Alpha Synuclein Research Paper

It is not rare for individuals with lupus to undergo muscle throbs and discomfort or have inflammation of certain muscle groups, which causes faintness and loss of intensity. More than 90 percent of people with lupus will encounter joint and/or muscle pain at some time during the path of their illness. In lupus, the immune system of the body raids its own cells and tissues. Precisely, the joints, skin, kidneys, lungs, heart, nervous system, and other organs of the body are affected. Lupus affects generally 10 times as many women as men. Most often, lupus develops in people 18 to 45 years old. (Lahita) Though lupus is most dominant among women, it also may affect men and children, as well as individuals of all ages. Lupus effects each person

According to Lupus.org, lupus is a chronic autoimmune disorder that can affect any of the systems of the body. The organization continues to state that an estimated 1.5 million people within the United States have lupus with more than 16,000 new cases being reported across the nation annually (Lupus.org). While lupus does not often lead to death itself, the complications that can arise will have an impact on how one would embalm a decedent who had the disease. Embalming is a technique used to preserve, sanitize, and present the dead to surviving family, and can be complicated by disease and condition of the body. This paper will discuss the two types of lupus, their effects on the body, treatment of the disease, and how the disease in conjunction

Even today, after so much study, Alzheimer’s is not fully understood. However, researchers do agree that this degenerative disease is caused by the gradual buildup of fibrous protein compounds in the brain, which are known in the scientific world as amyloids. These amyloids in the brain area act like plaque and as a result of their presence, the normal brain functioning is disrupted.

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 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

In damaged regions of the brain, the dysfunction and death of neurons is associated with cytoskeletal abnormalities and results in a reduction in the level of synaptic proteins in the regions of the brain within which these neurons terminate. The distribution and the spread of these abnormalities follow characteristic patterns that are area-specific and even cell-specific. Normal neurons contain neurofilaments, but no neurofibrillary tangles. Visualizing neurons with a marker for neurofilaments and a tau stain allow for the marking of neurons that are diseased or have died. Healthy neurons show no signs of tau while diseased neurons show both neurofilaments and some tau. Dead neurons show solely tau proteins without any

Alzheimer’s disease is characterized by the degeneration of the nervous system, mainly the neurons in the brain leads to nerve cell death and the loss of tissue throughout the whole brain (MacGill, 2009). Over a period, the brain shrinks dramatically, affecting almost all of its normal functions throughout ones life (MacGill, 2009). The brain size shrinks with AD and the tissue tends to have fewer nerve cells and connections (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).

Lupus tears families apart, ruins lives, and brings pain to the affected. “[SLE] is a multisystemic, autoimmune disease of unknown etiology, which affects multiple organ systems, including the central nervous system, or CNS” (Milovancevic et al.). This disease will literally turn a person’s body against itself. It leads to excruciating pain throughout the victim’s body, as if it were on fire. The optimistic side of this coin, however, is that many pharmacologists have created medications that can nullify the effects of most symptoms. These solutions include antimalarial drugs, non-steroidal anti-inflammatory drugs, anti-rheumatic drugs, immunosuppressives, a type of medication called Belimumab, and corticosteroids. While anyone can use the

This form of dementia accounts for 5-15% of dementia cases. Dementia with Lewy Bodies shares similar signs and symptoms with Alzheimer’s Disease and Parkinson’s Disease. This dementia forms due to tiny deposits of a protein called alpha-synuclein, also known as Lewy bodies (Peter V. Rabins, 2012). The signs and symptoms that individuals present with are attention problems, hallucinations, memory loss and motor impairments that are associated with Parkinson’s Disease. This form of dementia is can be difficult to diagnose because the early stages can look like Alzheimer’s disease. Also, it can be difficult because Lewy bodies are present in Parkinson’s Disease as well (Services U. D.,

PSEN1 and PSEN2 are polytopic membrane proteins (Davis et.al., 1998) that form the catalytic core in the protease γ-secretase (Francis et.al., 2002), which is responsible for the proteolysis of APP (Navivaeva & Turner, 2013). When there is a mutation at the loci for PSEN1 and PSEN2, located on chromosome 14 and 1 respectively, the activity of γ-secretase is altered resulting in changes in the proteolysis of APP and increased formation of Aβ (Qain et.al., 1998). Due to the increase of Aβ, amyloid plaques aggregate quickly causing early-onset of AD.

cell linages like astrocytes have been reported to have an elevated level of HSPs to

MJFF is officially ending the MJFF Research Grant 2013 project titled “Alpha-synuclein and other biomarkers in biological samples of LRRK2 PD” with the Fundacio Clinic Per A La Recerca Biomedica. All activities relating to this project ended at Fundacio Clinic Per A La Recerca Biomedica on April 6, 2016. The original funds awarded for the grant was $250,000.00, $125,000.00 payable to Fundacio Clinic Per A La Recerca Biomedica and $125,000.00 payable to Hebrew University Jerusalem. According to our records, MJFF has sent four payments totaling $125,000.00 to Fundacio Clinic Per A La Recerca Biomedica.

Due to the severity of these diseases that are linked with PrLPs and amyloid fibrils, many research groups are using new research on the structure of these infectious proteins to try and develop a method to inhibit the conversion. One such group, led

The brains of people with Alzheimer’s disease have an abundance of two abnormal structures – amyloid plaques and neurofibrillary tangles. These are made of misfolded proteins which can stick together with other misfolded proteins to form insoluble aggregates. If these aggregates build up, they can disrupt cellular communication and metabolism. The third main feature of Alzheimer’s is the loss of connections between cells leading to the ill-functioning and death of cells (Institute and Aging, 2011).

Multiple System Atrophy (MSA), is a progressive and ultimately terminal neurodegenerative disease which generally emerges in later adulthood (1,2). It is associated with the “adverse” accumulation of alpha-synuclein proteins in the pons, medulla, and cerebellar regions of the brain (1). There are two subtypes of MSA: MSA-Parkinsonian, which features symptoms similar to Parkinson’s disease, and MSA-Cerebellar, which manifests predominantly as oculomotor dysfunction in gait and speech.