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World Summit on Alzheimer’s Disease, Neurophysiology and Cognitive Neuroscience , will be organized around the theme “Emerging Concepts, Progressions and Awareness in Alzheimer’s Disease and Dementia”

Alzheimers Summit 2018 is comprised of keynote and speakers sessions on latest cutting edge research designed to offer comprehensive global discussions that address current issues in Alzheimers Summit 2018

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Alzheimer’s and dementia are still a mystery in many ways. This is why the two similar diseases are often mixed up in every day conversation and understanding. According to the National Institute on Aging (NIA), Dementia is a brain disorder that affects communication and performance of daily activities and Alzheimer’s disease is a form of dementia that specifically affects parts of the brain that control thought, memory and language.

In this track we can discuss on Neurological changes in brain, Amyloid protein, Genetic associations and susceptibility genes, Role of Apo lipoprotein E, Brain trauma, Metabolic syndrome and Alzheimer’s disease, Protein misfolding, aggregation and toxicity, Disease-causing mutations, Epidemiology and prevalence, Histone modification, DNA methylation, Alzheimer’s disease prevention.

Like all types of dementia, Alzheimer's is caused by brain cell death. It is a neurodegenerative disease, which means there is progressive brain cell death that happens over a course of time.

The total brain size shrinks with Alzheimer's - the tissue has progressively fewer nerve cells and connections. In Alzheimer’s,there are microscopic 'plaques' and 'tangles' between and within brain cells.

While they cannot be seen or tested in the living brain affected by Alzheimer's disease, postmortem/autopsy will always show tiny inclusions in the nerve tissue, called plaques and tangles

Plaques are found between the dying cells in the brain - from the build-up of a protein called beta-amyloid (you may hear the term "amyloid plaques").

The tangles are within the brain neurons - from a disintegration of another protein, called tau.

Alzheimer's disease is not simple to diagnose - there is no single test for it. For this reason, the first thing doctors do is to rule out other problems before confirming whether mental signs and symptoms are severe enough to be a kind of dementia or something. Arranging brain scans (possibly including CT,MRI and EEG).

Sometimes dementia symptoms are related to an inherited disorder such as Huntington's disease, so genetic testing may be done.

Again though, the above early tests are not for diagnosing Alzheimer's disease itself, but for ruling out other problems before starting to narrow down to dementia caused by AD. Central to this is checking memory loss and mental performance (cognitive testing).

There must be memory loss and impairment in one other area of cognition for a diagnosis of dementia such as Alzheimer's to be made. These criteria also need to be progressive (a worsening compared with how the person has been before), and severe enough to affect daily activities.

In this track we can discuss on Neurological changes in brain, Amyloid protein, Genetic associations and susceptibility genes, Role of Apo lipoprotein E, Brain trauma, Metabolic syndrome and Alzheimer’s disease, Protein misfolding, aggregation and toxicity, Disease-causing mutations, Epidemiology and prevalence, Histone modification, DNA methylation, Alzheimer’s disease prevention.

Persons with dementia have multiple psychological feature deficits that include each memory impairment, that affects the flexibility to find out new information 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.

This session includes Education and training of medical professionals, Care and quality of life, Person centered care, Cognitive training, Support and training for informal and professional careers, Putting scientific knowledge into practice, Non-pharmacological Interventions, Functional foods, Art, music and life style.

Over the past 30 years, research has linked moderate and severe traumatic brain injury to a greater risk of developing Alzheimer's disease or another type of dementia years after the original head injury.

One of the key studies showing an increased risk found that older adults with a history of moderate traumatic brain injury had a 2.3 times greater risk of developing Alzheimer's than seniors with no history of head injury, and those with a history of severe traumatic brain injury had a 4.5 times greater risk.

Emerging evidence suggests that individuals who have experienced repeated traumatic brain injuries (concussions) or multiple blows to the head without loss of consciousness, such as professional athletes and combat veterans, are at higher risk of developing a brain condition called chronic traumatic encephalopathy (CTE) than individuals who have not experienced repeated brain injuries.

This session includes current research on how traumatic brain injury changes brain chemistry indicates a relationship between traumatic brain injury and hallmark protein abnormalities (beta-amyloid and tau) linked to Alzheimer's.

