Alzheimer's Research Paper

Over the last 30 years, immense scientific progress in the fields of neuroscience, cell biology, genetics, and technology has allowed us to examine and understand the brain in much more detail than before. Recently, a team of ten researchers from the UCLA Research Center and the University of Wisconsin tested a new software produced in Denmark called Neuroreader, a program used for measuring hippocampal volume. With this new program, the slightest changes in brain volume can be detected rapidly, allowing for earlier diagnosis of brain disorders including Alzheimer's. Indeed, such advancements have altered the way scientists think about Alzheimer’s disease (AD), a progressive brain disorder that gradually eliminates the patient’s memory and

The final goal is to translate the information obtained from scientific discoveries into new treatments to improve cognitive function, slow the progression of AD, delay the onset, and ultimately prevent AD. Currently, there are an estimated 5.3 million Americans with AD, and the estimated cost of care in the US in 2010 for AD and other dementias was 172 billion dollars. (12) It is estimated that the worldwide prevalence of AD will be 30 million, and the number is expected to quadruple by 2050. (12) Evidently, Alzheimer’s is becoming one of the most prevalent and important global public health issues. Unfortunately, despite these statistics, Alzheimer’s research remains severely underfunded. AD requires more attention from the world, and should become an imminent

His examination of his patients with AD revealed their brains to be composed largely of amyloid-β peptide and hyperphosphorylated tau protein, a protein that stabilizes the microtubules of neurons. (10) Since 1907, evidence accumulated from ensuing experiments strongly suggests that the initiating event in Alzheimer's disease (AD) is related to abnormal processing of β-amyloid (Aβ) peptide, ultimately leading to formation of Aβ plaques in the brain. The amyloid cascade hypothesis has become the most widely accepted explanation for Alzheimer’s. The hypothesis states that the depositing of the amyloid-β peptide in the brain is a crucial step leading to Alzheimer's disease. (5) The onset of AD is associated with mutations four types of proteins: the precursor protein for Aβ called APP, presenilin-1 (PS1) or presenilin-2 (PS2), proteins associated with the growth of and development of nervous tissue, in apolipoprotein E, a major cholesterol carrier involved in lipid transport and injury repair in the brain, and tau protein. (13) Mutations in the proteins PS1 and PS2 enhances the processing of APP, leading to the development of large amounts of Aβ, which is toxic for the neurons. (7) Aβ can cause neurotoxic effects in many ways, including disruption of mitochondrial function by binding of the Aβ-binding alcohol dehydrogenase (ABAD) protein, induction of apoptotic genes through inhibition of Wnt, by