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Paper 183
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MEMORY ASSISTING NEURAL IMPLANTS IN PERSONS AFFLICTED WITH
ALZHEIMER’S DISEASE
Benjamin LeStourgeon, [email protected], Mahboobin 10:00, Michael Shulock, [email protected], Mahboobin 10:00
Abstract—This paper will discuss brain implants that are
used to improve memory function. Neural implants are small
devices placed on the surface or inside the brain that mimic
or alter functions of the brain. The brain communicates with
itself and with the rest of the body with electronic signals.
Neurons do this by transferring electronically charged
particles between them to relay signals. These electronic
signals can be measured when the electrodes of a brain
implant are placed on the surface of the brain. If the brain has
trouble forming memories, as with in Alzheimer victims, these
implants can help. If these implants are able to mimic neuron
activity, then they could bridge gaps caused by damaged
neurons. As a result, some memory function can be returned.
This paper will focus on how successes in memory storage
could alleviate the suffering of millions of Alzheimer’s
patients. The work of the University of Southern California’s
Dr. Theodore Berger will be extensively discussed in this
paper. Drawing from Dr. Berger’s studies, among others, this
paper will detail the progress of in vivo trials of brain
implants. Additionally, several codes of ethics, including that
of the Human Brain Project, will be used to evaluate the
ethicality of clinical use of memory enhancing neural
implants.
communicate by means of electric signals and form memories
by completing a path through certain areas of the brain. As
neurons deteriorate due to Alzheimer’s, these paths will be
increasingly more difficult to make, impeding memory.
Neural implants use electrodes that employ electrochemical
methods to measure brain signals, which are then transformed
into different signals that the implant outputs to other parts of
the brain. This process can be used to bypass deteriorated
parts of the brain that result from diseases such as
Alzheimer’s. This technology has shown growth over the
years; studies in a variety of non-human mammals have been
conducted. While the memory assistance functionality has not
been implemented in humans yet, brain implants have been
successful in treating other neurological disorders, such as
blindness, demonstrating that they have real medical
potential. While the potential for memory-assisting implants
exists, there are several issues that occur making progress
difficult, such as the invasiveness of electrodes in the brain
and the ethicality of the technology. However, the idea of
simulating a human brain using manmade materials gives
hope to many who wrestle with neurological issues.
Key Words- Alzheimer’s, Electrodes, Hippocampus, Memory,
Neural Implant, Neuron
The brain, an infinitely complex organ that dictates our
every thought and action, is composed of long cells called
neurons. According to “Mind and Body,” a magazine run by
the University of Campinas, neurons have distinct parts that
include the nucleus, the dendrites, the axon, the axon
terminals, and the myelin sheath [2]. Basic neuron structure is
shown in Figure 1, provided by “Mind and Body.”
OVERVIEW OF BRAIN FUNCTION
NEURAL IMPLANTS: A MODERN
MIRACLE
According to the UN News Centre, neurological disorders
afflict about one sixth of the world’s population [1], and
because the brain is the most vital and complex organ in the
body, these diseases are particularly destructive. Doctors and
researchers alike are constantly in search of new ways to
combat these common devastating diseases. One of these
technologies is the neural implant, which is a small device that
mimics the functions of a healthy portion of a brain. Neural
implants have the capability to restore memory function to
those that have lost it, and one of the most applicable uses for
neural implants is providing memory improvement for
individuals suffering with Alzheimer’s disease, a disorder
caused by brain deterioration. Sections of the brain
University of Pittsburgh Swanson School of Engineering
03.31.2017
FIGURE 1 [2]
Neuron with its parts labeled
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Michael Shulock
Benjamin LeStourgeon
The nucleus, depicted as an orange circle above and located
in the soma (cell body), encloses the DNA for the cell, which
is the blueprint for the necessary proteins that compose the
cell. The dendrites, labeled in the upper left of Figure 1,
receive signals from surrounding neurons, which are then
transferred to the soma. These signals are then carried by the
tube-like axon to the axon terminals, labeled on the right of
Figure 1. The myelin sheath, which is composed of proteins
and phospholipids, surrounds the axon. It serves to protect the
axon, preserve the signal it is carrying, and speed up the signal
[3]. The myelin sheath, depicted as orange segments in Figure
1, does so by being electrically insulative, meaning that
outside electrical signals will not affect the signal in the axon.
The dendrites from one neuron meet an axon terminal of
another neuron, and this meeting is called a synapse. Within
a synapse, the dendrites and the axon terminal are not actually
touching. They have a nanoscopic gap between them called
the synaptic cleft/gap, which is where the interneural
communication occurs.