Alzheimer's disease is a progressive neurodegenerative disease for which no cure exists. There is a substantial need for new therapies that offer improved symptomatic benefit and disease-slowing capabilities. In recent decades there has been substantial progress in understanding the molecular and cellular changes associated with Alzheimer's disease pathology. This has resulted in identification of a large number of new drug targets. These targets include, but are not limited to, therapies that aim to prevent production of or remove the amyloid-beta protein that accumulates in neuritic plaques; to prevent the hyperphosphorylation and aggregation into paired helical filaments of the microtubule-associated protein tau; and to keep neurons alive and functioning normally in the face of these pathologic challenges. We provide a review of these targets for drug development.

This session the various therapies or therapeutic targets characterized by an altered glutamatergic activation, and glutamate which can promote both Ca(2+) and Zn(2+) dyshomeostasis. The two cations can operate synergistically to promote the generation of free radicals that further intracellular Ca(2+) and Zn(2+) rises and set the stage for a self-perpetuating harmful loop. These phenomena can be the initial steps in the pathogenic cascade leading to AD, therefore, therapeutic interventions aiming at preventing Ca(2+) and Zn(2+) dyshomeostasis may offer a great opportunity for disease-modifying strategies.

Researches are going on to identify the specific differences in the brain between dementia with Lewy bodies and Parkinson’s disease dementia. Others are looking at the disease’s underlying biology, genetics, and environmental risk factors. Still other scientists are trying to identify biomarkers (biological indicators of disease), improve screening tests to aid diagnosis and research new treatments

This session includes a great deal to learn about Lewy body dementia (LBD). At a basic level, why does alpha-synuclein accumulate into Lewy bodies, and how do Lewy bodies cause the symptoms of LBD? It is also of increasing interest to the Alzheimer’s and Parkinson’s disease research communities. LBD represents an important link between these other brain disorders, and research into one disease often contributes to better understanding of the others.

A diagnosis of mixed dementia is made when Alzheimer pathology is thought to coexist with second neurodegenerative pathology. It is still unclear how the presence of specific secondary neuropathology interacts with the degree of Alzheimer pathology in determining rate of cognitive and functional decline over time. This information could be helpful in understanding and predicting rate of decline among mixed dementia patients. Methods: Retrospective analyses were conducted on longitudinal data from 498 subjects from the National Alzheimer’s Coordinating Center (NACC) database. At each Braak stage of AD pathology we determined the effect of each secondary neuropathology noted above on patient's neuropsychology profile and rate of functional decline over time on CDR-SB and CDR-Global. Results: We note that Lewy body pathology exhibits significant correlation with functional decline over time in the lower Braak stages(1-2) compared to Vascular disease and Hippocampal sclerosis which exhibit significant correlation with functional decline over time in the higher Braak stages. With Fronto-temporal dementia pathology when present in mixed dementia influencing cognitive and functional decline in both the high and low Braak stages.

This session include further note the neuropsychology profile for some of the mixed neuropathologies could often be distinguished from cases when AD is the primary neuropathology.

Alzheimer ’s disease (AD) is one of the most common form of dementia occurring in elderly population worldwide. Currently Aβ42, tau and p-tau in the cerebrospinal fluid is estimated for confirmation of AD. CSF which is being used as the potent source for biomarker screening is obtained by invasive lumbar punctures. Thus, there is an urgent need of minimal invasive methods for identification of diagnostic markers for early detection of AD. Blood serum and plasma serves as an appropriate source, due to minimal discomfort to the patients, promoting frequent testing, better follow-up and better consent to clinical trials. Hence, the need of the hour demands discovery of diagnostic and prognostic patient specific signature biomarkers by using emerging technologies of mass spectrometry, microarrays and peptidomics.

In this review we summarize the present scenario of AD biomarkers such as circulatory biomarkers, blood based amyloid markers, inflammatory markers and oxidative stress markers being investigated and also some of the potent biomarkers which might be able to predict early onset of Alzheimer’s and delay cognitive impairment.

In vascular dementia, changes in thinking skills sometimes occur suddenly following strokes that block major brain blood vessels. Thinking problems also may begin as mild changes that worsen gradually as a result of multiple minor strokes or other conditions that affect smaller blood vessels, leading to cumulative damage. A growing number of experts prefer the term "vascular cognitive impairment (VCI)" to "vascular dementia" because they feel it better expresses the concept that vascular thinking changes can range from mild to severe.

