The final assignment for this class will be a 10-page critical review of the drug treatment for a neuropsychological disorder. The review will use peer-reviewed and/or scholarly sources to provide an evidence base for the evaluation of current drug treatment modalities for the disorder. The disorder is the same disorder you selected in week 1 and for which you discussed its neurobiology in the Week 1 assignment (topic selection) and its drug management in the Week 2 assignment (drug treatment). Please remember – you will be analyzing the same disorder to complete the Week 6 assignment (comprehensive Critical Review of the same disorder and its management).
Reminder – your completed Week 1 and Week 2 assignments will be used as a foundation to help you complete your Week 6 assignment (Critical Review) on the same disorder. Thus, your work in Week 1 and in Week 2 will be used to support your work in Week 6. Utilize the previous references you researched in Week 1 and Week 2, and add any additional peer-reviewed/scholarly references that would support your comprehensive review. These sources should provide evidence-based information to help support your comprehensive analysis, focusing on the aspects described below. Be sure to cite your sources in your paper and include them on your References page. You may utilize required or recommended course materials in your work, but these will not count towards the reference requirements; however, you may cite and reference the American Psychiatric Association’s (2013) DSM-5 as one of your sources used for the grading credit.
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Alzheimer’s Disease and Neural Structures: Symptoms and Related Brain Structures
Jasmine Barbusca
PSY 625: Biological Bases of Behavior
Irene Kovacs- Donaghy
April 3, 2023
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Alzheimer’s Disease and Neural Structures: Symptoms and Related Brain Structures
According to various studies, Alzheimer’s disease is a chronic brain condition that
slowly robs the brain of its cognitive capacity. In addition, the disease interferes with human
memory and thinking skills. Ideally, all the symptoms that Alzheimer’s disease (AD) shows
in humans are closely related to the brain structures involved in the disease process.
Alzheimer’s disease’s initial signs and symptoms include forgetfulness, challenges with
learning new things, losing things, and communication difficulties. Confusion, mood swings,
and personality changes are some symptoms that worsen as the disease progresses.
Alzheimer’s patients may have trouble speaking or walking in the later stages of the illness
and may end up bedridden. These symptoms are linked to the alterations in the diseased
brain’s affected brain structures. Memory, reasoning, and behavior are all negatively impacted
by Alzheimer’s disease, a degenerative brain ailment (Roobini & Lakshmi, 2021). The study
investigates the neural structures that may have a role in Alzheimer’s disease by locating and
explicating the functions of three particular and significant areas of the brain or nervous
system, which will be the basis of this essay. Additionally, the paper discusses the various AD
symptoms and how they relate to damaged neural structures.
Relevant History of AD
Alois Alzheimer, a clinical psychiatrist and neuroanatomist discovered his unusual
cerebral cortex disease in 1906 while studying the brain tissue of a woman who had passed
away from an unidentified mental illness. According to Lock (2013), Dr. Alzheimer noticed
abnormal clusters and twisted fibers that have since been named beta-amyloid plaques and
tau tangles, respectively. Today, these plaques and tangles are recognized as characteristic
signs of AD. Additionally, the development and spread of beta-amyloid plaques and tau
tangles were the main topics of study for Alzheimer’s disease throughout the 20th century.
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Recent studies, however, have demonstrated that Alzheimer’s disease is a complex disorder
that impacts numerous brain systems. Imaging research has shown that the hippocampus,
amygdala, and prefrontal cortex are among the brain regions having structural and functional
abnormalities in Alzheimer’s disease.
Memory formation and retrieval depend heavily on the hippocampus, and its failure
may factor in the memory problems associated with Alzheimer’s disease. Since the amygdala
is essential in processing emotions, its malfunction may be a factor in the mood swings seen
in Alzheimer’s patients. Thinking, setting policy, and cognitive function are among the
executive skills impaired in people with AD. The prefrontal cortex of the brain is linked to
these cognitive processes. Neurotransmitters like acetylcholine have been studied concerning
how Alzheimer’s disease develops. Acetylcholine plays a crucial role in memory and
learning; therefore, problems with it may be part of why Alzheimer’s disease is associated
with memory difficulties. Thus, considerable strides in our comprehension of the underlying
molecular mechanisms of the disorder have been made throughout the history of Alzheimer’s
disease. According to imaging studies, numerous brain regions have structural and functional
abnormalities, and studies have centered on neurotransmitters’ role in AD progression. These
discoveries have aided in the creation of novel medications and treatments for individuals
suffering from AD.
Areas in the Brain Associated with Alzheimer’s Disease
Three distinct neurological areas are associated with Alzheimer’s disease: the
hippocampus, the entorhinal cortex, and the prefrontal cortex. A critical component in
forming new memories and committing them to long-term storage is a part of the brain called
the hippocampus. The entorhinal cortex is a part of the brain intimately related to the
hippocampus and is known for its significant contribution to spatial navigation and episodic
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memory (Neural Structures Involved in Speech Production, 2016). The prefrontal cortex is
part of the brain in charge of administrative processes, including attention, planning, and
decision-making.
When Alzheimer’s disease strikes, the hippocampus is one of the brain areas that is
impacted the first and in the most brutal way. It is accountable for the creation of new
memories, their consolidation, and the recovery of previously stored memories. Memory loss
is a symptom of Alzheimer’s disease, caused by the degradation of the hippocampus, which
occurs due to the buildup of beta-amyloid plaques and tau protein tangles in the brain (Neural
Structures Involved in Speech Production, 2016). Individuals who have Alzheimer’s disease
have a difficult time establishing new memories and may suffer from retrograde amnesia,
which is the loss of memories that were established before the commencement of the illness.