If the synaptic gap is very small, the synapse will be
deemed an electrical synapse. This term indicates that the
dendrite and axon terminal are close enough that they can
exchange ions, charged molecules, freely and directly. If the
dendrite and axon terminal are farther away, the synapse is a
chemical synapse, which requires the exchange of ions to be
done with neurotransmitters, small membranous sacs that
contain ions sent from the axon to the dendrite [2]. Regardless
of how ions are transferred from one neuron to the other, the
result is an action potential. Action potential is defined by the
University of Texas Medical School as a rapid movement of
ions through the axon [4]. This occurs due to the potential
energy, or stored energy, resulting from the attraction
between ions of opposite charges, hence the name. When a
neuron is in its resting state, or when there is no introduction
of charge, the inside of the axon is innately negative, while
the extracellular fluid outside the axon is positive. The
potential energy caused by this difference in charge is roughly
-70 meV (millielectronvolt) [4]. When an action potential
begins, a positive charge is introduced to the base of the axon,
via the soma, and small holes in the axon called ion channels
open, allowing positive ions into the base of the axon. The
result is a decrease in the potential energy between the
positive and negative charges, which is desirable by nature.
This triggers ion channels further down the axon to allow
more positives in the axon. Simultaneously, different
channels actively pump out the positive ions that have already
entered the axon, as shown in Figure 2 [3].
FIGURE 2 [3]
Diagram that shows how axon channels let plus ions in
and plus ions out, “moving” the charge down the axon
This process, action potential, “moves” the positive charge
from one end of the axon to the axon terminals, with the whole
progression lasting only about 1 millisecond [4]. After the
action potential is complete, small waves of voltage
difference occur for a short period of time as a result from this
rapid movement of charge. This is called the after-potential.
The action potential is the result of the initial stimulus, the
introduction of positive ions. The stimulus must be great
enough to cause the ion channels to open and begin the action
potential sequence. As a result, the action potential only
occurs at some threshold of stimuli. Additionally, action
potentials within a particular neuron do not vary in magnitude
or the speed at which they travel down the axon [4]. The
characteristic that distinguishes action potentials in a neuron
is their frequency. Different external stimuli and thought
processes cause a neuron to fire at different frequencies. The
signal’s frequency dictates the outcome of that thought.
Typically, more intense actions or thoughts result in higher
action potential frequency. Action potentials propagate
information throughout the brain; their frequency and
magnitude can be measured, and patterns can be observed [4].
These patterns of action potential are responsible for
everything we do, think, and remember. Dr. Theodore Berger,
a researcher at the University of Southern California who is
behind much of the research concerning neural implants,
defines memory as “A series of electrical pulses over time that
are generated by a given number of neurons” [5]. Thus, each
pattern of action potentials serves as a memory.
These memories, or patterns of action potentials, need to
be stored in order for them to be used by the brain later. The
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part of the brain responsible for generating long term
declarative memory, things learned consciously, is called the
hippocampus [6]. The hippocampal region receives electrical
signal via action potential from the prefrontal cortex. There is
then a circuitry within the hippocampus that the signal moves
through to produce a memory [5]. This circuitry is illustrated
below in Figure 3 and Figure 4.
states that along this same path, the memory is contextualized
by relating it with other information, such as emotion or
smell. One particular path, most studied by Dr. Berger, is one
that passes through the Cornu Ammonis (CA) 3 and then into
the CA1. These are the violet structures shown in Figure 3.
The path may possibly pass through the subiculum (sub), the
teal structure in Figure 3. Finally, like the majority of the
paths, it is terminated in a different part of the EC called the
deep EC [9]. This path has been highlighted in the bottom left
corner of Figure 4.
ALZHEIMER’S AND BRAIN
DETERIORATION
While the brain’s complex circuitry is necessary for
complex human function, any disruption can have a
devastating effect on the neural function. Since each part of
the brain works in tandem with other sections, a disturbance
in one area will usually prevent normal function in multiple
parts. One of the most common and deadly diseases that
causes this damage is Alzheimer’s disease. The Alzheimer’s
Association estimates that 5 million people are living with
Alzheimer’s in the U.S. alone, and that the disease kills more
than breast and prostate cancer combined [10].
According to the University of Maryland’s Medical
Center, Alzheimer’s disease is defined as “a progressive
degenerative disease of the brain from which there is no
recovery” [11]. While the cause of the disease is mysterious,
the symptoms are quite observable as the disease progresses.
Alzheimer’s ravages the neurons, disconnecting synapses and
breaking chains of action potential throughout the brain.
According to the National Institute of Aging, the
discontinuities throughout the brain caused by the disease
results in memory loss, confusion, mood disruption, and an
overall decrease in cognition [12].
