Findings from epidemiology, genetics, molecular and cell biology are fitting together in the Alzheimer's puzzle, helping researchers to identify some of the mechanisms that underlie it. Alzheimer's starts because the normal processing of certain proteins goes terribly wrong. This causes brain cells and the spaces between them to be cluttered with pieces of toxic protein. Closer investigating with microscopes has revealed a loss of nerve cells in certain regions of the brain. Some of these dying nerve cells communicate using the neurotransmitter acetylcholine, these compounds eventually break down by an enzyme called acetylcholinesterase.
If future research reveals that glutamine aggregates promote cell toxicity, we can direct research on how to inhibit these aggregations to slow down or possibly reverse the course of the disease. 2.) How aging in the infected organism influences the progression of Huntington's disease: Experiments with C. elegans expressing the age-1 genetic mutation not only had an extended the lifespan, but also had a delayed onset of Huntington's disease. This suggests that a substance produced as an organism ages can catalyzes the toxicity of Huntington's disease. With this in mind, further research could hunt for what this aging-related catalyst is.
One of these abnormalities is plaques that clump up, a protein called beta-amyloid which damages and destroys brain cells. In patients with Alzheimer’s the plaques created interfere with cell to cell communication. The other abnormality seen is tangles in the brain. Brain cells depend on an internal support and transport system to carry nutrients and other essential materials throughout their long extensions. This system requires the normal structure and functioning of a protein called tau.
INTRODUCTION: Alzheimer’s disease is a neurodegenerative disease mainly affecting people who are above 65 years of age. There have been various hypotheses that try to rationalize the cause of the disease. The major two hypotheses are the Amyloid hypothesis and Tau hypothesis. The amyloid hypothesis states that the aggregation of extra cellular amyloid-beta in the brain is the fundamental cause of the disease and the presence of Amyloid Precursor Protein (APP) on chromosome 21 supports the same. The Tau protein hypothesis states that a hyperphosphorylation of Tau inhibits its function of stabilizing the micro tubules in the brain thereby destroying its function of neuron transport.
It is suggested that neural apoptosis maybe through the intrinsic pathway or extrinsic. The accumulation of dysfunctional mitochondria because of inefficient removal of damaged mitochondria (mitophagy) causes an increase in free radical leakiness and the cycle of oxidative damage to the bio molecules and thus helping in apoptosis. 
Neurofibrillary tangles then kill the neuron. The final abnormality of Alzheimer’s disease is brain shrinkage. The brain shrink... ... middle of paper ... ... conclude that Alzheimer’s disease is becoming more common and the facts back that up. Just in a span of fourteen years the annual deaths related to Alzheimer’s has become twenty-five times greater. Both by external sources demonstrate that Alzheimer’s has been a problem for a while and will continue to increase if we do not find more efficient treatment methods in the near future.
Vitamin A has an effect on many of the metabolic markers of Alzheimer’s disease. These include inflammation, oxidative stress, and amyloid β in the extracellular. Targeting the receptors for these processes may slow down or reverse Alzheimer’s disease. The research into the effect Vitamin A has on Alzheimer’s disease needs to be furthered. One avenue to further it would be examining retinoic acids in vivo.
The alteration in redox potential may be a common feature in dividing cells, because ROS have been suggested to modulate the cell cycle in many cell lines (Han et al. 2006). Loosing of hepatocytes probably lead to be even worse the liver toxicity of ADR. Although it has been declared that some aspect of angiotensin signaling inhibition could be involved in alleviating adriamycin-induced cardiomyopathy (Octavia et al. 2012), and renopathy (Taskin et al.
This damages neurons that “react with neuron receptors and axon” (Lu & Bludau, 2011), which impinge the cells ability to function. Neurofibrillary tangles are made up of tau proteins. It plays a major role with microtubules, which are shaped like stacks of straws. Microtubules transport important cellular components and nutrients. The tau proteins separate from microtubules and twist into tangles.
Contrary to belief Alzheimer’s is not a normal part of aging. Different parts of the brain are affected causing multiple symptoms sometimes not diagnosed until later stages in the disease. Nerve cell death and tissue throughout the brain is the most significant affect over time. Naturally by age twenty-five the brain starts to decrease in size. With Alzheimer’s, the amount decrease is extremely significant.