Pathology: normal job, it is cut by other proteins

Pathology: How Alzheimer’s disease effects the brainApproximately 55,000 people in Ireland are affected by Alzheimer’s, a figure which is growing every day. Because this disease is so prominent in our society it is important for us, as chemists, to not only be aware of the facts and statistics, but also what chemical reaction and imbalances make this disease as devastating and fast acting as it is. In people diagnosed with dementia and Alzheimer’s the cerebral cortex is damaged and shrivels up. This is the outer layer of the brain and plays a key role in memory, attention, perception, cognition, awareness, thought, language, and consciousness. This Shrinkage is especially severe in the hippocampus, an area of the cortex that plays a key role in formation of new memories. Also evident from the picture is a growth in the size of the brain’s ventricles. These are fluid filled spaces within the brain and as they grow they further compress the cortex which further contributes to tissue loss within the brain. But what causes this to happen? (National institute of aging, n.d.)Beta Amyloid, which are peptides of amino acids, are crucially involved in Alzheimer’s disease. Beta-amyloid is a section of a larger protein which is called amyloid precursor protein or APP. Not much is actually known what service this amyloid precursor proteins actually does but from research scientists know a great deal about how it appears to function. In its complete form, APP extends from the inside to outside of the brain cell by passing through the membrane around the cell. When APP is “activated” to do its normal job, it is cut by other proteins called Alpha secretase and Gamma secretase into separate, smaller sections that stay inside and outside cells. There are several different ways APP can be cut by different enzymes. When cut by two certain enzymes in a certain place, the fragment produced is beta-amyloid. PlaquesThese plaques form when certain proteins within the cell of the neuron are processed differently. Normally, the previously mentioned enzyme alpha-secretase cuts the APP, which releases a fragment while another enzyme, Gamma secretase, also cuts the protein in a different place. Thesefragments are thought to benefit neurons. However, in the cells of an Alzheimer’s patient, the first snip of the protein is made usually by another enzyme Beta secretase. This enzyme plays a crucial role in the formation of sleeves of fatty tissues called myelin sheaths which encase the nerve cells protecting it from viruses and disease. (Alzheimers universal, 2010) When Beta secretase cleaves the APP, combined with the cut made by gamma secretase, this results in the release of short fragments called beta amyloid. (webmd, n.d.) beta amyloid fragments then come together and become insoluble eventually forming clumps and plaques. (Cognitive disorders, n.d.)Neurofibrillary tanglesAnother leading cause of Alzheimer’s are neurofibrillary tangles. These are created when a protein called Tau is modified. In normal brain cells, these proteins are crucial in the structural integrity of the cells internal transport system. Nutrients and other cellular cargo are carried up and down structures called microtubules to all parts of the neuron. In Alzheimer’s patients, abnormal Tau separates from the microtubules causing them to fall apart. Strands of this then dislodged Tau clump together and become insoluble to form tangles inside the neuron which can block the transport system. (Bailly, n.d.)The furthest away nerve endings from the nucleus of the cell, which are at the end of the axon, are the first microtubules to disintegrate. As time ges on the destruction travels up the axon moving closer to the nucleus. (Alzheimers universal, 2010) As a result, communication between the nerve endings and the cell brain is reduced and, once the entire neuron has degenerated, cut off completely. (Alzheimer’s Universal, n.d.)There are other cells within the brain which are tasked with clearing debris and other unwanted particles. These cells are called astrocyte and microglia. As the microglia cells attempt to clear away the plaques created by the beta amyloid, they are overwhelmed and chronic inflammation sets in. (Alzheimers universal, 2010)The astrocyte then react to the overwhelmed microglia but the damage is already done. With these defence cells disabled, Neurons eventually lose their ability to transport nutrients and 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 tissue loss within the brains cerebral cortex, and more precisely, the hippocampus.Other contributing factorsYears of research has pointed towards neurofibrillary tangles and beta-amyloid plaques being the two main contributing factors in the formation of Alzheimer’s disease, however, there are several other reasons responsible. (Roskey, n.d.)NeuroinflammationOther than beta-amyloid and the tau protein, Neuroinflammation is the third most prominent contributing factor in Alzheimer’s disease. When the APP’s are cut, they tend to deposit in the A? plaques. The APP protein previously mentioned, is released within the brain following a concussion or other trauma. The effects of neuroinflammation are controlled by microglial cells which are a potent generator of free radicals. Studies have revealed a number of abnormalities in the microglial cells reaction to Alzheimer’s disease. These abnormalities are triggered by Beta-amyloid and tau and in turn help them to spread throughout the brain. (Neuropthology, 2016)Free RadiclesAs the brain ages, it is put der stress by oxidation which in turn causes small mitochondrial DNA mutations. This process is speeded up in patients with Alzheimer’s disease by the presence of Beta-amyloid plaques and the previously mentioned microglia (Neuropthology, 2016)DiabetesBecause of low levels of insulin in people with type two diabetes, there is a high risk factor because of the low insulin resistance within the brain. This low resistance means the neurons metabolism is slowed which an adverse effect on the pathways has used to send signals by means of insulin. (Roskey, n.d.)Brain injuryIt’s only in the last 20 years that brain injuries have started to cause any concern in contact sports such as American football, boxing and ice hockey (, n.d.). Recent studies have shown that Parkinson’s and dementia develop more frequently in people who get concussed playing high contact sports such as the ones mentioned above. “We found that having a concussion was associated with lower cortical thickness in brain regions that are the first to be affected in Alzheimer’s disease,” Dr Jasmeet Hayes the assistant professor of psychiatry at BUSM explained “Our results suggest that when combined with genetic factors, concussions may be associated with accelerated cortical thickness and memory decline in Alzheimer’s disease relevant areas.” (Boston ~University Medical Centre, 2017)BibliographyAlzheimers universal, 2010. inside the brain. Online Available at: 26 january 2018.Alzheimer’s Universal, n.d. UNRAVELING THE MYSTERY OF ALZHEIMER’S DISEASE. Online Available at:’s universal, n.d. inside the brain. Online Available at: 22 january 2018.Bailly, D., n.d. amyloid plaques. Online Available at: 25 january, n.d. Real story behind concussion. Online Available at: 23 january 2018.Boston ~University Medical Centre, 2017. Link found between concussions, Alzheimer’s disease. Online Available at: 23 january 2018.Cognitive disorders, n.d. Dementia. Online Available at: 23 january 2018.Fox, L., 2015. Macroautophagy of Aggregation-Prone Proteins in Neurodegenerative Disease. Autophagy: Cancer, Other Pathologies, Inflammation, Immunity, Infection, and current, n.d. Inside the brain. Online Available at: institute of aging, 2017. How Alzheimer’s Changes the Brain. Online Available at: 22 january 2018.National institute of aging, n.d. Alzheimers disease facts. Online Available at:, 2016. Degenerative diseases. Online Available at: 21 january 2018.Roskey, A., n.d. Beta secretese. Online Available at: 24 january 2018.webmd, n.d. myelin sheath. Online Available at: 23 january 2018.Picture referenceFig.20) Alzheimer’s medication. Retrieved from: accessed on 17/01/18Fig.21) Amyloid beta and Alzheimer’s disease. Retrieved from: accessed on 21/01/18Fig.22) Nerve cell. Retrieved from: on 19/01/18Fig.23) Neurofibrillary tangle. Retrieved from: accessed on 24/01/18Fig.24) Oxidative medicine. Retrieved from: accessed on 27/01/18


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