FIGURE 3 [7]
Displays the hippocampal circuitry. This diagram
focusses on the areas closer to the CA regions
Neurofibrillary Tangles
There are two main causes of neural disruption as a result
of Alzheimer’s, one of which is the accumulation of
neurofibrillary tangles. Within the medical journal
Biochimica et Biophysica Acta, professor Lester Binder of
Northwestern expresses that these tangles are comprised of
the protein tau, and as a result are often referred to as tau
tangles [13]. Tau proteins in a healthy brain provide structure
to microtubules, which play a role in transporting necessary
nutrients throughout the neuron. In an Alzheimer’s patient’s
brain, these tau proteins become mutated and separate from
the microtubule, and as a result the microtubules’ structure is
compromised. These tau proteins accumulate and form
masses known as tau tangles. According to Binder, as the
system for nutrient distribution collapses, the neuron becomes
dysfunctional. This entails the loss of communication with
surrounding neurons. The tau tangles within the cell grow
FIGURE 4 [8]
Shows a more lifelike diagram of hippocampal anatomy
than Figure 3 and shows the direction signals move in it
According to Mark Mayford of the Scripps Research Institute,
the signal is generally received in the entorhinal cortex (EC),
which is labeled on the far left of Figure 4. Although action
potential movement through the hippocampal region is not
identical for each memory, there are a few patterns that seem
to occur more often than others. Regardless of the path, the
purpose of this stage is to create and strengthen the long-term
potentiation between the synapses, which means that the
action potentials are stronger along this path [6]. Mayford also
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until the cell can no longer allocate enough nutrients to
survive, and the cell dies.
Measurements of Action Potentials
Neural implants begin this process by detecting patterns in
action potentials. An action potential is actually a voltage
difference (measured in mV) between the outside and inside
of the axon. As described by University of Texas Medical
School, a voltage difference is the difference in potential
energy per charge [4]. Simply put, voltage difference is like
elevation. Increasing the elevation of an object increases its
potential energy. Similarly, as the voltage difference between
the inside and outside of the axon increases, potential energy
increases. During an action potential, a large spike in voltage
difference can be observe due to the flood of positive ions into
the axon [4]. Voltage difference can then be measured by the
electrodes of a brain implant using electrochemical methods.
Electrodes are simply needle-like conductors that carry
electricity. These electrodes measure voltage difference with
a process called voltammetry. Because the voltage difference
is a comparison, this process requires multiple electrodes. The
global publishing company Springer states one of these
electrodes must be a reference and have an unchanging
voltage. This reference electrode is often called the “zero”
voltage, and all the other electrodes’ measurements are
relative to this reference [16]. A common material, according
to Springer, used for this reference electrode is silver-silver
chloride, and is often seen in brain implants. When an
electrode is placed in a charged medium, an extremely small
amount of current passes through the electrode as a result of
the charge, which can be easily measured using an ammeter.
Using Ohm’s law, which states that voltage difference is
equal to the product of current and the resistance of the
measuring device, one can calculate the voltage difference of
the medium. However, prior to this calculation of voltage, the
voltage must be amplified to make the small magnitudes of
the electric signals manageable for the hardware of the brain
implant. The voltages are sent through a circuit within the
implant that amplifies the signal. The mechanism within that
circuit that performs the amplification is called an operational
amplifier, and is described in Tan Yin Qing’s paper, which
was included in the 3rd Kuala Lumpur International
Conference on Biomedical Engineering in 2006. An
operational amplifier takes the raw voltage in the electrode
and uses an external voltage, such as from battery, to linearly
increase it. The higher the external voltage, the more the
initial voltage is increased [17].
Senile Plaques
The second main cause of neural disruption is the buildup
of senile plaque in extracellular fluid. This plaque is generated
from a protein found on the exterior of the cell membrane.
Michael Murphy, of the University of Kentucky, performed a
study and wrote a paper depicting evidence that supports this
theory. According to Murphy’s work, alpha-secretase
enzymes cut these proteins from the membrane, which
proceed to float in the extracellular fluid and help to promote
neurogenesis, the generation of new neurons [14]. However,
in Alzheimer’s patients the beta-secretase enzyme cuts the
protein. Murphy’s paper states the protein is cut differently
and results in the release of Beta-Amyloid proteins. As this
process repeats, the small protein fragments have the
tendency to collect until they are no longer soluble in the extra
cellular fluid. At this point, these large chains of protein
entwine themselves into senile plaque and begin to block
neurotransmitters,
especially
acetylcholine,
a
neurotransmitter essential for memory [14]. This means
communication between neurons becomes interrupted.
The combination of neurofibrillary tangles and senile
plaque prevents action potentials from moving fluidly
throughout the brain. As groups of neurons succumb to cell
death or impeded signals, the circuitry required to generate
new memories is broken. As discussed in the previous section,
action potentials must make a path through the hippocampus
in order to form a memory. As Alzheimer’s erodes certain
parts of the hippocampus, this memory forming ability fades.
One study conducted by Dr. Aaron Bonner-Jackson of the
Lou Ruvo Center for Brain Health details how subjects with
early stage Alzheimer’s had a hippocampus of a higher
volume. The subjects with a more intact hippocampus
performed better on recollection exercises, affirming that
deterioration within hippocampal circuitry results in poor
memory [15].
HOW MEMORY RESTORING NEURAL
IMPLANTS OPERATE
Neural implants operate by mimicking the function of
neurons in the brain. If the neurons within a brain
communicate via action potential, a device can be created that
detects how often these action potentials occur and how
powerful they are. The device could then output signals to
other neurons based on the signals it receives, simulating a
group of healthy neurons. This relay of signals can bridge
gaps between parts of the hippocampus that have been
disconnected as a result of neural damage. This section will
detail how this progression is accomplished in the neural
implant.