With Alzheimer’s disease, the entorhinal cortex is another part of the brain that is impaired
early on and severely. It has strong ties to the hippocampus and is essential in forming
episodic memories and navigation across space. Deficits in spatial navigation and episodic
memory might be a symptom of Alzheimer’s disease, caused by the deposition of betaamyloid plaques and tau protein tangles in the entorhinal cortex (Roobini & Lakshmi, 2021).
This degradation can be traced back to Alzheimer’s disease. Alzheimer’s patients have
difficulties navigating familiar situations and are more likely to get disoriented or lost.
The prefrontal cortex is an area of the brain that controls administrative processes
such as attention, planning, and decision-making. The region also controls working memory.
Deficits in executive function are the outcome of Alzheimer’s disease, characterized by the
deposition of beta-amyloid plaques and tau protein tangles in the prefrontal cortex. This
degeneration of the prefrontal cortex causes the illness. Individuals affected by Alzheimer’s
disease often struggle with planning, making choices, and focusing on activities, and they
may also have memory problems in their working memory (Kamat, 2015). The prefrontal
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cortex is an integral part of the brain responsible for higher-level cognitive abilities, which
sets humans apart from other animals. It is situated in the front of the brain. It is essential in
various executive processes, including attention, working memory, planning, decisionmaking, and impulse control. In addition to regulating emotions and personality, the
prefrontal cortex is implicated in social interaction. With Alzheimer’s disease, on the other
hand, the buildup of beta-amyloid plaques and tau protein tangles causes this essential part of
the brain to deteriorate, a symptom of the illness (Kamat, 2015). These abnormal protein
deposits disrupt the normal functioning of neurons and lead to the loss of connections
between them, which results in the characteristic deficits in cognitive functions seen in
Alzheimer’s patients. Moreover, these deficiencies are caused by the loss of connections
between neurons.
The impairment or loss of executive functions, usually controlled by one’s prefrontal
cortex, is one of the most noticeable signs of Alzheimer’s disease. People who have
Alzheimer’s disease have a difficult time planning and carrying out challenging tasks, coming
to choices, and focusing their attention on activities that need it for an extended period. In
addition, they may have problems with their working memory, which refers to an individual’s
capacity to keep and manipulate information in their minds for brief periods (Kamat, 2015).
These cognitive deficiencies get increasingly severe as the illness advances and can
significantly affect day-to-day activities and quality of life. The prefrontal cortex is
responsible for regulating both emotional and social conduct, both of which may be
negatively impacted by Alzheimer’s disease in addition to the cognitive symptoms. Patients
could develop feelings of apathy, lose interest in participating in social activities, and go
through shifts in their personalities and mood. Since they may substantially affect the
patient’s quality of life and make it more challenging to provide care, these symptoms can be
challenging for caregivers and family members to deal with daily.
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Alzheimer’s is a degenerative brain condition that may harm a person’s behavior,
thinking, and memory over time. Three distinct neurological areas are associated with
Alzheimer’s disease: the hippocampus, the entorhinal cortex, and the prefrontal cortex. The
hippocampus and the entorhinal cortex are parts of the brain severely impaired early on in
Alzheimer’s disease (Kamat, 2015). Both regions are essential for memory loss and
difficulties with spatial navigation. Alzheimer’s disease causes a deterioration of the
prefrontal cortex, which is essential for organizational processes. Due to this degeneration,
patients with Alzheimer’s disease have difficulties with planning, decision-making, and
working memory. In order to provide successful therapies and interventions for people who
have Alzheimer’s disease, it is essential to have a solid understanding of the brain structures
that are implicated in the condition.
Memory Formation and the Locus Coeruleus
According to James et al. (2021), long-term memory formation and consolidation are
intricate processes involving numerous brain regions and neurotransmitter systems. The locus
coeruleus (LC), a tiny neuronal nucleus, helps to control attention, alertness, and aggravation.
According to recent studies, the LC may be crucial for memory formation and consolidation.
The LC is one of the first brain areas to degenerate in Alzheimer’s, impairing memory
formation and consolidation. The loss of LC neurons and a resulting drop in norepinephrine
levels could be a factor in the memory problems associated with AD (James et al., 2021).
Also, James et al. (2021) suggest that targeting the locus coeruleus may be a promising
therapeutic approach and that dysfunction of this region may contribute to the memory
impairment seen in AD.
Dysexecutive Syndrome (DES)
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DES is a collection of symptoms related to executive function deficits, including
challenges with task organization, planning, and execution. DES is a common aspect of AD
that can significantly affect the quality of life (Ribas et al., 2023). DES has been connected to
caregiver burden, decreased social engagement, and impairments in daily living activities.
Additionally, early on in the development of AD, the prefrontal cortex and basal ganglia, two
neural regions involved in executive function, are affected. According to Ribas et al. (2023),
the degeneration of the structures, as mentioned above, is a factor in the emergence of DES
and the associated behavioral symptoms. Cognitive rehabilitation and other interventions that
focus on executive function may help enhance the quality of life in AD sufferers.
Aging Theories and Alzheimer’s Disease
According to Trevisan et al. (2019), theories of aging assert that the buildup of
cellular damage over time causes the emergence of age-related diseases like Alzheimer’s.
According to the first oxidative stress theory, the buildup of reactive oxygen species in the
brain causes cellular damage and degeneration. Also, oxidative stress is thought to have a
massive effect on the degenerative changes of neural circuits like the hippocampus and the
prefrontal cortex in AD. Further, antioxidant therapy and other oxidative stress interventions
could slow AD progression.
