Call for Abstract
Scientific Program
5th International Conference on Alzheimer’s Disease & Dementia, will be organized around the theme “An Insight into Advanced Research and Diagnostic Approaches in Alzheimer’s Disease and Dementia”
Dementia 2016 is comprised of 10 tracks and 106 sessions designed to offer comprehensive sessions that address current issues in Dementia 2016.
Submit your abstract to any of the mentioned tracks. All related abstracts are accepted.
Register now for the conference by choosing an appropriate package suitable to you.
Alzheimer's is caused by brain cell death. It is a neurological disorder in which the death of brain cells causes memory loss and cognitive decline. The total size of the brain shrinks in Alzheimer's, nerve cells and connections in the tissue progressively reduced, which cannot be seen or tested in the living brain affected by Alzheimer's disease, post-mortem/autopsy will always show tiny inclusions in the nerve tissues, called as plaques and tangles. Plaques are found between the dying cells in the brain - from the build-up of a protein called beta-amyloid (amyloid plaques). The tangles exist in the brain neurons, from a disintegration of second protein, called tau.
- Track 1-1Neurological changes in brain
- Track 1-2Genetic associations and susceptibility genes
- Track 1-3Epidemiology and prevalence
- Track 1-4Amyloid protein: A protein of great concern
- Track 1-5Can Alzheimer’s disease be prevented or treated?
- Track 1-6Role of apolipoprotein E
- Track 1-7Age an important factor for Alzheimer’s disease?
- Track 1-8Brain trauma
- Track 1-9Metabolic syndrome and Alzheimer’s disease
- Track 1-10Protein misfolding, aggregation and toxicity
- Track 1-11Disease-causing mutations
- Track 1-12Histone modification, DNA methylation
- Track 1-13Nursing research and Dementia care
- Track 1-14Diabetes induced dementia
Dementia is the term used to describe the symptoms of a number of conditions that affecting the brain. The commonly seen condition is Alzheimer’s, and other includes Parkinson's disease. Symptoms seen at early stages are personality changes, withdrawal, memory loss, confusion and apathy. Early diagnosis helps with providing early treatment, support and planning. Medications might help with some symptoms of dementia, but no permanent cure.
- Track 2-1Vascular dementia
- Track 2-2Dementia with lewy bodies
- Track 2-3Fronto-temporal dementia
- Track 2-4Creutzfeldt-Jakob disease
- Track 2-5HIV-related cognitive impairment
- Track 2-6Mild cognitive impairment
- Track 2-7Korsakoffs syndrome
- Track 2-8Rarer causes of dementia
- Track 2-9Stroke Related Dementia
- Track 2-10Traumatic Brain Injury
- Track 2-11Rehabilitation therapy: Dementia
- Track 2-12Rehabilitation therapy: Stroke
Alzheimer’s disease is that the commonest type of dementia, it is a serious brain disorder and it impacts daily living through memory loss and cognitive changes. Although not all memory loss indicates Alzheimer’s disease, one in ten people over 65 years of age, and over half of those over 85 have Alzheimer’s disease. Currently, 26 million people worldwide have this dementia, and over 15 million Americans will be affected by the year 2050.
There is no single test that can show whether a person has Alzheimer's. While physicians can almost always determine if a person has dementia, it may be difficult to determine the exact cause. Diagnosing Alzheimer's requires careful medical evaluation, including medical history, mental status testing, physical and neurological exam, blood tests and brain imaging.
- Track 3-1Biomarkers
- Track 3-2Novel approaches in biomarkers
- Track 3-3Living with Alzheimer’s disease
- Track 3-4Patient’s psychological changes
- Track 3-5Neuropathology
- Track 3-6Neuropsychology
- Track 3-7Early detection possibilities
- Track 3-8Different diagnosis procedures
- Track 3-9New methods in diagnosis
- Track 3-10Normal brain aging
Scientists look at the brain’s grey matter when investigating about Alzheimer’s disease. A fresh study, found that degenerating white matter in the brain could be an early indicator of disease. A study was published in Radiology which concludes that white matter plays an important role in how the disease strikes and progresses. Abnormal deposits of proteins that form amyloid plaques and tau tangles all over the brain in Alzheimer’s disease. It can also be characterized by shrinkage of brain tissues due to neurons loss.