Interpreting the Signals
When the voltages have been amplified and calculated by
the implant using Ohm’s law, the implant hardware begins to
decode the patterns of signals. The microchip Dr. Berger
places in the brain is made up of a series of multi-input,
single-output (MISO) models [9]. These models mimic the
function of a neuron by decoding the signals received from
the electrodes and producing a single signal that can be
interpreted as an action potential. This process is similar to
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how a neuron receives many signals from its dendrites and
outputs a single signal via its axon.
FIGURE 6 [9]
Equations for the algorithm used in the MISO. K is the
feedforward block and H is the feedback block
The first variable is the action potential received by the
electrode. This is altered by a feed-forward term (K), a term
that reacts in a set way to certain stimuli without correcting
itself based on the result. The result is the synaptic potential
interpreted by the algorithm [9]. In addition, an uncertainty
coefficient corrects the system uncertainty resulting from the
electrodes detecting signals from neurons outside the target
area. Finally, a feedback (H) term accounts for the afterpotential if the voltage of the neuron before it fires is greater
than a certain value. This represents the output action
potential of the MISO model.
These MISO models are implemented on very large scale
integration (VLSI) circuits. As described by the
Massachusetts Institute of Technology, VLSI circuits are a
semiconductor material on which there are several smaller
electric circuits that involve thousands of transistors to imitate
a series of synapses. The silicon chip can adapt to the
introduction of new information, similarly to how learning
and memory occur in the brain. Instead of operating in binary,
as most computer chips do, current flows in analog through
the transistors in the VLSI circuit, meaning the voltage can be
varied to produce different currents [18]. This is because
transistors are made of semiconductors, or materials that only
allow for the passage of current at some threshold voltage. As
different voltages are applied to the circuits, different
transistors allow for the passage of current, changing the
overall path of current [18]. This threshold voltage for a
transistor is similar to the threshold stimuli of a neuron [4],
which is why these transistors mimic neurons with success.
The output voltage patterns of the MIMO model are directed
to another region of the hippocampus via electrodes specific
to output function.
FIGURE 5 [9]
Shows how a MISO unit receives multiple signals, and
outputs only one. Shows MISO’s compose a MIMO
Note how in Figure 5 the MISO has multiple patterns directed
into it, but only one pattern is produced. A series of single
output (MISO) models is referred to as a multi-input, multiout design (MIMO). This MIMO simulates a group of
neurons by receiving multiple signals from the surrounding
neurons and relaying multiple signals to another section of the
hippocampal region [9].
According to Berger’s algorithm, depicted below in Figure
6, the MISO model requires several input variables to
determine the single output.
Memory Boosting Implants for Alzheimer’s Patients
Since these implants are able to receive signals from one
part of the brain and then send a respective output to another
part of the brain, Berger believes these implants can be used
as a replacement in hippocampal circuitry if a part of this
circuitry is broken [9]. In Alzheimer’s, research described by
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Yangling Muhas within the Molecular Neurodegeneration
journal shows that the hippocampus is one of the first parts of
the brain that suffers from the disease [19]. According to the
University of Maryland Medical Center [11], the lifespan of
someone afflicted with Alzheimer’s is 3-20 years after
diagnosis. Because victims live with disease so long, this
implant could be used to retain normal memory function, as
the hippocampus decays in the early stages of the disease, for
years. While the implant cannot cure the disease, it is able to
provide a more normal life for an extended period of time by
replacing parts of the hippocampal circuitry.
generate signals that can be relayed to other neurons and
bridge gaps between sections of the hippocampus.
Studies in Nonhuman Primates
The next logical step in neural implant testing is the
implementation of the technology in a brain more similar to
that of a human. To accomplish this, Berger and Deadwyler
began studying the possibility of implants in non-human
primates. Five rhesus macaque monkeys were selected and
trained to perform a delayed-match-to-sample task for a juice
reward. The non-human primates were shown an image. This
image faded and the subjects were then shown a random
dispersion of images after a delay of 1 to 90 seconds [21]. In
order to receive the reward, the test subject had to make a
hand gesture to select the image they had seen previously.
After 100 to 150 trials per subject, the monkeys were able to
select the correct image with an accuracy of 70 to 75 percent.
Recording tools were used to gather information on the action
potential patterns in a healthy, functioning primate brain
during these baseline tests [21].
Implants containing the MIMO chip were then placed in
the prefrontal cortex, a region of the brain involved in short
term memory and decision making. Berger then provided
these monkeys with a dosage of cocaine via IV to impair their
memory and cognition. Cocaine directly affects the
functionality of the prefrontal cortex. The same test that was
done in the control group, in which the monkeys lacked a
MIMO chip and were not drugged, was repeated. Some tests
were conducted while the MIMO chip was active, and others
were conducted when it was inactive; there was a sizeable
difference in performance as this parameter was adjusted.
NEURAL IMPLANT PROGRESS
Although the memory assisting implant is a developing
innovation, there have been successful tests using this
technology that demonstrate its progress and potential to
become a widely-used treatment for neurological issues.