Brain Structures
Hippocampus
The hippocampus in the brain is a vital structure developed for functions such as memory,
learning, and spatial navigation (James et al., 2021). Hippocampus is one of the most
vulnerable parts of the brain to be affected by AD. Any case of destruction of the
hippocampus can result in memory loss for the individual with AD.
Cortical Entorhinum
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The parietal cortex is a part of the brain that aids memory consolidation and spatial
navigation (Li et al., 2019). Alzheimer’s patients may struggle with spatial navigation and
have trouble creating new memories as the entorhinal cortex becomes damaged.
Prefrontal Cortex
The prefrontal cortex is a region of the human brain involved with executive function,
social behavior, and decision-making. The prefrontal cortex is susceptible to damage in
people with AD, and when its condition deteriorates, behavioral symptoms associated with
the prefrontal cortex are seen. Aggressive behavior and irritation are two additional typical
behavioral features of Alzheimer’s disease (Marco & Redolat, 2023). However, outbursts,
verbal and physical, restlessness, and wandering are examples. However, the inability to
recognize people and objects is another typical sign of Alzheimer’s disease. Such can cause
confusion and disorientation, making interacting with others or navigating their environment
challenging (James et al., 2021). Alzheimer’s disease negatively impacts the temporal and
parietal lobes, which are in charge of processing sensory data and recognizing familiar faces
and objects (Ribas et al., 2023). As the illness worsens, people may also struggle with
language, including difficulty finding the right words and difficulties communicating their
thoughts. Generally speaking, AD’s incredibly complex and multidimensional symptoms
affect various intellectual, sentimental, and behavioral functions (James et al., 2021). The
structural changes in the brain associated with these symptoms are particularly detrimental to
the hippocampus, entorhinal cortex, and other brain areas involved in memory and cognitive
processing.
Role of the Brain in AD
Neuroanatomy of AD
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A neurodegenerative disorder that affects different parts of the brain and neural
networks is Alzheimer’s disease. The disorder’s defining feature is the slow loss of neurons
and synapses, which causes significant brain atrophy and cognitive deterioration. The
complex neuroanatomy of AD includes numerous brain areas, neurotransmitter systems, and
structural alterations. The hippocampus, a vital memory storage and retrieval structure, is the
most severely impacted area in AD. It is particularly prone to amyloid-beta (A) protein
buildup, a pathological characteristic of Alzheimer’s disease (Slattery et al., 2019). A buildup
results in the development of plaques, which can impair brain signaling and result in neuronal
death. The hippocampus also undergoes considerable shrinkage in AD, which is thought to be
a factor in the disorder’s memory problems.
The prefrontal cortex, which is essential because it plays a role in executive function,
attention, and decision-making, is another crucial area AD impacts. With Alzheimer’s disease,
the prefrontal cortex also exhibits considerable shrinkage, with decreases in gray matter
volume seen even in the early stages of the illness. AD also impacts the temporal lobes
responsible for language, auditory processing, and memory. In the condition’s early stages,
the entorhinal cortex, an area of the temporal lobe crucial for memory consolidation, exhibits
substantial atrophy and is particularly susceptible to Aβ accumulation (Tarawneh et al.,
2022). In addition to these parts of the brain, AD also affects the basal forebrain, which
contains cholinergic neurons crucial for learning and memory, and the parietal cortex, which
is essential to sensory processing and spatial cognition. With Alzheimer’s disease, the
cholinergic system is particularly damaged, contributing to the cognitive difficulties seen in
the condition.
Neurotransmitter Systems
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The complex neurological disease known as AD impacts numerous neurotransmitter
systems. The most well-known is the cholinergic system, crucial to memory and learning.
Acetylcholine, the primary neurotransmitter of the cholinergic system, declines with AD and
is linked to cognitive problems. The loss of cholinergic neurons in the basal forebrain and
their connections to the hippocampus and neocortex compromises the cholinergic system in
Alzheimer’s disease. Acetylcholine activity and release are thus decreased, which is thought
to be a factor in the memory problems seen in Alzheimer’s disease (Sahana et al., 2020).
Several neurotransmitters (glutamatergic and GABAergic) are most affected by AD. The
degenerative alterations of Alzheimer’s disease impact the brain’s glutamatergic system,
which is in charge of excitatory transmission. Alzheimer’s disease also affects the GABAergic
system, essential in inhibitory signalling; reduced GABAergic activity has been seen in the
hippocampus and neocortex.
Other neurotransmitters, including serotonin, norepinephrine, and dopamine, might
add more to the pathophysiology of AD. The mood-regulating neurotransmitters serotonin
and norepinephrine have been linked to depression in Alzheimer’s patients. Dopamine plays a
role in processing rewards and may also be responsible for the apathy and anhedonia are seen
in the illness (Sahana et al., 2020). The cholinergic system is severely damaged, which affects
cognition and contributes to the disorder’s cognitive deficiencies. It is essential to
comprehend the neurological underpinnings of Alzheimer’s disease to create efficient
interventions and treatments for this life-altering condition.
Other Biological Systems
Hormonal changes have also been connected to Alzheimer’s disease. For instance,
estrogen is recognized for its neuroprotective and role in memory consolidation effects. At
menopause, estrogen levels drop, which may lead to why women are more prone than men to
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suffer from AD. Also, it has been proven that stress chemicals like cortisol harm Alzheimer’s
sufferers’ cognitive function.
