Track 1: Alzheimers disease

Alzheimer’s disease (AD), likewise referred to just as Alzheimer's, is a chronic neurodegenerative illness that typically begins gradually and get serious over time. It is the reason for 60% to 70% of cases of dementia. The most widely recognized early side effect is trouble in recollecting recent event short-term memory loss. [As the disease getting worse, indications can incorporate issues with language, disorientation (counting effectively getting lost), mood swings, and loss of inspiration, not overseeing self-care, and conduct issues. As an individual's condition decreases, they frequently pull back from family and society. Slowly, bodily function is lost, at last leading to death.

Track 2:  Causes and Prevention of Alzheimer’s

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 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 3:   Managing 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.

Majority of people with dementia are above age 65, the condition is not normal for all older people. The occurrence of dementia gets high with age, but it’s not given that an older person will develop it. While only 1-in-4 people with Alzheimer’s disease or Dementia has been diagnosed.

Vascular dementia is the second most common cause of dementia in older people. Vascular dementia occurs when vessels that provide blood to the brain become blocked or narrowed. Because it has a lower profile than Alzheimer's, many people don't suspect vascular dementia when forgetfulness becomes problematic. It's also difficult to diagnose so it's difficult to know exactly how many people suffer from vascular dementia.

Track 4:   Alzheimer’s disease Diagnosis and Symptoms

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 illness.

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.

Symptoms of Alzheimer’s disease usually develop slowly and gradually worsen over time, progressing from mild forgetfulness to widespread brain impairment. Chemical and structural changes within brain slowly destroy the ability to create, remember, learn, reason, and relate to others. As critical cells die, drastic personality loss occurs and body systems fail.

Track 5:   Alzheimer’s disease Imaging

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 6:   Alzheimer’s disease Pathophysiology and Disease Mechanisms

Alzheimer’s disease (AD) 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 enviornment. 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 7:   Amyloid Protein in Alzheimer’s and Dementia

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.

Neurofibrillary Tangles: Neurofibrillary tangles are insoluble twisted fibers found inside the brain's cells, consisting primarily of a protein called tau, which forms structure called a microtubule. Transport of nutrients and other important substances from one part of the nerve cell to another done by help of microtubule. In Alzheimer's disease, the tau protein is abnormal and results in collapse of the microtubule structures.

Track 8:   Geriatrics and Cognitive Disorder

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 speciality 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.

Cognitive disorders square measure a class of mental state disorders that primarily have an effect on learning, memory, perception, and drawback determination, and embody blackout, dementia, and delirium. Whereas anxiety disorders, mood disorders, and psychotic disorders can even have an effect on psychological feature and memory functions, the DSM-IV-TR doesn't contemplate these psychological feature disorders, because loss of cognitive function is not the primary (causal) symptom. Causes vary between the various sorts of disorders however most include damage to the memory parts of the brain. Treatments rely on however the disorder is caused. Medication and therapies square measure the foremost common treatments but, for a few sorts of disorders like amnesia, treatments will suppress the symptoms however there is presently no cure.

Track 9:   Care Practice and Awareness

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 10:   Therapeutic Targets and Mechanisms for Treatment

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 11:   Animal Models and Translational Medicine

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.

Patients with Alzheimer’s disease will display both amyloidopathy and tauopathy; however, scientists often focus, in a reductionist way, on one or the other in an animal model. A participant added that even though the anatomy in the mouse is different than the human, mutant tau mice are relatively good models in that they recapitulate tau-dependent neurodegeneration. This has led a number of companies to focus on antibodies that block tau-dependent neurodegeneration in these mouse models.

Track 12: Neurodegenerative Diseases

Neurodegenerative disease causes your mind and nerves to crumble after some time. They can change your character and cause confusion. They can likewise decimate your brain tissue and nerves. Some brain disease, for example, Alzheimer's disease, may develop as you getting old. They can gradually debilitate your memory and thought process. Different disease, for example, Tay-Sachs disease, is hereditary and starts at an early age.