Studies have progressed from small rodents to preliminary
human trials. This section will provide insight on these
studies.
Studies in Rats
In 2011, Dr. Theodore Berger of USC and Sam A.
Deadwyler of Wake Forest began experiments with these
memory-assisting neural implants in vivo. Rats were trained
to remember which of two levers released water [20]. They
then had a series of electrodes placed into the hippocampal
regions CA1 and CA3 in order to detect action potentials.
These electrodes could perform the electrochemical methods
previously described by the global publishing company
“Springer”, including cyclic voltammetry and Ohm’s law
calculations [16]. At this point in time, the MISO/MIMO
model microchip had not been fully developed. Due to the
lack of hardware to decode brain signals within the implant,
the electrodes were wired directly to a computer, which
simply recorded the pattern of signals that occurred when the
rat chose which lever to pull. After these signal patterns were
recorded, the rats were given a dose of a drug that disabled
function in the CA1. According to Berger, this hole in the
hippocampus made it impossible for the rats to remember that
a particular lever provided water [20].
The researchers then used the signal pattern stored in the
computer to project an identical pattern back into the CA
regions, as if the rat was able to form a healthy memory. The
rats were able to remember which lever provided water, as the
electrodes were acting as a replacement for the disabled CA1.
When the signal from the electrodes was stopped, the rats
could no longer remember which lever to push. In Dr.
Berger’s words “'Turn the switch on, the animal has the
memory; turn it off and they don't: that's exactly how it
worked” [20]. This study proves that machine generated
electric signals can be interpreted as memory by the brain.
Thus, the study proves an implant placed in the brain can
FIGURE 7 [21]
Graph of the percent of images the monkeys correctly
matched vs the number of image choices. Performance
when the MIMO is activated (green) was better
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In Figure 7, the blue points represent the performance
without the MIMO, and the green points represent
performance with the MIMO. According to this graph, when
the task the monkey performs is moderately difficult, i.e.
when the number of pictures they are shown range between 3
and 6, the difference in performance is about 10-20%. These
results indicate that the brain implant successfully improved
memory function [21].
Cocaine inhibits function in the prefrontal cortex, which
impedes the action potentials from being sent to the
hippocampus, in order to form memories. This study shows
that the MIMO chip implant has the potential to adjust to the
signal it receives and subsequently outputs. The MIMO chip
does not memorize a singular image; it improves memory
throughout multiple trials as the image changes. This
adaptation to situation demonstrates how the MIMO model
adjusts to different signals. Since learning is not a linear
process this study validates that the MIMO model can
simulate healthy neurons. The study is additionally useful
because the parameters within it, such as implant placement,
will be similar to those used in humans. This is due to the
similarity between human and monkey neural process. With
this new knowledge, Dr. Berger is predicting that human trials
will occur within the next decade.
implants allowed two men who, in the words of the scientists
“had a significant disability with large implications on quality
of life,” see again [22].
Parkinson’s Disease
As defined by James Macintosh of Medical News Today,
Parkinson’s disease is a neurological disorder that is a result
of the death of dopaminergic neurons, or the neurons in the
brain that produce the neurotransmitter dopamine. Since
dopamine regulates bodily control, this neuronal death causes
bodily tremors to occur [23]. The neural implant technology
used to treat these tremors is called deep brain stimulation.
Electrodes are placed into target areas of the brain that are
suspected of causing the tremors in the patient. An electric
voltage is applied in an effort to stimulate these parts of the
brain. The goal is to disrupt the erratic signals resulting from
the lack of dopamine. While the exact reason for why this is
effective is unclear, patients receiving deep brain epilepsy see
a significant reduction in symptoms [23].
Epilepsy
The Institute of Electrical and Electronics Engineers
(IEEE), a professional engineering association, defines
epilepsy as the recurring, abnormal electrical activity in the
brain that causes seizures. This abnormal activity is caused by
imbalanced neurotransmitters, tumors, strokes, or external
injury to the brain [24]. Different types of abnormal activity
cause different types of seizures. When this activity resides
on only one half of the brain, a focal seizure occurs, resulting
in loss of function in whatever body part this particular section
of the brain controls and possible unconsciousness. For
example, a focal seizure may affect the occipital lobe of the
brain, and in turn will impair vision [24]. If the abnormal
activity is present in both sides of the brain, the outcome is a
generalized seizure, which is a seizure that effects the victim’s
whole body and results in definite loss of consciousness [24].
The neural implants used to treat epilepsy consist of
electrodes connected to the regions where the abnormal
activity that causes seizures appears. Using the same
electrochemical methods as the memory assisting implants
discussed previously, voltammetry and Ohm’s law [16], the
electrodes measure signals in the brain. Instead of having a
microchip that relays electric signals to other neurons, like in
memory assisting implants, the microchip within epileptic
implants is designed to recognize patterns in action potential
preceding epileptic fits. According to IEEE, if the microchip
identifies one of these patterns, the implant delivers electric
signals to its surroundings in order to impede the progress of
the signals that would cause the seizure [24].