Lifespan Effects of AD
A person’s risk of developing AD increases with age, usually after age 65. The most
prevalent type of dementia in older people is Alzheimer’s disease, which affects women more
frequently than men. Alzheimer’s illness has serious negative consequences on longevity. In
addition to a loss of independence and a deterioration in cognitive function, the condition is
gradual and irreversible. Alzheimer’s disease patients may struggle to carry out daily tasks
and interact socially because they may have memory loss, language impairments, and
executive function issues (Walhovd et al., 2020). Caregivers and family members of people
with Alzheimer’s also suffer when trying to take care of such individuals. Caring for people
with AD can be emotionally and physically draining, resulting in caregiver burnout and
elevated stress levels. Also, the economic toll that AD takes on society is significant. The cost
of caring for those with AD is high and is expected to rise in the upcoming years as the
population ages. As a result of carers frequently needing to reduce their work schedules or
abandon their jobs to care for their loved ones, Alzheimer’s disease also has a detrimental
influence on productivity and employment.
Studying Alzheimer’s Disease
Neuroimaging, genetics, and animal models are only a few methods to research
Alzheimer’s disease. Researchers can see the structure and operation of a living person’s brain
using neuroimaging methods like magnetic resonance imaging (MRI), positron emission
tomography (PET), and solitary laser computed tomography. These methods can spot
abnormalities in the brain’s structure and function brought on by Alzheimer’s disease, like
aberrant protein accumulation and neuronal loss (Andrews et al., 2020). Genetic research can
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help identify people at risk for AD and shed light on the biological processes underlying the
disorder. There are many advantages to researching Alzheimer’s illness. Studying the
disorder’s biological underpinnings can help find potential treatment and preventative
options. For those with Alzheimer’s, early detection and therapies can also help delay the
onset of symptoms and enhance the quality of life (Andrews et al., 2020). The frequency of
Alzheimer’s disease is predicted to rise with an aging population; researching the condition is
essential for creating effective treatments and lessening the disease’s toll on patients and
society.
Behavioral Processes
Memory, language, attention, executive function, and mood management are all
affected by the neurodegenerative disorder known as Alzheimer’s disease. While the
disorder’s most apparent and upsetting symptoms are frequently the cognitive losses seen in
Alzheimer’s disease, other behavioral changes can also be very severe. Memory impairment
is one of the earliest and most apparent behavioral changes in AD. According to Kales et al.
(2019), individuals with AD struggle with recent memory, including recalling conversations
or recent experiences. More distant memories may also be impacted as the condition worsens,
making it harder to carry out regular tasks. The impact of this memory loss on daily life may
be significant.
Alzheimer’s patients also have language impairment, making it difficult to find words
to understand and express themselves. Communication can be difficult due to such linguistic
deficiencies, which can cause social isolation and dissatisfaction. Alzheimer’s disease also
exhibits abnormalities in attention and executive function, which make it harder to plan,
organize, solve problems, and make decisions (Kamat, 2015). Starting and finishing tasks
become more challenging, making daily activities more difficult. Depression is a prevalent
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symptom of Alzheimer’s disease, affecting mood control (Kales et al., 2019). Cognitive
deficiencies can be exacerbated by depression, which also affects memory and other
cognitive processes. Unrest and disinterest are additional AD symptoms that make interacting
with others and performing daily tasks difficult. Consequently, Alzheimer’s disease, a
complex ailment, impacts various behavioral processes, including cognition, speech,
concentration, executive function, and emotional regulation.
Conclusion
A neurodegenerative ailment called Alzheimer’s affects the neuroanatomy and
neurotransmitter systems of the brain, impairing cognitive performance and causing
substantial behavioral abnormalities. Many neurotransmitter systems become dysfunctional
due to amyloid beta protein buildup, neurofibrillary tangles, and the death of neurons in
critical brain regions. These alterations may result in memory, language, attention, executive
function, and mood management issues. It is crucial to comprehend the behavioral
mechanisms at play in Alzheimer’s disease to create effective interventions and treatments.
The condition’s behavioral alterations can cause problems with daily tasks, communication,
and social relationships and a general reduction in quality of life. It is essential to
comprehend the neurobiological and behavioral mechanisms behind Alzheimer’s disease to
create effective interventions and treatments. Research into Alzheimer’s disease has advanced
significantly in recent years, providing fresh insights into the disorder’s origin and novel
treatment approaches. Yet, much must be done to create efficient therapies for this severe
condition. Overall, Alzheimer’s disease is a multifaceted ailment that has an impact on a
variety of brain and behavioral functions. Developing efficient interventions and treatments
to enhance the quality of life for those afflicted with the disease requires a better
understanding of the disorder’s etiology.
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References
Andrews, S. J., Fulton-Howard, B., & Goate, A. (2020). Interpretation of risk loci from
genome-wide association studies of Alzheimer’s disease. The Lancet
Neurology, 19(4), 326-335.
James, T., Kula, B., Choi, S., Khan, S. S., Bekar, L. K., & Smith, N. A. (2021). Locus
coeruleus in memory formation and Alzheimer’s disease. European Journal of
Neuroscience, 54(8), 6948-6959
Kales, H. C., Lyketsos, C. G., Miller, E. M., & Ballard, C. (2019). Management of behavioral
and psychological symptoms in people with Alzheimer’s disease: an international
Delphi consensus. International psychogeriatrics, 31(1), 83-90.
