Pathology: The effects Alzheimer’sdisease has on the brainApproximately55,000 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, perception, attention,awareness, cognition, thought, language, and consciousness. This Shrinkage isespecially severe in the hippocampus, an area of the cortex that plays a keyrole 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, n.d.)        BetaAmyloid, which are peptides of amino acids, are crucially involved inAlzheimer’s disease.

Beta-amyloid is a section of a protein which iscalled an “amyloid precursor protein”or APP. Not much is actually known what servicethis amyloid precursor proteins actually does but from research scientists knowa great deal about how it appears to function. In its complete form, APPextends from 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 certain proteins within the cell of the neuron are processeddifferently.

Normally, the previously mentioned enzyme alpha-secretase cuts theAPP, which releases a fragment while another enzyme, Gamma secretase, also cutsthe protein in a different place. These fragments are thought to benefitneurons. However, in the cells of an Alzheimer’s patient, the first snip of theprotein is made usually by another enzyme Beta secretase.

(Anderson, 2014)This enzyme plays a crucial role in the formationof a protective layer of fatty tissues called myelin sheaths which cover the celland prevent the spread of viruses and disease. (Alzheimers universal, 2010)When Beta secretase cleaves the APP, combined with the cut made by gammasecretase, this results in the release of short fragments called Beta-amyloid. (webmd, n.d.) All the releasesBeta-amyloid fragments then begin to tangle up and clump together becominginsoluble which forms clumps and eventually plaques. (Cognitive disorders, n.d.

) (Anderson, 2014)       Neurofibrillarytangles.The otherleading 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 central transport system.Nutrients and signals are carried up and down structures in the cells, whichare called microtubules, to all parts of the neuron.

In Alzheimer’s patients,abnormal Tau separates from the microtubules causing them to break up and disintegrate.The dislodged Tau then start to tangle and clumptogether. These clumps and tangles then block the cellular transport system andlead to the death of the nerve cell.

(Bailly, n.d.) The nerve endings at the end of theaxon are the first microtubules to disintegrate. As time goes on thedestruction travels up the axon moving closer to the nucleus. (Alzheimers universal, 2010)As a result, communicationbetween the nerve endings and the cell is reduced and, once the neuron has degenerated,communication is cut off completly. (Alzheimer’s Universal, n.

d.)        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 try to clear away the plaques created by the beta amyloid, theyare overwhelmed and chronic inflammation sets in (Alzheimers universal, 2010). The astrocyte thenreact to aid the overwhelmed microglia but the damage has already beensustained.

With these defence cells disabled, Neurons eventually lose theirability to transport nutrients and information to each other and become dethatchedand die. (national institute of aging, 2017)As time goes on, tanglesand plaques form in and around millions of neurons which begin to breakup and stopworking.It is this mass wipe-out of neurons that leads to the aforementioned tissueloss inside 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. (Roskey, n.

d.)NeuroinflammationThe third most prominentcontributing factor of Alzheimer’s disease is Neuroinflammation. When the APP’sare cut, they deposit in the A? plaques. TheAPP protein previously mentioned, is released within the brain following aconcussion or other trauma. The effects of neuroinflammation are controlled bymicroglial cells which are a potent free radicle generators. Studies haverevealed a number of abnormalities within the microglial cells reaction to Alzheimer’sdisease.

These abnormalities are triggered by Beta-amyloid and tau and in turnhelp them to spread within the brain. (Neuropthology, 2016) Free RadiclesAs you getolder, the brain can be put under stress by means of oxidation which in turncauses small mitochondrial DNA mutations. This process is speeded up inpatients with Alzheimer’s disease by the presence of Beta-amyloid plaques andthe 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. (Roskey, n.d.

)Brain injuryIt’s only inthe last 20 years that brain injuries have started to cause any concern incontact sports such as American football, boxing and ice hockey (, n.d.).Recent studies have shown that dementia and Parkinson’s develop more frequentlyand earlier in people who get concussed playing high contact sports such as theones mentioned above. “We found that having a concussion was associatedwith lower cortical thickness in brain regions that are the first to beaffected in Alzheimer’s disease,” Dr Jasmeet Hayes the assistantprofessor of psychiatry at BUSM explained “Our results suggest that whencombined with genetic factors, concussions may be associated with acceleratedcortical thickness and memory decline in Alzheimer’s disease relevantareas.” (Boston ~University Medical Centre, 2017) Bibliography Alzheimers universal, 2010.

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Retrieved from: accessed on 17/01/18Fig.21) Amyloid beta and Alzheimer’s disease.Retrieved from: on 21/01/18Fig.22) Nerve cell.

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