Vascular brain changes often coexist with changes linked to other types of dementia, including Alzheimer's disease and dementia with Lewy bodies. Several studies have found that vascular changes and other brain abnormalities may interact in ways that increase the likelihood of dementia diagnosis.

Vascular dementia is widely considered the second most common cause of dementia after Alzheimer's disease, accounting for 10 percent of cases. Many experts believe that vascular dementia remains underdiagnosed — like Alzheimer's disease — even though it's recognized as common.

Neurodegeneration is the progressive loss of structure or function of neurons, including death of neurons. Many neurodegenerative diseases – including amyotrophic lateral sclerosis, Parkinson's, Alzheimer's, and Huntington's – occur as a result of neurodegenerative processes. Such diseases are incurable, resulting in progressive degeneration and/or death of neuron cells. As research progresses, many similarities appear that relate these diseases to one another on a sub-cellular level. Discovering these similarities offers hope for therapeutic advances that could ameliorate many diseases simultaneously. There are many parallels between different neurodegenerative disorders including atypical protein assemblies as well as induced cell death. Neurodegeneration can be found in many different levels of neuronal circuitry ranging from molecular to systemic.

Parkinson's disease (PD) is a long-term degenerative disorder of the central nervous system that mainly affects the motor system. The symptoms generally come on slowly over time. Early in the disease, the most obvious are shaking, rigidity, slowness of movement, and difficulty with walking. Thinking and behavioural problems may also occur. Dementia becomes common in the advanced stages of the disease. Depression and anxiety are also common occurring in more than a third of people with PD. Other symptoms include sensory, sleep, and emotional problems. The main motor symptoms are collectively called "parkinsonism", or a "parkinsonian syndrome

Wernicke–Korsakoff syndrome (WKS) is the combined presence of Wernicke's encephalopathy (WE) and Korsakoff's syndrome. Due to the close relationship between these two disorders, people with either are usually diagnosed with WKS, as a single syndrome.

The cause of the disorder is thiamine (vitamin B1) deficiency, which can cause a range of disorders including beriberi, Wernicke's encephalopathy, and Korsakoff's psychosis. These disorders may manifest together or separately. WKS is usually secondary to alcohol abuse. It mainly causes vision changes, ataxia and impaired memory.

Wernicke's encephalopathy and WKS are most commonly seen in people who are alcoholic, and only 20% of cases are identified before death. This failure in diagnosis of WE and thus treatment of the disease leads to death in approximately 20% of cases, while 75% are left with permanent brain damage associated with WKS. Of those affected, 25% require long-term institutionalization in order to receive effective care.

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.

This session includes Transgenic models, Pharmacological and lesion models, Natural and semi natural models, Primate models, Zebra fish models, Animal models of human cognitive aging, Development of new animal models, Genetics of translational models, Protein-protein interactions, Ethical issues with animal models.

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.

This session includes Amyloid and Tau imaging, Imaging animal models, Imaging and genetics, New methods in imaging, Structural and functional MRI, Positron emission tomography, MR spectroscopy, EEG and brain mapping, SPECT imaging, Imaging correlates of clinical, cognitive and biomarker variables.

Recent therapeutic approaches have been strongly influenced by five neuropathological hallmarks of AD: acetylcholine deficiency, glutamate excitotoxicity, extracellular deposition of amyloid-β (Aβ plague), formation of intraneuronal neurofibrillary tangles (NTFs), and neuroinflammation. The lowered concentrations of acetylcholine (ACh) in AD result in a progressive and significant loss of cognitive and behavioral function. Current AD medications, memantine and acetylcholinesterase inhibitors (AChEIs) alleviate some of these symptoms by enhancing cholinergic signaling, but they are not curative. Since 2003, no new drugs have been approved for the treatment of AD.

This session focuses on the current research in clinical trials targeting the neuropathological findings of AD including acetylcholine response, glutamate transmission, Aβ clearance, tau protein deposits, and neuroinflammation. These investigations include acetylcholinesterase inhibitors, agonists and antagonists of neurotransmitter receptors, β-secretase (BACE) or γ-secretase inhibitors, vaccines or antibodies targeting Aβ clearance or tau protein, as well as anti-inflammation compounds.