Kamat, P. K. (2015). Streptozotocin induced Alzheimer′s disease like changes and the
underlying neural degeneration and regeneration mechanism. Neural Regeneration
Research, 10(7), 1050. https://doi.org/10.4103/1673-5374.160076
Li, H. W., Zhang, L., & Qin, C. (2019). Current state of research on non‐human primate
models of Alzheimer’s disease. Animal Models and Experimental Medicine, 2(4),
227-238
Lock, M. (2013). Making and remaking Alzheimer disease. The Alzheimer Conundrum.
https://doi.org/10.23943/princeton/9780691149783.003.0002
Marco, P., & Redolat, R. (2023). Art therapy approaches in Alzheimer’s disease: A systematic
review. Activities, Adaptation & Aging, 47(1), 75-106
Neural Structures Involved in Speech Production. (2016). Neural Control of Speech.
https://doi.org/10.7551/mitpress/10471.003.0004
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Ribas, M. Z., Paticcié, G. F., Noleto, F. M., Ramanzini, L. G., de Oliveira Veras, A.,
Dall’Oglio, R., … & Dos Santos, J. C. C. (2023). IMPACT OF DYSEXECUTIVE
SYNDROME IN QUALITY OF LIFE IN ALZHEIMER DISEASE: WHAT WE
KNOW NOW AND WHERE WE ARE HEADED. Ageing Research Reviews,
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Roobini, M. S., & Lakshmi, M. (2021). Prediction of Alzheimer disease using Pearson
recursive graph convolutional neural network. https://doi.org/10.21203/rs.3.rs935323/v1
Sahana, S., Kumar, R., Nag, S., Paul, R., Chatterjee, I., & Guha, N. (2020). A Review On
Alzheimer Disease And Future Prospects.
Slattery, C. F., Agustus, J. L., Paterson, R. W., McCallion, O., Foulkes, A. J., Macpherson, K.,
… & Warren, J. D. (2019). The functional neuroanatomy of musical memory in
Alzheimer’s disease. Cortex, 115, 357-370.
Tarawneh, H. Y., Menegola, H. K., Peou, A., Tarawneh, H., & Jayakody, D. M. (2022).
Central auditory functions of Alzheimer’s disease and its preclinical stages: a
systematic review and meta-analysis. Cells, 11(6), 1007.
Trevisan, K., Cristina-Pereira, R., Silva-Amaral, D., & Aversi-Ferreira, T. A. (2019). Theories
of Aging and the Prevalence of Alzheimer’s Disease. BioMed research international,
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Walhovd, K. B., Fjell, A. M., Sørensen, Ø., Mowinckel, A. M., Reinbold, C. S., Idland, A. V.,
… & Wang, Y. (2020). Genetic risk for Alzheimer disease predicts hippocampal
volume through the human lifespan. Neurology Genetics, 6(5).
Critical Review
The final assignment for this class will be a 10-page critical review of the drug treatment for
a neuropsychological disorder. The review will use peer-reviewed and/or scholarly sources
to provide an evidence base for the evaluation of current drug treatment modalities for the
disorder. The disorder is the same disorder you selected in week 1 and for which you
discussed its neurobiology in the Week 1 assignment (topic selection) and its drug
management in the Week 2 assignment (drug treatment). Please remember – you will be
analyzing the same disorder to complete the Week 6 assignment (comprehensive Critical
Review of the same disorder and its management).
Reminder – your completed Week 1 and Week 2 assignments will be used as a foundation to
help you complete your Week 6 assignment (Critical Review) on the same disorder. Thus,
your work in Week 1 and in Week 2 will be used to support your work in Week 6. Utilize
the previous references you researched in Week 1 and Week 2, and add any additional peerreviewed/scholarly references that would support your comprehensive review. These sources
should provide evidence-based information to help support your comprehensive analysis,
focusing on the aspects described below. Be sure to cite your sources in your paper and
include them on your References page. You may utilize required or recommended course
materials in your work, but these will not count towards the reference requirements;
however, you may cite and reference the American Psychiatric Association’s (2013) DSM5 as one of your sources used for the grading credit.
The paper will be evaluated on the inclusion of the following information.
Introduction:
Evaluate the disorder in terms of symptomatic and behavioral presentation. Include the time,
course, and progression of the disorder. Evaluate and explain special features of the disease
epidemiology including risk factors for development of the disorder, lifespan and
reproductive factors increasing risk of developing the disorder, and any genetic,
environmental, or behavioral factors that increase risk.
Theory:
Evaluate the predominant theory or theories regarding the biological basis of the disorder.
Explain the disorder in terms of pertinent neurotransmitter and receptor theories and use
your references to provide an evidence base for these theories. Analyze neurotransmitter
system(s) involved in the pathology of the disorder, including a description of: 1) the
involved neurotransmitter(s) and receptor(s), 2) regions of the nervous system (brain, spinal
cord, or peripheral nervous system) involved with any pathological anatomical changes, and
3) abnormalities of neural circuits and pathways. Include an explanation of how receptor
agonists or antagonists would theoretically treat the disorder to reverse the pathology and
restore normal function, or why they would be expected to improve symptoms.
Treatment:
Evaluate drug therapies for treating the disorder based on the current understanding of the
biological basis of the disorder. Include a description of the behavioral symptoms and
physical signs of the disorder, and identify the drug class(es) used in pharmacological therapy
with a discussion of the mechanism of action of the drug class(es). Explain why the
pharmacodynamics of the drug class(es) would affect the pathology of the disorder to restore
function and/or improve symptoms. Include a discussion of the drug pharmacokinetics for
each drug class. Provide examples of available marketed drugs within each class. Describe
any drug side effects and/or adverse effects of the drug treatment and their biological basis,
including issues related to contraindications, interactions, drug metabolism, and elimination.