OTHER SUCCESSES USING NEURAL
IMPLANT TECHNOLOGY
Sight Restoration
Some brain implant technology is able to restore sight to
patients that suffer from hereditary retinal deterioration, also
called blindness. German scientists Ziad M. Hafed, Katarina
Stingl, Karl-Ulrich Bartz-Schmidt, Florian Gekeler, and
Eberhart Zrenner, tested the effectiveness of a neural-retinal
implant to restore sight [22]. They placed a chip in the
subjects’ eyes that essentially replaces photoreceptors in the
eye with light-sensitive photodetectors. These photodetectors
are semiconductors that emit electrons when exposed to
different types of light [22]. The emitted electrons generate a
current, or flow of charges, which is then directed to a series
of amplifiers. After the current is amplified, a computer chip
uses an algorithm to determine the voltage that will be output
via electrodes. The algorithm is determined by tests on
healthy eyes. This determined voltage will be applied to the
part of the brain that controls sight, mimicking the signals this
part of the brain would receive from healthy eyes [22].
The results of the tests with this implant are impressive.
Two male subjects rendered blind by a hereditary disease
were asked to partake in an experiment where they would
have one of these implants placed in their eye. They sat in a
dark room and were asked to fixate their eyes on a white circle
when it appeared. Surprisingly, the subjects were able to
fixate their eyes on the circle quite well (within 2 degrees of
accuracy), after having this implant placed in their eye. These
Cochlear Implants
As stated by the National Institute on Deafness and Other
Communication Disorders cochlear implants serve to restore
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Benjamin LeStourgeon
hearing to deaf individuals by imitating the signals that the
inner ear produces and relays to the temporal lobe of the brain
[25]. Professor Jeffery Hess describes the structure of the ear
in the following way. The inner ear contains an eardrum,
which vibrates in response to soundwaves. These vibrations
are transferred to a liquid in the part of the ear known as the
cochlea and move sensory hairs within this liquid [26]. The
movement of these hairs produces a different electric signal
for each sound frequency, which are then interpreted by the
temporal lobe as sound. If the inner ear is damaged, these
signals will not be produced, thus hearing will not occur.
The National Institute on Deafness and Other
Communication Disorders reveals cochlear implants use a
microphone to receive soundwaves, which are then
transformed to electric signals similar to those produced by a
healthy cochlea [25]. The microchip in the implant dictates
the signal produced by each type of soundwave based on
information determined experimentally from healthy ears.
These signals are then run through wires to the auditory nerve,
which connects to the temporal lobe. Through practice, the
brain will come to understand these signals as sound [25].
FIGURE 8 [29]
Shows an MRI of a person with scar tissue, arrows
showing location, in their brain
DIFFICULTIES WITH NEURAL IMPLANTS
Additionally, this scar tissue can have negative health impacts
on the patient. For example, Del Prado details how the
presence of scar tissue in the brain has been linked to seizures,
due to the abnormal activity caused by extra pressure on
certain areas of the brain [28]. The brain implants must be
biocompatible, meaning they are not perceived as a threat and
thus do not react toxically with the body.
Even if the initial insertion of the implant does not cause
scar tissue formation, the shifting of brain tissue relative to
the skull can dislodge the implant from its intended neuron
location. While the implant is fixed to the skull, the brain is
submerged in a fluid and is allowed to undergo subtle
movements. If this movement of the brain is great enough, the
implant’s electrodes will no longer be reading and distributing
signals from the correct neurons. Furthermore, this movement
can also cause scar tissue over time, as the electrode can
irritate the brain as it rubs against it [28].
Complexity of the brain
As with any emerging technology, there are many hurdles
that must be overcome in memory enhancing neural implants.
One of these issues is the overwhelming complexity of the
brain. Mario Garret of Psychology Today states that there are
over 1,000 to 10,000 synapses per neuron, and this results in
over 125 trillion synapses in the human brain; more than the
number of stars in our galaxy. These synapses are constantly
changing as the brain learns [27]. This changing allows the
brain to continually adapt to its environment and predict the
world around it. Consisting of over 100,000 miles of neurons,
the brain is so unfathomably complicated, it would take
millions of years to map all of the action potential paths. For
this reason, the implants will only be able to mimic a very
small portion of the brain’s function for a long time to come.
Process Variation
Invasiveness and Displacement of Neurons
Process variation refers to the error during production of
VLSI circuits. Dr. Berger remarks that this is a difficulty he
encounters when constructing hippocampal cognitive
prostheses. There is always a threshold of error associated
with the manufacture of products. When the size of the
product approaches nanoscopic scale, the effect of any
variation is amplified because the error becomes a larger
percentage of the overall dimensions of the product. Within a
VLSI circuit, variations in the size of the transistors that make
up the circuit can impact the way a signal is processed [9].
