ology: institute of aging, n.d.) Beta Amyloid, which

ology: How Alzheimer’s disease effects the brain

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.)

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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.












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. These fragments 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 a protective layer of fatty tissues called
myelin sheaths which cover the cell and prevent the spread of 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.) All the releases
Beta-amyloid fragments then begin to tangle up and clump together becoming
insoluble which forms clumps and eventually plaques . (Cognitive
disorders, n.d.)









The other
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 central transport system.
Nutrients and signals are carried up and down structures in the cells, which
are called microtubules, to all parts of the neuron. In Alzheimer’s patients,
abnormal Tau separates from the microtubules causing them to break up and
disintigrate. The dislodged Tau then
start to tangle and clump together. These clumps and tangles then block the cellular
transport system and lead to the death of the nerve cell. (Bailly, n.d.) The nerve endings at
the end of the axon are the first microtubules to disintegrate. As time goes 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 is reduced and, once the neuron has degenerated,
communication is cut off completly. (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 try 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 aid the overwhelmed microglia but the damage has already been
sustained. 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, tangles
and 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 tissue
loss inside the brains cerebral cortex, and more precisely, the hippocampus.

contributing factors

Years 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.)


The third most prominent
contributing factor of Alzheimer’s disease is Neuroinflammation. When the APP’s
are cut, they 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 free radicle generators. Studies have
revealed a number of abnormalities within the microglial cells reaction to Alzheimer’s
disease. These abnormalities are triggered by Beta-amyloid and tau and in turn
help them to spread within the brain. (Neuropthology, 2016)



As you get
older, the brain can be put under stress by means of 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).


Because 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.)


It’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 (Biography.com,
Recent studies have shown that dementia and Parkinson’s develop more frequently
and earlier 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)


Alzheimers universal, 2010. inside
the brain. Online
Available at: https://www.youtube.com/watch?v=NjgBnx1jVIU
Accessed 26 january 2018.
Alzheimer’s Universal, n.d. UNRAVELING THE MYSTERY
Available at: http://hdvideo2018.download/download-Inside-the-Brain-Unraveling-the-Mystery-of-Alzheimer-s-Disease-HQ_NjgBnx1jVIU.html
alzheimer’s universal, n.d. inside the brain. Online

Available at: http://hdvideo2018.download/download-Inside-the-Brain-Unraveling-the-Mystery-of-Alzheimer-s-Disease-HQ_NjgBnx1jVIU.html
Accessed 22 january 2018.
Bailly, D., n.d. amyloid plaques. Online
Available at: http://thebrain.mcgill.ca/flash/d/d_08/d_08_cl/d_08_cl_alz/d_08_cl_alz.html
Accessed 25 january 2018.
Biography.com, n.d. Real story behind concussion. Online

Available at: https://www.biography.com/news/concussion-movie-true-story
Accessed 23 january 2018.
Boston ~University Medical Centre, 2017. Link
found between concussions, Alzheimer’s disease. Online
Available at: https://www.sciencedaily.com/releases/2017/01/170112110804.htm
Accessed 23 january 2018.
Cognitive disorders, n.d. Dementia. Online
Available at: https://cognitivedisorders.weebly.com/pathophysiology.html
Accessed 23 january 2018.
Fox, L., 2015. Macroautophagy of Aggregation-Prone
Proteins in Neurodegenerative Disease. Autophagy: Cancer, Other
Pathologies, Inflammation, Immunity, Infection, and Aging.
md current, n.d. Inside the brain. Online
Available at: http://mdcurrent.in/patients/inside-brain-unraveling-mystery-alzheimers-disease/
Accessed 24 january 2018.
national institute of aging, 2017. How Alzheimer’s
Changes the Brain. Online
Available at: https://www.nia.nih.gov/health/video-how-alzheimers-changes-brain
Accessed 22 january 2018.
National institute of aging, n.d. Alzheimers
disease facts. Online
Available at: https://www.nia.nih.gov/health/alzheimers-disease-fact-sheet
Neuropthology, 2016. Degenerative diseases. Online

Available at: http://neuropathology-web.org/chapter9/chapter9bAD.html
Accessed 21 january 2018.
Roskey, A., n.d. Beta secretese. Online
Available at: http://proteopedia.org/wiki/index.php/Beta_Secretase_%28BACE1%29_1SGZ
Accessed 24 january 2018.
webmd, n.d. myelin sheath. Online
Available at: https://www.webmd.com/multiple-sclerosis/myelin-sheath-facts
Accessed 23 january 2018.



Picture reference


Fig.20) Alzheimer’s medication. Retrieved from: https://www.discountdrugnetwork.com/the-struggle-to-afford-alzheimers-medication/ accessed on 17/01/18

Fig.21) Amyloid beta and Alzheimer’s disease.
Retrieved from: http://sage.buckinstitute.org/amyloid-beta-and-alzheimers-disease/
accessed on 21/01/18

Fig.22) Nerve cell. Retrieved from: http://mcat-review.org/specialized-eukaryotic-cells-tissues.php
accessed on 19/01/18

Fig.23) Neurofibrillary tangle. Retrieved from: http://www.alamy.com/stock-photo/neurofibrillary-tangle.html accessed on 24/01/18

Fig.24) Oxidative medicine. Retrieved from: https://www.researchgate.net/figure/289586526_A-diagram-of-amyloid-precursor-protein-APP-processing-pathway-The-transmembrane
accessed on 27/01/18