In addition, explain risks, benefits, and ethical implications for high-risk and exceptional
treatment conditions.
Conclusion:
Summarize theories of neuropsychological disorders as they relate to principles of drug
action for that selected disorder. Provide a synopsis of the evidence base that supports or
disproves current theories regarding the pathology of the disorder, advantages and
disadvantages of current drug treatment(s). Lastly, evaluate any controversies regarding
ethical and/or risk-benefit perspectives associated with the current treatment(s). Describe
possible areas for future research.
Attention Students: The Masters of Arts in Psychology program is utilizing the Folio
portfolio tool as a repository for student scholarly work in the form of signature assignments
completed within the program. After receiving feedback for this Integrative Literature
Review, please implement any changes recommended by the instructor, go to your Folio
account and upload the revised Integrative Literature Review as a project in your portfolio.
(Use the Setting Up and Using FolioLinks to an external site. guide to create an account if
you do not already have one.) The upload of signature assignments will take place after
completing each course. Be certain to upload revised signature assignments throughout the
program as the portfolio and its contents will be used in other courses and may be used by
individual students as a professional resource tool.
The paper:
•
Must be 10 to 12 double-spaced pages in length (not including title and reference pages)
and formatted according to APA style as outlined in the Writing Center.Links to an
external site.
•
•
•
•
Must include a separate title page with the following:
o Title of paper
o Student’s name
o Course name and number
o Instructor’s name
o Date submitted
Must use at least six peer-reviewed and/or scholarly sources to provide an evidence base
for your analysis. It is expected that you will use the references researched in Week 1 and
Week 2, as well as any additional references you need to provide additional support for
your work. You may utilize required or recommended course materials in your work, but
these will not count towards the reference requirements; however, you may cite and
reference the American Psychiatric Association’s (2013) DSM-5 as one of your sources
used for the grading credit.
Must document all sources in APA style as outlined in the Writing Center.
Must include a separate reference page that is formatted according to APA style as
outlined in the Writing Center.
Carefully review the Grading RubricLinks to an external site. for the criteria that will be
used to evaluate your assignment.
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Schizophrenia
Jasmine Barbusca
PSY 630 Psychopharmacology
Dr. Laura Green
April 10, 2023
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Schizophrenia
Schizophrenia is a severe neuropsychological condition with a long history of affecting
an individual’s thoughts, feelings, perceptions, and behavior. Other scholars suggest that
Schizophrenia is a psychotic disorder. According to research, the disease first appears in late
adolescence or early adulthood. Further, Torrey & Yolken (2019) categorizes Schizophrenia as a
complex and multiple etiology influenced by genetic, environmental, and neurological variables.
In this paper, we will explore the theories of the etiology of Schizophrenia with a focus on the
neurobiology of the disorder, including the pathology of nervous system structures and function,
neurotransmitter abnormalities, anatomical changes, and how these factors contribute to the
physical signs and behavioral symptoms displayed by individuals diagnosed with Schizophrenia.
Etiological Theories
Today, the exact cause of Schizophrenia has not yet been understood. However, several
studies suggest that the disorder is likely from genetic and environmental factors. Genetic studies
have proven that individuals with a family history of the disorder are at a greater risk of suffering
from the disorder. Nevertheless, it is vital to remember that researchers have not yet identified
any particular gene to be the cause of Schizophrenia. Thus, Schizophrenia is most likely to be
associated with the interaction of more than one gene and various environmental factors.
Neurotransmitters are the brain chemicals that transmit multiple signals between nerve cells.
According to most scholars, Schizophrenia’s pathogenesis has been linked to abnormalities in
neurotransmitter systems. First, one of the most well-known theories of Schizophrenia is the
dopamine supposition, which suggests that excessive dopamine transmission in particular brain
regions, especially the mesolimbic pathway, may contribute to the emergence of positive
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manifestations of the disorder, for example, delusions and hallucinations (Saparia, 2023).
Antipsychotic drugs’ success in treating patients, which block dopamine receptors and lessen
dopamine transmission in the brain, supports the notion. Apart from dopamine, some other
neurotransmitters, for instance, GABA, glutamate, and serotonin have been associated with the
etiology of Schizophrenia (Saparia, 2023). An excitatory neurotransmitter called glutamate is
thought to regulate dopamine release, and abnormalities in glutamate signaling have been
observed in people with Schizophrenia. Serotonin, a neurotransmitter important in mood
regulation, has also been linked to Schizophrenia because serotonin receptors are changed in the
brains of patients with the disorder.
Symptomatology of Schizophrenia
Despite the symptomatology of Schizophrenia being broad, the disorder is most
commonly associated with symptoms like delusions, hallucinations, disorganized behavior, and
some cognitive deficits. The symptoms, as mentioned earlier, are the outcome of the disorder
affecting and dysregulating neurotransmitter systems, for instance, dopamine, glutamate, and
GABA. Typically, the two symptoms, hallucinations and delusion, can be categorized as positive
symptoms and are mostly linked to the hyperactivity of the dopamine system (Bègue et al.,
2020). Conversely, symptoms such as apathy and social disengagement are mostly related to the
hypoactivity of the dopamine system and are deduced to be negative symptoms. Additionally,
regarding the GABA neurotransmitter system, scholars have established that GABAergic
disruption may cause the emergence of various psychotic symptoms. On the other hand,
glutamatergic dysregulation has been linked to multiple cognitive deficiencies, for instance,
decreased working memory and reduced executive function.
