Pathology: How Alzheimer’s Disease effects the brainApproximately48,000 people in Ireland are affected by Alzheimer’s, a figure which is growing every day.

Because this disease is so prominent in our societyit is important for us, as chemists, to not only be aware of the facts andstatistics, but also what chemical reaction and imbalances make this disease asdevastating and fast acting as it is. In people diagnosed with dementia andAlzheimer’s the cerebral cortex is damaged and shrivels up. This isthe outer layer of the brain and plays a key role in memory, attention,perception, cognition, awareness, thought, language, and consciousness. ThisShrinkage is especially severe in the hippocampus, an area of the cortex thatplays a key role in formation of new memories. Also evident from the picture is a growth in the size of the brain’sventricles. These are fluid filled spaces within the brain and as they growthey further compress the cortex which further contributes to tissue losswithin the brain. But what causes this to happen? (National institute of aging)        BetaAmyloid, which are peptides of amino acids, are crucially involved inAlzheimer’s disease.

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Beta-amyloid is a section of a larger protein whichis called amyloid precursor protein or APP. Little is known what purpose thisamyloid precursor proteins actually serve but from research scientists know agreat deal about how it appears to function. In its complete form, APP extendsfrom the inside to outside of the brain cell by passing through the membranearound the cell.

When APP is “activated” to do its normal job, it is cut byother proteins called Alpha secretase and Gamma secretase into separate,smaller sections that stay inside and outside cells. There are severaldifferent ways APP can be cut by different enzymes. When cut by two certainenzymes in a certain place, the fragment produced is beta-amyloid. PlaquesTheseplaques form when specific proteins in the neurons cell membrane are processeddifferently. Normally, the alpha-secretase enzyme snips the APP, which releasesa fragment while a second enzyme, Gamma secretase, also cuts the protein in separateplace. These released fragments are thought to benefit neurons. However, in thecells of an alzheimer’s patient, the first snip of the protein is made usuallyby another enzyme Beta secretase. This enzyme plays a crucial role in theformation of sleeves of fatty tissues called myelin sheaths which encase thenerve cells protecting it from viruses and disease.

When Beta secretase cleavesthe APP, combined with the cut made by gamma secretase, this results in therelease of short fragments called beta amyloid. (webmd) When these beta amyloidfragments come together and become insoluble eventually forming clumps andplaques.     NeurofibrillarytanglesAnotherleading cause of Alzheimer’s are neurofibrillary tangles. These are createdwhen a protein called Tau is modified. In normal brain cells, these proteins arecrucial in the structural integrity of the cells internal transport system.Nutrients and other cellular cargo are carried up and down structures calledmicrotubules to all parts of the neuron. In Alzheimer’s patients, abnormal Tauseparates from the microtubules causing them to fall apart. Strands of thisthen dislodged Tau clump together and becomeinsoluble to form tangles inside the neuron which can block the transport system.

(Bailly)The furthest away nerveendings from the nucleus of the cell, which are at the end of the axon, are thefirst microtubules to disintegrate. As time ges on the destruction travels upthe axon moving closer to the nucleus. As a result, communicationbetween the nerve endings and the cell brain is reduced and, once theentire neuron has degenerated, cut off completely. (Alzheimer’s Universal)       There areother cells within the brain which are tasked with clearing debris and otherunwanted particles.

These cells are called astrocyte and microglia. As themicroglia cells attempt to clear away the plaques created by the beta amyloid,they are overwhelmed and chronic inflammation sets in. The astrocyte then reactto the overwhelmed microglia but the damage is already done. With these defencecells disabled, Neurons eventually lose their ability to transport nutrientsand information to each other and become dethatched and die. (national institute of aging, 2017)As time goes on,plaques and tangles effect millions of neurons which begin to breakup and die.It is this mass wipe-out of neurons that leads to the aforementioned tissueloss within the brains cerebral cortex, and more precisely, the hippocampus.

 Other contributing factorsYears of research has pointed towardsneurofibrillary tangles and beta-amyloid plaques being the two maincontributing factors in the formation of Alzheimer’s disease, However, thereare several other reasons responsible.NeuroinflammationOther than beta-amyloid and the tau protein,Neuroinflammation is the third most prominent contributing factor inAlzheimer’s disease. When the APP’s are cut, they tend to deposit in the A?plaques. The APP protein previously mentioned, isreleased throughout the brain following an injury or other trauma. The effects of neuroinflammation are mediatedby microglial cells which are a potent generator of free radicals. Studies haverevealed several abnormalities in the microglial cellsresponse in Alzheimer’sdisease. These abnormailities are triggered by Beta-amyloid and tau and in turnhelp themto spread throughout the brain. (Neuropthology, 2016)Free RadiclesAs the brain ages,it is put der stress by oxidation which in turn causes small mitochondrial DNAmutations.

This process is speeded up in patients with Alzheimer’s disease bythe presence of Beta-amyloid plaques and the previously mentioned microglia (Neuropthology, 2016)DiabetesBecause of low levels of insulin in people withtype two diabetes, there is a high risk factor because of the low insulinresistance within the brain. This low resistance means the neurons metabolismis slowed which an adverse effect on the pathways has used to send signals bymeans of insulin. Brain injuryIt’s Only inthe last 20 years that brain injuries have started to cause any concern in contactsports such as American football, boxing and ice hockey (Biography.com). Recent studies haveshown that Parkinson’s and dementia develop more frequently in people who getconcussed playing high contact sports such as the ones mentioned above. “Wefound that having a concussion was associated with lower cortical thickness inbrain regions that are the first to be affected in Alzheimer’s disease,” DrJasmeet Hayes the assistant professor of psychiatry at BUSM explained “Ourresults suggest that when combined with genetic factors, concussions may beassociated with accelerated cortical thickness and memory decline inAlzheimer’s disease relevant areas.” (Boston ~University Medical Centre, 2017)      Bibliography Alzheimer’s Universal. (n.

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html Bailly, D. (n.d.). amyloid plaques.

Retrieved from thebrain: http://thebrain.mcgill.ca/flash/d/d_08/d_08_cl/d_08_cl_alz/d_08_cl_alz.html Biography.com. (n.d.

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com: https://www.biography.com/news/concussion-movie-true-story Boston ~University Medical Centre. (2017, January 12). Link found between concussions, Alzheimer’s disease.

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html webmd. (n.d.). myelin sheath.

Retrieved from webmd: https://www.webmd.com/multiple-sclerosis/myelin-sheath-facts         Picture referenceFig.10) Alzheimer’s medication.

Retrieved from: https://www.discountdrugnetwork.com/the-struggle-to-afford-alzheimers-medication/Fig.11) Fig.13) Nerve cell. Retrieved from: http://mcat-review.

org/specialized-eukaryotic-cells-tissues.phpFig.14) Neurofibrillary tangle. Retrieved from: http://www.alamy.com/stock-photo/neurofibrillary-tangle.html