- Track 4-1Amyloid and Tau imaging
- Track 4-2Imaging animal models
- Track 4-3Imaging and genetics
- Track 4-4New methods in imaging
- Track 4-5Structural and functional MRI
- Track 4-6Positron emission tomography
- Track 4-7MR spectroscopy
- Track 4-8EEG and brain mapping
- Track 4-9SPECT imaging
- Track 4-10Imaging correlates of clinical, cognitive, and biomarker variables
Alzheimer’s disease is a progressive dementia with loss of neurons and the presence of two main microscopic neuropathological hallmarks: extracellular amyloid plaques and intracellular neurofibrillary tangles. Early onset AD, a rare familial form, is caused due to mutation of one out of three genes: (amyloid precursor protein), (presenilin 2) or (presenilin 1). Sporadic form occurs usually after age of 65 and accounts for most cases; it most likely results from a combination of genetic and influence of environment. Confirmed risk factors for sporadic AD are age and the presence of the E4 allele of (Apo lipoprotein E). Amyloid plaques comprise mainly of the neurotoxic peptide amyloid (Aβ, Abeta), cleaved sequentially from a larger precursor protein (APP) by two enzymes: β-secretase (also called BACE1) and γ-secretase (comprising four proteins, presenilin is one of them). If APP is first cleaved by the enzyme α-secretase rather than β-secretase then Aβ is not formed. Neurofibrillary tangles comprise mainly of the protein tau which binds with microtubules, which facilitating the neuronal transport system. Tau uncoupling from microtubules and aggregation into tangles inhibits transport and results in disassembly of microtubule. Phosphorylation of tau might have an important role in this. Selective vulnerability of neuronal systems such as the cholinergic, serotonergic, and noradrenergic and glutamatergic systems form the basis of current rational pharmacological treatment.
- Track 5-1Aging
- Track 5-2Prions and Alzheimer’s disease
- Track 5-3Cellular signaling and cell to cell transmission?
- Track 5-4Oxidative damage
- Track 5-5Mitochondrial dysfunction
- Track 5-6Autoimmunity in Alzheimer’s
- Track 5-7Blood-brain barrier and transport
- Track 5-8Neurogenesis and stem cells
- Track 5-9Cell death
Geriatrics or geriatric medication may be a specialty that focuses on health care of older people. It aims to push health by preventing and treating diseases and disabilities in older adults. there's no set age at that patients is also underneath the care of a specialist or geriatric MD, a MD United Nations agency makes a specialty of the care of older people. Rather, this call is set by the individual patient’s needs, and therefore the availableness of a specialist. It’s vital to notice the distinction between gerontology, the care of aged people, and geriatrics, that is that the study of the aging method itself.
- Track 6-1Neurodegenerative diseases
- Track 6-2Geriatric emergency medicine
- Track 6-3Geriatric diagnostics
- Track 6-4Geriatric neurology
- Track 6-5Geriatric oncology
- Track 6-6Geriatric psychiatry or psychogeriatric
- Track 6-7Geriatric pharmacotherapy
- Track 6-8Alcohol addiction and mental health
- Track 6-9Nutritional deficiency
- Track 6-10Preventions: Mental activity and healthy lifestyle
The amyloid plaques and neurofibrillary tangles formation are thought to contribute to the degradation of the neurons (nerve cells) in the brain and the subsequent symptoms of Alzheimer's disease.
Amyloid Plaques: One of the hallmarks of Alzheimer's disease is the accumulation of amyloid plaques between nerve cells (neurons) in brain. Amyloid generally indicates protein fragments that the body produces normally. Beta amyloid is a protein fragment from an amyloid precursor protein (APP). In a healthy brain, these protein fragments are broke down and get eliminated. In Alzheimer’s, the fragments gets accumulated to form hard &insoluble plaques.