Track 13: Vascular Dementia

A decrease in a man's psychological limits and academic limits that is adequately marvelous to influence the individual's ordinary day by day working. Dementia is a Syndrome result of sores of the cerebrum, Vascular in cause, regardless of their ischemic, haemorrhagic or hypoxic nature. Vascular dementia is more ordinary in men than in women (maybe considering the way that men are more likely than women to encounter the evil impacts of (Strokes). Vascular dementia ends up being continuously normal as people become increasingly settled. The number of people affected by vascular dementia rises altogether in the midst of and after the Sixth decade. Vascular dementia generally occurs at a more youthful age than Alzheimer's disease. Vascular dementia conventionally displays in an extraordinary and stepwise form meaning an "stage" is lost after each event.

Track 14:  Animal Models and Translational Medicine

Animal models for Alzheimer's disease it is basic to consider the human phenotype and what is being shown similar to the animal phenotype. The judge, Bradley Hyman, teacher of nervous system science at Harvard Medical School, said that animal models of Alzheimer's disease, in perspective on the hereditary characteristics of the sickness and the solidly related front temporal dementia, impersonate at any rate a segment of the pathology. Specialists have been productive at showing specific type of Alzheimer's disease in the mouse (e.g., plaques, tangles). Regardless of the way that these are inadequate models of the human disease, they have been for the most part invited in the field as possibly significant models for use in calm disclosure.Patients with Alzheimer's disease will show both amyloidopathy and tauopathy; in any case, researchers every now and again focus, reductionist, on either in an animal showcase. A part incorporated that notwithstanding the way that the existence structures in the mouse is one of a kind in connection to the human, freak tau mice are modestly incredible models in that they repeat tau-subordinate neurodegeneration. This has driven different associations to focus on antibodies that piece tau-subordinate neurodegeneration in these mouse models.This session incorporates Transgenic models, Pharmacological and injury models, Natural and semi natural models, Primate models, Zebra edge models, Animal models of human intellectually developing, Development of new animal models, Genetics of translational models, Protein-protein collaborations, Ethical issues with animal models

Track 15:  Current Research in Therapeutic Targets

Alzheimer's disease (AD) starting at now shows one of the best therapeutic administrations issues in the created nations. There is no effective treatment prepared for backing off contamination development. Starting late the crucial focus of research on novel pharmacotherapies relied upon the amyloid genic hypothesis of AD, which puts that the beta amyloid (Aβ) peptide is essentially accountable for abstract impediment and neuronal end. The target of such drugs is (a) to reduce Aβ creation through the restriction of β and γ secretes synthetic concoctions and (b) to propel breaking down of existing cerebral Aβ plaques. In any case, this methodology has ended up being simply unpretentiously reasonable. Late examinations propose an alternative strategy focused on the limitation of the downstream Aβ hailing, particularly at the neural association. Aβ oligomers may cause degenerate N-methyl-D-aspartate receptor (NMDAR) commencement postsynaptically by forming structures with the telephone surface prion protein (PrPC). PrPC is improved at the neuronal postsynaptic thickness, where it works together with Fyn tyrosine kinase. Fyn sanctioning happens when Aβ is bound to PrPC-Fyn complex. Fyn causes tyrosine phosphorylation of the NR2B subunit of metabotropic glutamate receptor 5 (mGluR5). Fyn kinase blockers masitinib and saracatinib have wound up being successful in treating AD symptoms in preliminary mouse models of the ailment.

