Small Molecule Screen For Modulators Of Kinesin Function

Alzheimer 's disease (AD) was discovered by a German doctor Alois Alzheimer in 1906 when he found amyloid plaques and neurofibrillary tangles in the autopsy of a woman who died of an unknown mental disease. The extracellular amyloid plaque deposits, composed of insoluble amyloid-Beta peptide were hypothesized to be the main etiological factor. “The most important abnormality is an excess of Amyloid-beta peptides brought about through either overproduction or failure in degradation.” (Uzun, Kozumplik, & Folnegović-Smalc, 2011) Later, it was discovered that intracellular neurofibrillary tangles composed of hyper-phosphorylated, helically-paired tau

1.1 Dementia is an umbrella term for a range of diseases that affect memory, behaviour and motor skills. The causes vary depending on the disease but largely the presence of “plaques” and “tangles” on the neurons of the brain is found in people with Alzheimer’s. Plaques are protein that the body no longer breaks down and allows to build up; these get between the neurons and disrupt the message transmission. Tangles destroy a vital cell transport system made of proteins. The transport system is organised in orderly parallel strands like rail tracks. In healthy areas a protein call “tau” helps the tracks stay straight but in areas where tangles

One of the most prominent and perhaps most feared condition associated with aging is dementia. The family of disorders can cause individuals to lose their mind, reducing one from being a complex, thinking, feeling human being to being confused and vegetative, unable to recognize their loved ones. Serious dementia affects nearly 37 million people globally, but predictions of how those numbers will change over the next few decades are conflicting (textbook). Although we know dementia as to do with damage to nerve cells in the brain, there are ongoing studies looking at correlations between other health issues and these types of diseases.

The damage then alters the permeability of the axon membrane resulting in a large inflow of calcium, and the release of apoptotic cell death mediators that may be responsible for the phosphorylation, shortening, misfolding and aggregation of tau proteins (2011). Thus, the neurodegeneration that begins in the cortical sulci and initially surrounding only small blood vessels, spreads to larger portions of the brain. This tau-toxic factor associated systemic degeneration in regions of the brain that regulate emotion, memory, and other cognitive functions, leads to the physical and neuropsychological sequelae of CTE (McKee, et al., 2010).

Some pathologic symptoms of Alzheimer’s include the breaking-down of certain nerve cells, along with the presence of neurotic plaques and tangles. Some believe that if there was a way to reduce or break down these plaques and tangles, then people would not be forgetful (Nierenberg, 2016). Over long term testing, most patients with Alzheimer’s showed similar declines, initially with memory, moving to language, praxis, and visual perception (Mckhann, etc. all, 1984).

Dementia is a syndrome which is progressive in nature, characterized by impairment of memory and loss of intellectual ability.1 Decreased level of Acetylcholine in the brain, neuro-inflammatory reaction, rise in the oxidative stress and hypercholesterolemia have been reported to play an important etiological role in the memory decline.2 Alzheimer’s Disease (AD) is the most common form of dementia which is a progressive and a neurodegenerative disease characterized by the presence of senile plaques rich in insoluble aggregates of β amyloid and neurofibrillary tangles in the brain. AD has been estimated to account for 50–60% of dementia cases in persons over 65 years of age worldwide.3 Alzheimer’s Disease International

Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most widespread age-related neurodegenerative diseases. Both diseases impact a considerable number of people, where AD occurs in around 10 percent of the population greater than the age of 65 while PD occurs in roughly 1 percent of the population above the age of 65. AD is considered to be the most widespread cause of dementia, characterised by the progressive memory and cognitive deficits which impair ones day to day activities. The pathological hallmark of AD comprises of extracellular accumulation of senile plaques consisting of mainly amyloid-beta (Aβ) peptides, along with neurofibrillary tangles which are composed of the phosphorylated tau protein, located in the hippocampus and cortex. Conversely, PD is considered to be the most widespread movement disorder that is characterised by symptoms such as rigidity slow movements, resting tremor and other instabilities. The extreme loss of dopaminergic neurones in the substantia nigra is what defines PD, as the loss of this nerve cell can be linked to Lewy bodies containing aggregates of a soluble protein called α-synuclein.