This is because the variation in the size of the transistor can
change the threshold of current passage. If one erroneous
transistor is inaccurate enough to raise its threshold passage,
When foreign objects are placed into the brain, the body’s
immune system recognizes this as a potential danger and can
react negatively with the object. This negative reaction is
summarized by Guia Marie Del Prado of the “Business
Insider.” When devices are embedded into brain tissue, the
body’s natural immune-response results in inflammation
around the device. This swelling can lead to scar formation,
or the increased presence of connective tissue called glial
tissue, as the body tries to heal the wound [28]. The presence
of this scar tissue around the neural implant’s electrodes can
obstruct accurate signal readings because the glial tissue acts
as an insulator, preventing the electrodes from being exposed
to the voltage differences in the neurons.
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Michael Shulock
Benjamin LeStourgeon
this will alter the entire successive path of that signal through
the VLSI circuit. The desired outcome of certain action
potential patterns will not be processed as desired, giving
incorrect outputs [9].
intelligence between the rich and poor would increase the
socioeconomic gap between these groups. Another potential
ethical danger concerning neural implants is the potential for
the technology to be used maliciously. For example, a power
such as a government could require the implant be placed in
every citizen’s brain in order to force the citizens to comply
with the law [32].
At the present, neural implants do not seem to be widely
accepted by the public. Based on a 2016 Pew Research Center
public poll, 69% of Americans say they are at least somewhat
worried about neural implants becoming a reality. Only 29%
of Americans, based on the poll, are not worried about these
brain-altering devices [33].
THE ETHICAL ISSUES OF BRAIN
IMPLANTS
Developing technologies, especially those involved with
human cognition, often draw a great deal of scrutiny and
debate over their ethicality. There are many concerns as to the
extent that neural implants could alter human identity. Some
ethicists argue that a neural implant that alters brain function
is consequently altering the personality of that individual.
This raises the issue that scientists could be playing God by
manipulating innate human characteristics. Nicholas Agar, an
ethicist of Victoria University of Wellington, wrote a book
called “Humanities End: Why We Should Reject Radical
Enhancement,” where he argues that electronics should not be
used to alter brain function [30]. One of his primary
arguments is that alteration of cognitive function will allow
human thought process to be reshaped, at will, by other people
via technology. The Human Brain Project (HBP) is a
European Commission Future and Emerging Technologies
Flagship that is dedicated to collaboration concerning human
brain research. The HBP, a continental organization, declares
that research that effects the “human essence” may be
unethical [31].
On the more tangible level, some researchers view brain
implants as a significant risk to brain health rather than a
treatment. Among these researchers is Charles Lieber, of
Harvard University. This is because of the difficulties that can
arise from the immune system attacking the implant and
creating scar tissue in the brain. Lieber states, "If you look at
implanted electronics in the brain over the past 10 to 20 years,
all suffer from a common problem which is the implant's
electronic probes... create scarring in brain tissue" [28].
Procedures that may have negative outcomes often require the
patient to decide whether the reward outweighs the risk.
Although any surgery entails some risks, brain surgery is far
more dangerous and can cause many serious problems,
including a change in personality or death.
Another concern is the progression of neural implants
beyond treatment to neural ailments. The Columbia
University of the State of New York’s neurology department
believes if neural implants that could theoretically improve
learning and memory were available to healthy individuals, a
superhuman like class of individuals may be developed.
These individuals would have capabilities beyond that of
typical humans. Aptitude would no longer be determined by
nature or effort of an individual, rather it would be determined
by the abilities of the implant placed in the brain. This would
create an unnatural hierarchy of intelligence due to the fact
that the rich could afford these upgrades of intellect. The
university asserts that theoretically, the difference in
FIGURE 9 [33]
Shows the dispersion of American’s opinion on neural
implants
People seem to think the ethicality of brain implants is low
and as a result do not embrace the technology.
COST SUSTAINABILITY OF TREATING
ALZHEIMER’S WITH NEURAL IMPLANTS
Sustainability is defined by Cambridge Dictionary as “the
ability to continue at a particular level for a period of time”
[34]. The sustainability of neural implants as a treatment for
Alzheimer’s predominately relies on cost. The implants must
be economically feasible for a significant number of
Alzheimer’s patients in order to perpetuate their use because
money drives production. If the cost of treatment via implant
is far more expensive than other forms of treatment, it would
not be worthwhile to consumers. However, if the implant is
less expensive overall than coping with the disease and
increases quality of life, the technology will flourish with use.
Ultimately, the cost sustainability will depend on the balance
of several variables. These variables include the service cost
of placing the implant in the patient’s brain, the cost of having
Alzheimer’s without the implant, and the improvement of the
quality of life as a result of the implant.
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Benjamin LeStourgeon
like jumping out a window, and assist them in daily tasks such
as eating and going to the bathroom. Another way to increase
the patients’ quality of life is to provide them medications that
decrease the symptoms of the disease. Unfortunately, these
medications are expensive and not largely effective in
assisting the patient.
