PhD in 1979 at University of Helsinki, Finland and; Post-doctoral studies from 1980-1983 at Imperial Cancer Research Fund, Mill Hill, London, UK. He was an Assistant Professor from 1984-1986, at Rutgers Medical School, Piscataway, New Jersey, USA; Associate Professor 1986-1992, and Division Chief, Connective Tissue Research, Robert Wood Johnson Medical School, Piscataway, New Jersey, USA. He is Professor at Wayne State University School of Medicine, Detroit, Michigan, USA. He has published more than 100 papers, reviews and book chapters.

Abstract:

According to the amyloid hypothesis, Alzheimer dementia begins in the brain with Aβ peptides accumulation and amyloid formation. However, clinical drug trials targeting Aβ peptides and brain amyloid have failed to help anybody living with Alzheimer. Instead of repeating similar trials and errors of 25 years, we have to discover novel drug targets and better our research to prevent and treat Alzheimer. Glutamate is the synaptic signaling molecule of neurons. As soon as the glutamate signaling starts it is stopped in 0.1-2 ms by astrocytes, which take up and clear glutamate from synapses. This prevents glutamate neurotoxicity causing synapse loss and neuron cell death. Astrocytes make EAAT2 (excitatory amino acid transporter-2), the major glutamate transporter and 1% of brain protein. In Alzheimer dementia, astrocytes are impaired in glutamate uptake. In experimental mouse models of Alzheimer, increasing EAAT2 expression slows dementia progression. To discover drugs that can activate EAAT2 in glutamate uptake; we describe a simple assay that targets the EAAT2 protein reconstituted in liposomes and measures glutamate uptake with Oxonol VI red light. By directly targeting the EAAT2 protein, the assay should limit ‘off-targeting’ of drugs and adverse events, which are the main problems in Alzheimer’s drug discovery and clinical development. We may have to screen a million or more drugs, chemical compounds and natural products, before we find what we are looking for. We believe our drug assay of liposome glutamate uptake, in a high-throughput screening (HTS) format, can do exactly that. For efficacy, specificity and safety, the EAAT2 activating drugs are studied in an experimental C elegans model of Alzheimer.