Pathology: attention, perception, cognition, awareness, thought, language, and consciousness.

Pathology: How Alzheimer’s disease effects the brain

Approximately
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.
Another side-effect from Azheimer’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.)

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Beta
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. Not much is actually known what function or
role this amyloid precursor proteins actually plays 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.

 

 

 

 

 

 

 

 

 

 

Plaques

These
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. (Anderson, 2014)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.) (Anderson,
2014)

 

 

 

 

 

 

 

Neurofibrillary
tangles.

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 disintegrate.
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.

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.)

Neuroinflammation

The third most prominent
contributing factor of Alzheimer’s disease is Neuroinflammation. When the Amyloid
precursor proteins are cut, they deposit in the Beta amyloidf 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)

 

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).

Diabetes

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.)

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 (Biography.com,
n.d.).
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)

Bibliography

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Biography.com, n.d. Real story behind concussion. Online

Available at: https://www.biography.com/news/concussion-movie-true-story
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Available at: http://neuropathology-web.org/chapter9/chapter9bAD.html
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Roskey, A., n.d. Beta secretese. Online
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webmd, n.d. myelin sheath. Online
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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