Amyloid precursor protein

neurodegenerative processes. Scientists believe that both tau and amyloid work together to instigate the disease. Amyloid is believed to facilitate the spread of tau. However, there is no scientific evidence to back up this statement. Amyloid is a general term for protein fragments that the body naturally produces. Beta amyloid is a protein fragment trimmed from an amyloid precursor protein (APP), (O’Brien & Wong 2011). These protein fragments are usually broken down and removed naturally within healthy

Alzheimer 's disease is a condition that affects the cognitive status of many people around the world regardless of wealth, ethnicity, intelligence or any other factor. A specific case study that demonstrates the destructive nature of the disease can be seen in the case of Akram. Akram was an 80-year-old woman with a past medical history of hypertension, diverticulitis, transient ischemic attack (TIA), and diabetes. Her history did include a serious head injury at the age of 45 from an automobile

invertebrates. Specifically for human Calpain genes, there are nine classical Calpains and six non-classical Calpains, giving a total of 15 Calpain genes for humans. For human Calpain genes, there two genes for regulatory subunits and one specific inhibitor protein. Classical Calpains, especially those found in humans, are ubiquioltly expressed and are controlled through the inhibitor of Calpastain (Trinchese et al., 2008). Although the role of calcium inducing change to enable Calpastatin to bind to Calpain

result is death of the nerve cell within the brain, also referred to as synaptic failure (6). Synaptic failure takes place when amyloid plaque and neurofibrillary tangles develop (7). Amyloid plaque develops from amyloid beta proteins, which are released by enzymes from the amyloid precursor protein that is located on the surface of the neuron (7). The amyloid beta proteins are normally cleared within the body once they are released however, in

cells and it also leads to brain shrinkage. In the brain tissue there are two types of abnormalities that are considered toward the disease, Plaques and Tangles. Plaques are clumps of proteins that may hurt and destroy brain cells. Tangles are a system that requires the normal structure and functioning of a protein. There are many symptoms when it comes to Alzheimer’s disease. For example, memory, you forget conversations you had, misplace possessions, and eventually will forget the names of everyday

people in the UK. The term dementia describes a loss of mental ability associated with gradual death of brain cells (NHS, 2013). This essay, provides an overview of Alzheimer’s disease, focusing on the amyloid hypothesis, which states that the accumulation and deposition of fibrillar -amyloid (beta-amyloid) is the primary driver of neurodegeneration and cognitive decline leading to dementia (Tanzi, 2005). Neurodegeneration is the progressive damage of nerve cells (News medical, 2014), and cognitive decline

According to Alzheimer.net, forty-four million people, worldwide, are diagnosed with Alzheimer’s disease. In the United States, one out of nine people over the age of 65 are diagnosed with this disease, and it ranks as the sixth leading cause of death in the United States. Two out of three people diagnosed with Alzheimer’s are women. Five point three million dollars are depleted every year from citizens diagnosed with Alzheimer’s. Alzheimer’s is “a progressive and fatal disease of the brain” (Lu

Dementia is a general term that is used to describe a disease or disorder that affects brain functioning by a decline in metal ability that can progress enough to interfere with daily life. There are different forms of dementia, such as Huntington’s, Parkinson’s, Vascular, and Frontotemporal, but the number one type of dementia is Alzheimer’s disease. According to the Alzheimer’s Association, one in nine Americans older than the age of 65 currently have been diagnosed with Alzheimer’s disease. Alzheimer’s

When AD is suspected, patients will undergo MRI, PET Scans, and lumbar punctures to look for brain atrophy, beta-amyloid plaques, or increased phosphorylated tau in cerebral spinal fluid (Hyman et al., 2012). The two main biomarkers of AD are beta-amyloid (Aβ) and tau and are highly debated in regards to their function in AD pathophysiology. The production of beta-amyloid plaques may be due to improper functioning of the proteasome preventing the breakdown of Aβ. Support for this theory comes

The protein misfolding induces structural conversion of a soluble protein to insoluble amyloids through self-assembling. The protein aggregation induces the loss of biological function and gain of disease and is well connected to several diseases such as neurodegenerative disorders, prion diseases and type-II diabetes. Several studies have been carried out to elucidate the role of protein misfolding and aggregation in the pathogenesis of a number of protein conformational diseases (ref). Among several