Track 16:  Alzheimer’s disease and Type 2 Diabetes

Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) are extraordinarily dominating developing related disease related with gigantic dismalness and mortality. A couple of discoveries in human and animal models have associated T2DM to AD-type dementia. Despite epidemiological connection between the T2DM and mental weakness, the interpretational instruments are unclear. the commonness of evidence in longitudinal assessments with dismemberment confirmation have indicated that vascular parts, rather than excellent AD-type pathologies, underlie the psychological decay frequently found in self-revealed T2DM. T2DM is related with cardiovascular and cerebrovascular infection (CVD), and is related with extended risk of infarcts and little vessel illness in the brain and various organs.Neuropathological evaluations of after death cerebrums demonstrated proof of cerebrovascular sickness and no relationship among T2DM and β-amyloid stores or neurofibrillary tangles. Before long, the parts upstream of early AD-express pathology stay obscure. In such way, there may to be certain be spread between the pathologic frameworks of T2DM/"metabolic issue," and AD.

Track 17:  Front temporal Dementia

The nerve cell harm caused by frontotemporal dementia prompts loss of capacity in these mind areas, which dynamically cause weakening in conduct and identity, dialect unsettling influences, or changes in muscle or engine capacities.There are various diverse sicknesses that reason frontotemporal degenerations. The two most conspicuous is 1) a gathering of cerebrum issue including the protein tau and 2) a gathering of mind issue including the protein called TDP43. For reasons that don't seem to be however notable, these 2 gatherings have Associate in Nursing inclination for the frontal and momentary projections that reason insanity.

Track 18: Vascular Dementia

A decrease in a man's psychological limits and academic limits that is adequately marvelous to influence the individual's ordinary day by day working. Dementia is a Syndrome result of sores of the cerebrum, Vascular in cause, regardless of their ischemic, haemorrhagic or hypoxic nature. Vascular dementia is more ordinary in men than in women (maybe considering the way that men are more likely than women to encounter the evil impacts of (Strokes). Vascular dementia ends up being continuously normal as people become increasingly settled. The number of people affected by vascular dementia rises altogether in the midst of and after the Sixth decade. Vascular dementia generally occurs at a more youthful age than Alzheimer's disease. Vascular dementia conventionally displays in an extraordinary and stepwise form meaning an "stage" is lost after each event.

Track 19:  Insulin Resistance on the development of Alzheimer’s disease

Convincing preclinical and clinical confirmation underpins a pathophysiological association between Alzheimer's disease (AD) and diabetes. Modified digestion, aggravation, and insulin resistance are key neurotic components of the two maladies. For a long time, it was for the most part considered that the cerebrum was unfeeling to insulin; however it is presently acknowledged that this hormone has focal neuromodulatory capacities, incorporating parts in learning and memory, which are debilitated in Alzheimer's Disease. Be that as it may, up to this point, the sub-atomic components representing cerebrum insulin resistance in AD have stayed tricky. Here, we survey late proof that reveals insight into how cerebrum insulin brokenness is started at an atomic level and why anomalous insulin flagging comes full circle in synaptic disappointment and memory decay. We likewise examine the phone premise basic the gainful impacts of incitement of cerebrum insulin motioning on perception. Disclosures outlined here give pathophysiological foundation to recognizable proof of novel sub-atomic targets and for improvement of option helpful methodologies in AD.

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Alzheimer’s is a form of disease that affects the functioning of the brain resulting in decline in memory or other thinking skills. Alzheimer’s disease is the most common and largest form of dementia (in over 60% cases), which is observed among people aged 65 years and above. Accumulation of a protein called beta amyloid, in the spaces between nerve cells due to genetic mutation is a major cause of dementia. Although dementia disease is not treatable, symptomatic treatment is followed in all cases. Research is being carried out to develop treatment centered on the role of beta-amyloid in dementia.

The global dementia drugs market estimated to be valued at US$ 13,900.0 million in 2017 and is expected to witness a CAGR of 8.4% over the forecast period (2018–2026).