Alzheimer’s disease, considered the most common form of dementia, is a degenerative brain disorder which leads to loss of memory and decline of cognitive thinking. Alzheimer’s disease effects over 5 million Americans, a number which is expected to triple in the projected future, and is the sixth leading cause of death in the United States (Dougherty, R.J., et al). Majority of these affected people are sixty-five years of age or older and have what is called late-onset Alzheimer’s, whilst a smaller margin of individuals is younger than sixty-five years of age and are said to have early-onset Alzheimer’s. Alzheimer’s disease presents itself in three main stages, is caused by the degeneration of neurons and by the changes in protein composition in the brain, and despite the lack of definitive, early diagnosis or preventative treatment the disease can to a certain degree be detected and managed.

Alzheimer’s disease or AD is an incurable disorder of the brain that results in loss of normal brain structure and function. In an AD brain, normal brain tissue is slowly replaced by structures called plaques and neurofibrillary tangles. The plaques represent a naturally occurring sticky protein called beta amyloid and in an Alzheimer’s brain, sufferer’s tend to accumulate too much of this protein. Neurofibrillary tangles represent collapsed tau proteins which, in a normal brain along with microtubules, form a skeleton that maintains the shape of the nerve cells. In Alzheimer’s disease, the tau proteins break loose from their normal location and form tangles. Without the support of these molecules, nerve cells collapse and die. As normal

Alzheimer’s Disease is indicated by the break down of the nervous system, essentially the neurons within the brain (MacGill, 2009). The break down leads to nerve cell eradication, and the casualty of tissue throughout the brain (MacGill, 2009). As the disease progress, the brain begins to shrink fiercely, developing loss of its normal functioning (MacGill, 2009). Abnormal protein groups and structures of plaques and tangles characterize the disease (MacGill, 2009). Plagues and tangles are not able to be viewed or tested in the living brain, but are able to be observed in an autopsy of an infected deceased (MacGill, 2009).

Dementia is a drastic failure of cognitive ability that correlates with shrinkage of the hippocampus; the greater the impairment, the likely the smaller the size of the hippocampus. Alzheimer’s Disease is a neurodegenerative disorder, and a form of senile dementia that is characterized by progressive cognitive and sensory impairment in the form of: having a greater difficulty performing tasks, forgetting material that one just read, memory loss, slowed metabolism and atrophy and loss of awareness. With Alzheimer’s being the most common form of dementia, it is estimated that the disease affects 10% of people by the age of 65 and over 50% of people over the age of 85. This disease

Alzheimer’s is an irreversible disease normally affecting the elderly population and is progressive in nature causing degeneration that leads to impairments in memory, reasoning, planning, and behaviour. It is a neurodegenerative disorder that adversely affects neurons in the brain, ultimately resulting in loss of memory and language, behavioural disturbances, and dependence on caregivers (Phillips, Baktir, Das, Lin & Salehi, 2015, p. 1047). Alzheimer’s has 3

Alzheimer 's disease which chronically leads to Senile Dementia, is a horrific change in homeostasis for human beings. The most obvious change in homeostasis from Alzheimer 's is loss of memory. Memory loss can vary from short term to long term. Alzheimer 's disease has been occurring in humans for a long time. This is a disease that affects different body systems, and interrupts homeostasis to a significant point. As Alzheimer 's disease is further investigated, there are more discoveries with how it is caused, what it affects, and how to reduce the risk of developing it. Alzheimer 's disease is a frightening disease that is represented in humans. There are many concerns with this disease that are worth finding out for the future victims

A new study shows Alzheimer’s disease is spread from brain cell to brain cell and slowly moves to cover larger areas of the brain. Before the twentieth century scientists weren’t sure how it was transmitted. It moves along paths that nerve cells use to communicate between. Eventually, patients can lose all memory.

Dementia is a disease that affects a vast number of Americans, and people worldwide. As people grow and live longer in today’s world the cases of clinical dementia are increasing. There are many causes of dementia, equally leading to different forms and symptoms of this disease. Most causes of dementia are known, and labeled in order to establish proper treatment. Alzheimer’s disease is the most common form of dementia, accounting for more than half of all people with dementia. The cause, and symptoms of Alzheimer’s disease are well known within the scientific community, but a cure is yet to be discovered. This show that there is still much improvement to be done within the scientific and medical