Amyloid precursor protein

gene and its corresponding protein does not guarantee onset (Hardy). Rather, external elements such as lifestyles, coupled with the action of multiple genes characterize AD as a complex trait. One hallmark of AD is amyloid beta plaques, large aggregates found in the patient brains composed of the peptide, amyloid beta. These amyloid plaques form the basis for the primary hypothesis behind AD, the amyloid cascade hypothesis. The cascade begins with amyloid precursor protein (APP). APP is cleaved by

Abstract: Neurodegenerative diseases are progressive disorders that mainly affect neuronal cells and functions, and commonly characterized by abnormal protein metabolism and aggregations i.e. Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease, Prion diseases, Motor neurone disease, Amyotrophic lateral sclerosis (ALS), Lou Gehrig’s disease, among others. Currently, there is no single cure out there to treat these debilitating diseases. However, present therapies available either

deterioration of memory a personality that’s marked by the formation of plaques of beta-amyloid protein and tangles of fat in the brain. Abnormalities destroy the ability of neurons to communicate with one another. The brain has a plaque that is located in the tissues surrounding neurons. The tangles are twisted mass of threads made of a protein called tau within the neurons. Normal brains contain beta-amyloid and some tau, but brains with AD plaques and tangles causing proliferate in the hippocampus

predominantly composed of the protein tau, a microtubule-associated protein (Forsyth and Ritzline 1998). Normal tau protein promotes axonal integrity and transport by playing an important role in the assembly of microtubules throughout the nervous system. The gene responsible for tau synthesis is subject to alternative splicing and as a result, six isoforms of tau are found in the human brain (Buee et.al. 2000). These isoforms vary in their state of phosphorylation, altering the proteins’ binding affinity for

(ApoE4) which is located in chromosome 19 is linked to the onset and progression of AD. The synaptic loss is due to a loss of cholinergic neurones which transmits nerve signals in the brain which are known to be linked to memory formation (figure 2). Amyloid plaques cause this loss. S.McGREEVEY et al,2013. J. Cerebral Blood Flow & Metabolism, 2006,1562–1576. ACh and memory ACh helps in memory formation by facilitating cell to cell signalling of the cholinergic neurones in the frontal

(Seyedabadi, 2014 as cited by Boulougouris & Tsaltas, 2008; Kiser et al., 2012; Meltzer et al., 2012). The cause of AD can be associated with many mutations; one specific mutation is in the amyloid precursor protein (APP). The amyloid protein in normal functioning is 40 amino acids long. In AD, this amino chain is 42 amino acids long and cut in the wrong places. Some serotonin modulators are associated with this change in the expression of APP (Seyedabadi, 2014 as

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by β-amyloid plaque formation caused by aggregation of β-amyloid42 within the brain leading to a progressive decline in cognitive function and memory loss (2). Hyperphosphorylated tau protein is occasionally found in brains of AD patients with advanced pathology however, it is not necessarily an indicator of AD but considered a sign of disease severity (2, 4, Kosik et al, 1986). AD is separated into two subcategories following

What is Alzheimer’s Disease? Alzheimer’s Disease (AD) is a type of dementia that is irreversible and it causes problems with memory, thinking and behavior. The symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks. (“Alzheimer’s Disease & Dementia,” n.d.). Dementia is a term for a decrease in the intellectual ability which it can be severe enough to interfere with an individual’s day to day life. The German neurologist Alois Alzheimer was the

Alzheimer’s disease is a progressive decline in cognitive function. It affects the brain by damaging brain cells resulting in a decreased in cognitive function, physical mobility, swallowing and fine motor skills. This disease approximately 5.1 million Americans aged sixty-five or older (Alzheimer 's Association, 2015) of which approximately 700,000 will likely die this year (Alzheimer 's Association, 2015) of related symptoms such as aspiration pneumonia due to decreased swallowing ability. The

and immature, proteins in the endoplasmic reticulum (ER) of the cell. Aggregation of misfolded proteins in this region produces neurofibrillary tangles that correlated to loss of memory in patients. Mutations in the Amyloid Precursor Protein (APP) have displayed direct causes of increased concentration of β-amyloid, which are involved in the production of the neurofibrillary tangles. Chaperone protein, GRP78 in the endoplasmic reticulum increases availability to assist in protein folding, and prevention