 Alzheimer's Disease and Therapeutic Market

GlobalData estimated sales of AD therapeutics in 2016 to have been around $3 billion over the seven major markets (7MM), which are the US, the five major European markets (5EU: France, Germany, Italy, Spain, and UK), and Japan. By 2026, Global Data foresees the AD market will have developed at a solid Compound Annual Growth Rate (CAGR) of 17.5%, arriving at sales of $14.8 billion over the 7MM. This is mostly credited to the developing pervasiveness of both AD and mild cognitive impairment (MCI) and the quick take-up of biologics and other novel disease therapies (DMTs

The Alzheimer's Therapeutics Market is required to reach USD 12.43 Billion by 2026, as indicated by another report by Reports and Data. This can be essentially connected with the developing pipeline drug development, investment in biomarkers for drug development which are expected to further quicken the market development globally. Based on statistics, increase in advanced diagnostics for early identification, along with more scientific drug development, and emerging innovative diagnostics technologies are additionally a portion of the elements that are likewise developing the size of the worldwide market.

Importance and Scope:

Dementia is a general term that depicts a social affair of reactions, for instance, loss of memory, judgment, tongue, complex motor capacities, and other insightful limit caused by the enduring mischief or going of the cerebrum's nerve cells, or neurons. Dementia, including Alzheimer's disease, is one of the best overall general prosperity challenges standing up to our period.

All around, eventual outcomes of a current meta-examination prescribe that 44 million people lived with dementia worldwide in 2010, with numbers foreseen that would twofold at standard interims, to 65.7 million of each 2030 and 115.4 million out of 2050. In 2010, 58 percent shockingly with dementia lived in countries with low or focus compensation, with this degree predicted to rise to 63 percent in 2030 and 71 percent in 2050. This number is depended upon to twofold by 2030 and more than triple by 2050 to 115 million.

In the United States alone, experts gage that upwards of five million people age 65 and more settled experience the evil impacts of Alzheimer's affliction The AD advertise has an absence of helpful alternatives. Which classes of medication overwhelm the market?

The conference was focused on the theme, “Decoding Dementia & Alzheimer's disease.” and facilitated by the Conference Series LLC Ltd. Liberal reaction and cooperation was received from the Editorial Board Members of Associated Journals, Vascular Dementia 2019 Organizing Committee Members and researchers, analysts and pioneers in Dementia, and Vascular Dementia.

The conference was started by the Keynote Forum and we are pleased to thank all our Keynote Speakers, Honourable Guests, Speakers and Conference Attendees for creating a successful meeting.

The conference has encrusted through the following sessions:

• Vascular Dementia and Stroke
• Causes and Prevention
• Vascular Cognitive Impairment
• Dementia: Risk Factors
• Prevention of Dementia
• Dementia Stages
• Ageing and Dementia
• Advances in Dementia Diagnosis
• Dementia Care Management
• Dementia Nursing
• Neuropharmacology
• Novel Therapeutics
• Treating Dementia
• Neurodegenerative Disorders

We would like to specially mention our Keynote Speakers who participated very enthusiastically and actively:

Hans von Holst, Karolinska University Hospital, Sweden

Anne L. Foundas, Brain Institute of Louisiana, USA

Brian Norris, Founder, Executive Director Living Memories C.I.C.UK

Shu G. Chen, USA Case Western Reserve University School of Medicine, USA

Nancy D. Broz, Rowan University, USA

Kyaien O. Conner, University of South Florida, USA

Morejoy Saineti, Greenwich University London, UK

Amarnath Mallik, Consultant Psychiatrist, India

Taheri Saeid, Byrd Alzheimers Institute, USA

David Truswell, Dementia Alliance for Culture and Ethnicity, UK

Jacqueline A Hinds, Society of Emotional Intelligence UK

Workshop:

Olessia Gorkovenko, oulos, UNISA, South Africa

The speakers gave their productive commitment as exceptionally enlightening presentations and made the meeting an extraordinary achievement.

We thank all the members who supported the conference by encouraging the healthy discussions. Vascular Dementia 2019 expresses gratitude to the Organizing Committee Members for their generous response, support and help towards

After the immense idealistic reaction from logical crew, prestigious identities and the Editorial Board Members we are pleased to announce our forth coming conference International conference on Alzheimer's disease and Dementia to be held in at Prague, Czech Republic, during June 22-23, 2020.