Services that are necessary to keep Alzheimer’s victims
from harming themselves and allow them to survive come
with a large economic burden. According to research
conducted by the Alzheimer’s Association, an average a
person with Alzheimer’s, that is experiencing symptoms, pays
$49,126 annually on care and medication [37]. Furthermore,
as of 2015, a typical person afflicted with Alzheimer’s has to
pay $32,781 for nursing home care. This table shows the
different expenses of a typical person with Alzheimer’s.
The Cost of Neural Implant Implementation
CostHelper, a team of journalists who compile information
about the costs of health services, states the average cost of
brain surgery ranges from $50,000 to $100,000 [35]. With the
cost of surgery so high, a large economic strain is associated
with neural implant implementation. The cost of neural
implant surgery includes the hospital fee, the doctor fees, and
complication fees. The hospital fee pays for the employment
of non-doctor hospital employees, the cost of using a bed
space in the hospital, usage of hospital technology such as
MRIs, and the cost of various supplies the hospital uses during
the surgery [35]. These supplies include the anesthesia used
to subdue the patient during surgery, the antiseptic to clean
the patient’s skin, any medication the patient takes, and other
miscellaneous costs. The doctor fees pay the surgeons and the
anesthesiologist for their service [35]. As reported by
CostHelper, doctor fees at the Baptist Memorial Healthcare in
Memphis, Tennessee, are often $30,000 or more for a typical
brain surgery. When the other fees are added to the doctor
fees, this cost can add up to $50,000-$80,000. If
complications arise during the surgery, this amount can easily
double [35].
Since neural implants that assist Alzheimer’s patients are
not currently developed enough to be utilized, a close estimate
to their cost can be made by looking at an implant that is
produced presently. As discussed in prior sections, James
Macintosh of Medical News Today states that Parkinson’s
disease is currently being treated with a deep brain stimulation
implant (DBS) [23]. According to Michael S. Okun of the
National Parkinson’s Foundation, it typically costs $30,000 to
$50,000 to place a DBS in the brain. This estimate includes
the hospital and doctor fees [36], and is on the less expensive
end when it comes to the cost of neural surgery. Both
Parkinson’s and Alzheimer’s treating implants are essentially
small groups of electrodes placed in the brain. Due to this
similarity in construction and procedure, $30,000-$50,000 is
a reasonable estimate of how much an Alzheimer’s treating
implant surgery would cost.
FIGURE 10 [37]
Shows the different expenses a person with Alzheimer’s
has and how much, on average, each one is.
The inpatient hospital service expense is the fee paid to the
hospital itself. The Alzheimer’s patient could be going to the
hospital for diagnosis, to get scans done to show the
progression of the disease, or to get evaluated for the purpose
of prescribing medicine. The medical provider expense is the
money paid directly to the doctor themselves [37]. The care
that these various expenses pay for manages the symptoms of
Alzheimer’s disease and keeps patients safe, but
unfortunately the care does not prevent the symptoms from
occurring.
Cost of Alzheimer’s Without the Implant
The Alzheimer’s Association states that Alzheimer’s
patients require constant care to keep them comfortable and
to prevent them from harming themselves. As patients’
memory deteriorates, their independence also diminishes
because the lack of memory causes the victim to have an
inability to make rational decisions [37]. They might forget
where they live, where the bathroom is located, or even who
they are. Additionally, the disease can also impact physical
movement, making it difficult for the victim to be mobile and
perform simple tasks, like bathe themselves. In order to keep
them safe and comfortable, Alzheimer’s patients might have
a nurse that looks after them at their house, or they may be
placed in a nursing home with access to fulltime care. These
nurses prevent the patients from performing irrational things,
WHAT DO NEURAL IMPLANTS MEAN
FOR THE WORLD?
Neural implants possess the ability to return memory to
individuals who have lost this function as a result of a
neurological disease and show great potential in returning
cognition to Alzheimer’s patients. Since the brain
communicates by passing along electric signals from one
section of the organ to the next, neural implants can detect
these signals and them to another part of the brain. Memories
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Michael Shulock
Benjamin LeStourgeon
are formed by sending signals through a certain path of
neurons, but within an Alzheimer’s patient’s brain neurons
are disconnected in some areas, making the formation of
memory difficult. Neural implants placed at the locations
where these disconnections occur can serve as replacement
neurons and complete the necessary paths to produce
memory. Studies on memory assisting implants have
progressed from rodents to nonhuman primates,
demonstrating that the implants have real potential in the
medical field. Additionally, similar neural implant technology
has been used to successfully treat other medical disorders,
such as Parkinson’s. Despite a seeming aversion from the
general public toward brain implants, these devices could one
day prevent memory loss for millions of people.
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ACKNOWLEDGEMENTS
I, Michael Shulock, would like to thank my parents, for
putting me into the position to write this paper. I would not be
where I am without them. I would also like to thank my
roommate Shloke Nair for proofreading this paper and
keeping us motivated when we needed it.
I, Benjamin LeStourgeon, would like to thank my parents,
for supporting me on my journey to college and giving me the
opportunity to be where I am today. I would also like to thank
Abigail Pinto and Jesse Carpenter for proofreading our paper.
12