Pathology: is called an “amyloid precursor protein “or

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Pathology: How Alzheimer’s disease effects the brain

Close to
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, 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.
Another side-effect of Alzheimer’s disease is a growth in the size of the
brain’s ventricles which can be seen in the picture below. 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.)50








Amyloid, which are peptides of amino acids, play a crucial role in Alzheimer’s
disease. Beta-amyloid is a segment of a certain protein which is called an
“amyloid precursor protein “or APP. Very little is actually known about what
role this amyloid precursor proteins plays within the brain but from research, scientists
know a great deal about how it appears to function. In its full form, APP
extends from the inside to outside of the brain cell by passing through the membrane
which surrounds the cell. When APP is “activated” to do its normal job, it is
snipped by other proteins known as Alpha secretase and Gamma secretase into
separate, smaller sections that stay inside and outside cells. There are various
different ways in which APP can be cut by different enzymes. When cut by two certain
enzymes in a certain place, the fragment produced is beta-amyloid.

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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 known to
benefit neurons. However, in the brain cells of an Alzheimer’s patient, the
first snip of the protein is usually made by another enzyme Beta secretase. (Anderson, 2014)51This
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)52 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.)53 All the
releases Beta-amyloid fragments then begin to get tangled up and clump together
becoming insoluble which forms clumps and eventually Beta-amyloid plaques. (Cognitive
disorders, n.d.)54 (Anderson,









leading cause of Alzheimer’s disease are neurofibrillary tangles. These are formed
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. Signals
and nutrients 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 which causes them to break up and disintegrate.
The dislodged Tau then start to clump and tangle
together. (cognitive disorders, n.d.)These clumps and
tangles then block the internal transport system and lead to the death of the
nerve cell. (Bailly, n.d.)56 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)57
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.)58








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)59. 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)60As time
goes on, tangles and plaques form in and around millions of neurons which begin
to breakup and stop working. 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.

Other 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.)61


The third most prominent
contributing factor of Alzheimer’s disease is Neuroinflammation. When the Amyloid
precursor proteins are cut, they deposit in the Beta amyloid plaques. The cut APP is released throughout the brain
following a concussion or other trauma. The effects of neuroinflammation are controlled
by microglial cells which are 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)62


Free Radicles

As you get
older, the brain can be put under stress by means of oxidation which in turn
causes small mitochondrial mutations of the DNA. This process is hastened in
patients with Alzheimer’s disease by the presence of plaques and the previously
mentioned microglia (Neuropthology, 2016)63.


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.)64

Brain injury

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 (,
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 and repeated head trauma may be
associated with accelerated cortical thickness and memory decline in
Alzheimer’s disease relevant areas.” (Boston ~University Medical
Centre, 2017)66


50Alzheimers universal, 2010. inside the brain. Online

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51Alzheimer’s Universal, n.d. UNRAVELING THE MYSTERY
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52alzheimer’s universal, n.d. inside the brain. Online

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53Bailly, D., n.d. amyloid plaques. Online
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Accessed 25 january 2018., n.d. Real story behind concussion. Online

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61 Cognitive
disorders, nd Available at :
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55Boston ~University Medical Centre, 2017. Link
found between concussions, Alzheimer’s disease. Online
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Accessed 23 january 2018.
56Cognitive disorders, n.d. Dementia. Online
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Accessed 23 january 2018.
57Fox, L., 2015. Macroautophagy of Aggregation-Prone
Proteins in Neurodegenerative Disease. Autophagy: Cancer, Other
Pathologies, Inflammation, Immunity, Infection, and Aging.
58md current, n.d. Inside the brain. Online
Available at:
Accessed 24 january 2018.
59national institute of aging, 2017. How Alzheimer’s
Changes the Brain. Online
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Accessed 22 january 2018.
60National institute of aging, n.d. Alzheimers
disease facts. Online
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61Neuropthology, 2016. Degenerative diseases. Online

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Accessed 21 january 2018.
62Roskey, A., n.d. Beta secretese. Online
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63webmd, n.d. myelin sheath. Online
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Fig.20) Alzheimer’s medication. Retrieved from: accessed on 17/01/18

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

Fig.22) Nerve cell. Retrieved from:
accessed on 19/01/18

Fig.23) Neurofibrillary tangle. Retrieved from: accessed on 24/01/18

Fig.24) Oxidative medicine. Retrieved from:
accessed on 27/01/18



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