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Anatomical Changes Associated with Schizophrenia
The dysregulation of neurotransmitter systems and underlying structural abnormalities
can explain schizophrenia patients’ physical and behavioral symptoms. As previously mentioned,
hallucinations and delusions are examples of positive symptoms of Schizophrenia that are linked
to dopamine system hyperactivity, whereas negative symptoms are related to dopamine system
hypoactivity (Ding & Hu, 2021). Cognitive and memory problems and negative symptoms like
apathy and social disengagement are linked to anatomical alterations like lower grey matter
volume in the prefrontal cortex and hippocampus and increased ventricular volume.
Summary of Dysregulation of Neurotransmitters
The physical and behavioral symptoms experienced by people with Schizophrenia can be
explained by the dysregulation of neurotransmitters and structural abnormalities in this
condition. Positive signs of Schizophrenia, such as delusions and hallucinations, might result
from excessive dopamine neurotransmission in some brain areas, especially the mesolimbic
pathway. Dopamine and other neurotransmitter systems in different brain parts, like the
prefrontal cortex, may be underactive, contributing to Schizophrenia’s negative symptoms like
decreased motivation and social disengagement (Chatterjee et al., 2020). Cognitive deficiencies
frequently seen in Schizophrenia can be explained by anatomical abnormalities in the brain,
particularly in the prefrontal cortex and hippocampus. Ideally, treating the disorder is based on
correcting the dysregulated neurotransmitter systems. Medications such as antipsychotic ones,
which are dopamine antagonists, help treat positive symptoms of the disorder. Further, newer
drugs, such as the antipsychotic ones mentioned above, have been created to target glutamate and
other neurotransmitter systems, thus improving the cognitive deficits and the negative symptoms
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of the disease, such as apathy. Despite the effectiveness of these medications, they have various
side effects on the individuals using them. For instance, the use of antipsychotic medicines might
result in the individual gaining massive amounts of weight and experiencing multiple metabolic
changes in their body, which might cause the limitation of the efficacy of the various body parts.
In conclusion, Schizophrenia is a neuropsychological condition marked by various issues
in the general development and functioning of the neurological system, for instance, the multiple
neurotransmitter systems. As the paper mentions, the disorder is associated with various
neurotransmitter systems such as glutamate, serotonin, and GABA. Further, individuals suffering
from the disease have been associated with multiple brain structural alterations, for instance,
lower volume of the brain and some cognitive difficulties. So, in order to properly treat the
disorder, it is vital to have a deeper understanding of its pathophysiology.
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References
Bègue, I., Kaiser, S., & Kirschner, M. (2020). Pathophysiology of negative symptom dimensions
of Schizophrenia–current developments and implications for treatment. Neuroscience &
Biobehavioral Reviews, 116, 74-88.
Chatterjee, I., Kumar, V., Rana, B., Agarwal, M., & Kumar, N. (2020). Identification of changes
in grey matter volume using an evolutionary approach: an MRI study of Schizophrenia.
Multimedia Systems, 26, 383-396.
Ding, J. B., & Hu, K. (2021). Cigarette smoking and schizophrenia: Etiology, clinical,
pharmacological, and treatment implications. Schizophrenia research and
treatment, 2021.
Saparia, P. (2023). Schizophrenia: A Systematic Review. Clinical and Experimental
Psychology, 9(1), 8-14.
Torrey, E. F., & Yolken, R. H. (2019). Schizophrenia as a pseudogenetic disease: A call for more
gene-environmental studies. Psychiatry research, 278, 146-150.
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Schizophrenia
Jasmine Barbusca
PSY 630 Psychopharmacology
Dr. Laura Green
April 17, 2023
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Schizophrenia
Antipsychotic drugs, commonly referred to as neuroleptics, are frequently used in the
pharmacological treatment of schizophrenia (Ceraso et al., 2020). These medications
(Antipsychotics, Atypical Antipsychotics, and Antidepressants), which have various mechanisms
of action, are used to treat the agitation, hallucinations, delusions, and disorganized thinking that
are hallmarks of schizophrenia. Dopamine is involved in the brain’s signaling process (Ceraso et
al., 2020). Excessive dopamine activity has been linked to the pathophysiology of schizophrenia.
Haloperidol, fluphenazine, and chlorpromazine are a few examples of common antipsychotic
medications. The named medications are frequently used to treat hallucinations and delusions,
which are various symptoms of schizophrenia.
Atypical antipsychotics have a more complicated mechanism of action, including both
dopamine and serotonin receptors, making them partial agonists or antagonists. Depending on
the situation, they can either activate or inhibit the action of these receptors, which may help
explain their broader range of activity in treating schizophrenia symptoms. These drugs
frequently work by antagonistically interacting with dopamine D2 receptors to reduce the
elevated dopamine activity associated with psychosis (Tendilla-Beltrán et al., 2021). However,
they also show partial agonist or antagonist activity at other receptors, including the serotonin 5HT2A receptors, which likely contributed to their unique pharmacological profile. Atypical
antipsychotics are primarily used to treat the symptoms of schizophrenia and other psychotic
disorders, rather than stopping or reducing the underlying disease process, in terms of the disease
process (Tendilla-Beltrán et al., 2021). These medications are often used to treat acute psychotic
episodes and long-term maintenance therapy is frequently needed to control symptoms and avoid
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relapse. By inhibiting excessive dopamine activity, atypical antipsychotics can assist in lessening
the positive symptoms of psychosis, such as delusions and hallucinations.
