Essay on Alzheimer S Disease

Alzheimer S Disease Term Papers

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Alzheimer’s Disease is a progressive, degenerative disease that affects the

brain. Individuals with AD experience a progressive and specific loss of

cognitive function resulting from the differentiation of the limbic system,

association neocortex, and basal forebrain. It is also accompanied by the

deposition of amyloid in plaques and cerebrovasculature, and the formation of

neurofibrillary tangles in neurons. Alois Alzheimer, a German doctor, diagnosed

this disease for the first time in 1907. At that time it was considered a rare

disorder. Currently, this tragic brain disorder affects approximately four

million people; It is the most common type of dementia and the fourth leading

cause of death in the United States. Many studies have been done and are still

being conducted to determine the exact cause of AD. The molecular and biological

basis for the degeneration of neurons in AD is incompletely understood. However,

the APP(Amyloid Precursor Protein) and its proteolytic fragments have been

implicated more often than not and is the focus of most current studies. Several

lines of evidence have strengthened the amyloid hypothesis for Alzheimer’s

Disease. The first being the identification of point mutations with the APP gene

in groups of patients afflicted with the familial forms of AD. Second, amyloid

deposition temporally precedes the formation of neurofibrillary changes. In

addition, b-amyloid has been shown to be toxic to neurons. In Alzheimer’s

Disease, b-Amyloid proteins derived from APP are the main component of neuritic

plaques. It is believed that errantly processed APP derivatives may induce

physiological processes that lead to neurodegeneration and plague formation.

Many studies have successfully linked APP with AD. One study on transgenic mice

with human APP717(associated with familial AD) displayed subcellular

neurodegeneration similar to those observed in AD, including dystrophic neurites,

disruption of synaptic junction, and intracellular amyloid and reactive gliosis.

Amyloid deposits in the tg mice were very similar to those found in AD and was

readily recognized by anti-b-amyloid antibody. In other studies, Hippocampal

pyramidal neurons in AD display an intense immunostaining with 10 different

antibodies against subsequences of APP. The area containing the stained neurons

were consistent with those showing the most neuropathology in AD. Collectively,

these data show APP as being closely associated with neurodegeneration. However,

it is still unclear if APP is the cause of cell death in the AD brain. APP could

be one of many factors participating with differnent intracellular processes to

cause cell death. In hope of finding more information on Alzheimer’s disease,

researchers look for similarities and connections to other more understood

illnesses, one being the prion disease. This disorder is a neurodegenerative

disease characterized by prion protein deposits and is associated with reactive

astrocytes and microglial cells. Alzheimer’s disease is similarly

characterized by plagues and inflammatory astrocytes. Many earlier studies found

that prion peptides and b-amyloid proteins activate microglial cells by

secreting cytokines, reactive oxygen species, and other neurotoxins. Analogous

to typical inflammatory signaling response such as those mediated through

classical immune receptors, b-amyloid and prion proteins activate a common

tyosine kinase-dependent pathway. This was indicated by an elevated level of

phosphotyrosine in plaque associated microglials of AD. Microglial treated with

inhibitors of specific protein in the tyrosine kinase-based pathway successfully

blocked amyloid-stimulated secretion of neurotoxins and reduced the number of

cell death. Despite this documentation on amyloid-induced production of

neurotoxins, it does not resolve the issue of what causes AD. The species

responsible for neurodegeneration in AD still remain controversial. However, it

does implicate b-amyloid peptide along with numerous coordinated response

pathways and mediating species. Neurodegeneration in AD is suspected to be

caused by apoptosis or programmed cell death. Research with andenovirus-mediated

APP gene transfer, demonstrate that neurons in vivo are vulnerable to

intracellular accumulation of APP. Hippocampal pyramidal neurons show severe

atrophy and nuclear DNA fragmentation, a typical feature of apoptosis. Infection

of rat hippocampal cells with an adonovirus contain APP695 cDNA enhanced

glutamate induced rise of intracellular Ca2+ concentration. Elevation of Ca2+

level in the cellular compartment can cause activation of a numbers

Ca2+-dependent degradative processes, including apoptosis. Interestingly, one of

the newly discovered "apoptosis-linked genes" encodes a Ca2+ binding

site. The increase in intracellular level of Ca2+ could come from the impairment

of glucose transporters. Data from studies in AD shows that the transporters for

Glucose uptake, GLUT3, to be decreased. When glucose uptake is compromised, ATP

production diminishes, Na/K+ pumps stops and the neuron depolarizes releasing

glutamate. Large release of glutamate can cause a Ca2+ overload in the neuron.

Thus, neurons with a compromised Ca2+ buffering system such as those found in

the aging or AD will be most affected by changes to Ca2+...

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