- Track 7-1Amyloid Protein and Alzheimer's Disease
- Track 7-2Amyloid-beta metabolism in Alzheimer's
- Track 7-3Brain accumulation of toxic amyloid β (Aβ)
- Track 7-4Amyloid Plaques & Neurofibrillary Tangles
- Track 7-5Amyloid neuroimaging and biomarkers
- Track 7-6Amyloidosis and Neurodegeneration
- Track 7-7Aβ deposition, cognition and brain volume
- Track 7-8The amyloid hypothesis and potential treatments
Persons with dementia have multiple psychological feature deficits that include each memory impairment, that affects the flexibility to find out new info or recall information previously learned, and one or additional of the subsequent symptoms-aphasia, apraxia, agnosia, or executive dysfunction-such that the psychological feature deficits negatively have an effect on social or activity functioning with a big decline in previous talents. Additionally, persons with dementia typically suffer from comorbid conditions that additional complicate care and impede best outcomes. Therefore, developing caregiving methods people with dementia is urgent, given this increasing prevalence and therefore the associated burden that dementia places not only on the individuals, however on the caregivers, relations, and therefore the resources of the health care system. Conventional views bearing on geriatric nursing typically paint an image of the care as being slow paced certain and less demanding than acute care. However, care of the aged, and particularly those with dementia, is usually complicated, unpredictable, and unstable.
- Track 8-1Education and training of medical professionals
- Track 8-2Care and quality of life
- Track 8-3Caregiver support
- Track 8-4Person centered care
- Track 8-5Cognitive training
- Track 8-6Support and training for informal and professional carers
- Track 8-7Putting scientific knowledge into practice
- Track 8-8Non-pharmacological Interventions
- Track 8-9Functional foods
- Track 8-10Art, music & life style
- Track 8-11Nursing and Care Practice
Alzheimer's disease is a progressive neurodegenerative disease that is characterized histopathologically by the presence of plaques, mainly composed of Abeta amyloid and the tangles, mainly composed of hyperphosphorylated tau. To date, there is no treatment that can reverse the disease, and all the current therapeutics is directed to cope with the symptoms of the disease. Here we describe the efforts dedicated to attack the plaques and, in more detail, the process of neurofibrillary degeneration, linked to the presence of the hyperphosphorylated microtubule associated protein tau. We have identified the different putative targets for therapeutics and the current knowledge on them.
Treatment for Alzheimer's disease is entering a new and exciting phase, with several new drugs beginning clinical trials. Many of these new therapies are based on our best current understanding of the pathogenesis of Alzheimer's disease, and are designed to try to either slow or halt the progression of the disease. There are several different theories underlying the current efforts, and these are briefly reviewed. Therapies directed against some aspect of beta-amyloid formation, against neurofibrillary tangle formation and against the inflammatory response are all considered, as are the problems associated with each area. It is as yet unclear which, if any, of these approaches will be successful, but the high level of activity in each of these three fields provides some hope that an effective treatment for Alzheimer's disease is on the horizon.
- Track 9-1Abeta, truncated and pGlu-Abeta
- Track 9-2Immunotherapy
- Track 9-3Neurotransmitter-based targets
- Track 9-4Anti-oxidants
- Track 9-5Neurotrophic factors
- Track 9-6Protein aggregation
- Track 9-7Deep brain stimulation
- Track 9-8Misfolding and chaperones
- Track 9-9Gene therapy
- Track 9-10Nanotechnology
- Track 9-11Drug-delivery systems
- Track 9-12Anti-inflammatory targets
Animal models for Alzheimer’s disease it is important to think about the human phenotype and what is being modeled in terms of the animal phenotype. The moderator, Bradley Hyman, professor of neurology at Harvard Medical School, said that animal models of Alzheimer’s disease, based on the genetics of the disease and the closely related frontotemporal dementia, replicate at least some of the pathology. Researchers have been successful at modeling very specific aspects of Alzheimer’s disease in the mouse (e.g., plaques, tangles). Although these are incomplete models of the human disease, they have been well received in the field as potentially relevant models for use in drug discovery.
- Track 10-1Transgenic models
- Track 10-2Pharmacological and lesion models
- Track 10-3Natural and semi natural models
- Track 10-4Primate models
- Track 10-5Zebra fish models
- Track 10-6Animal models of human cognitive aging
- Track 10-7Development of new animal models
- Track 10-8Genetics of translational models
- Track 10-9Protein-protein interactions
- Track 10-10Ethical issues with animal models