Although they may also treat depression and other mental health issues, antidepressant
drugs are typically used to treat schizophrenia. One example of an antidepressant is the Tricyclic
Antidepressant (Adell, 2020). Serotonin, norepinephrine, and dopamine, neurotransmitters
involved in mood regulation, are increased in the brain due to these medications’ actions.
Fluoxetine (Prozac), sertraline (Zoloft), venlafaxine (Effexor), and bupropion (Wellbutrin) are
some examples of regularly prescribed antidepressants. The ability of antidepressant medications
to either increase (agonist) or inhibit (antagonist) the activation of specific receptors in the brain
is referred to as their agonist-antagonist action. For instance, agonists that increase the
availability of serotonin in the brain by blocking the absorption of serotonin include fluoxetine
and sertraline (Adell, 2020). Reestablishing the balance of serotonin levels in the brain is thought
to aid in easing the symptoms of depression.
Certain receptor types and subtypes in the brain, including serotonin (5-HT receptors)
and norepinephrine receptors, are where antidepressant medications work pharmacologically
(NE receptors). These receptors on nerve cells are essential for controlling mood, emotion, and
other neurological functions. It is crucial to remember that antidepressant medications are not
usually used to stop or slow the onset of depression or other mood disorders (Adell, 2020).
Instead, they treat the disorders’ symptoms, such as low mood, loss of interest or pleasure,
changes in food or sleep, and difficulty concentrating. Antidepressants are typically used as a
component of an all-encompassing treatment strategy that may involve counseling, dietary
changes, and other supporting strategies to manage mood disorders effectively. Antidepressant
medications’ precise mechanisms of action and efficacy can vary based on the substance in
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question and unique patient features, so a trained healthcare expert should carefully evaluate and
treat these factors.
When weighing the potential benefits of symptom relief and increased quality of life
against the potential hazards of side effects, a risk-benefit analysis of drug use for schizophrenia
is performed. Antipsychotic medications are frequently prescribed as a part of a thorough
treatment program for those diagnosed with psychotic disorders. Psychiatrists or other qualified
healthcare experts typically prescribe antipsychotic medicines and doses. They depend on the
precise diagnosis, the severity of the patient’s symptoms, unique traits, and other considerations.
Reducing psychotic symptoms linked to psychotic diseases is the main advantage of
antipsychotic medication use (Bjarke et al., 2020). Antipsychotics can aid with hallucinations,
delusions, thinking disorders, and agitation, significantly enhancing the patient’s capacity for
clear thought, everyday functioning, and a higher quality of life. Sedation, movement
abnormalities (including extrapyramidal symptoms such as tremors and rigidity), and hormone
imbalances are typical side effects of conventional antipsychotics (Bjarke et al., 2020). Regular
antipsychotic usage over an extended period can also increase the chance of tardive dyskinesia, a
possibly irreversible movement disease. However, the effectiveness of conventional
antipsychotics in treating negative symptoms of schizophrenia, such as cognitive impairment and
social disengagement, may be limited. Patients may find these side effects upsetting, affecting
their willingness to comply with treatment.
Contrarily, atypical antipsychotic medications may raise the risk of metabolic side effects
such as weight gain, diabetes, and dyslipidemia while having a decreased risk of extrapyramidal
side effects (Carli et al., 2021). Atypical antipsychotics frequently cause weight gain, metabolic
issues (including diabetes and dyslipidemia), drowsiness, and mobility difficulties as side effects
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(although generally less severe than typical antipsychotics). Also, it is advised to regularly check
metabolic parameters while receiving medication because some atypical antipsychotics may raise
the risk of cerebrovascular and cardiovascular events. These metabolic side effects may need to
be monitored and managed because they may have long-term health repercussions (Carli et al.,
2021). Generally, atypical antipsychotic drug use can be very beneficial in treating
schizophrenia, despite any possible adverse effects. These medications are frequently successful
in lowering the intensity and frequency of symptoms, allowing patients to live more comfortably.
Relapses and hospitalizations, which may be expensive and disruptive for patients and their
families, can also be avoided with their assistance. Atypical antipsychotic medicine is commonly
used following a thorough treatment plan that includes ongoing side effect monitoring and
appropriate dosage and medication change recommendations.
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References
Adell, A. (2020). Brain NMDA receptors in schizophrenia and depression. Biomolecules, 10(6),
947.
Bjarke, J., Sinkeviciute, I., Kroken, R. A., Løberg, E. M., Jørgensen, H. A., Johnsen, E., &
Gjestad, R. (2020). Different response patterns in hallucinations and delusions to
antipsychotic treatment. Nordic Journal of Psychiatry, 74(7), 497-504.
Carli, M., Kolachalam, S., Longoni, B., Pintaudi, A., Baldini, M., Aringhieri, S., … & Scarselli,
M. (2021). Atypical antipsychotics and metabolic syndrome: From molecular
mechanisms to clinical differences. Pharmaceuticals, 14(3), 238.
Ceraso, A., Lin, J. J., Schneider-Thoma, J., Siafis, S., Tardy, M., Komossa, K., … & Leucht, S.
(2020). Maintenance treatment with antipsychotic drugs for schizophrenia. Cochrane
Database of Systematic Reviews, (8).
Tendilla-Beltrán, H., del Carmen Sanchez-Islas, N., Marina-Ramos, M., Leza, J. C., & Flores, G.
(2021). The prefrontal cortex as a target for atypical antipsychotics in schizophrenia,
lessons of neurodevelopmental animal models. Progress in neurobiology, 199, 101967.
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