





































Berkeley
Pharma Tech
Journal of Medicine

Correspondence: 
segaljasmine7@gmail.com

Keywords:
Disease Treatment and Therapies, 
Pre-Clinical Studies, Alzheimer's 
Disease, Stem Cell Therapy, Neural 
Stem Cells, Mesenchymal Stem 
Cells, Embryonic Stem 
Cells

Submitted August 9, 2023 
Accepted March 15, 2024 
Published June 28, 2024

Full Open Access

Creative Commons Attribution 
License 4.0

Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder, a form of dementia 
commonly affecting people aged 40-65. Growing more prevalent in society, 
approximately 6.2 million Americans aged 65 and older live with AD. AD is a 
progressive, long-term neurological disorder that worsens cognitive skills, memory, and 
communication abilities, leading to a performative decline in daily tasks. 

Characterized by the accumulation of extracellular amyloid beta (Aβ) plaque and 
neurofibrillary tangles (NFTs) of tau in the central nervous system. AD accounts for 
neuronal death in the brain. Unfortunately, even with its detrimental impacts, 
clinical trials of therapeutic drugs are still to be tested and not available to the 
public. Current research on stem cell transplantation has shown to alleviate 
neuropathology and is explored as a prospective treatment for AD. This literature 
review assesses the important uses of stem cell therapy for AD patients to provide a 
new clinical approach for future treatment. Further clinical research should be 
conducted on the long-term outcomes of stem cell therapy for deeper 
analysis of its therapeutic effects for AD. 

Stem Cell Therapy as a Target for 
Alzheimer’s Disease 
By: Jasmine Segal



1. Introduction

Alzheimer's Disease (AD) is a form of dementia a�ecting memory and
behavioral capabilities, resulting in the deterioration of cognitive function.
As of 2023, this neurodegenerative disease has impacted around 50-75% of
the United States population.1 Symptoms of AD are characterized by
impairments in memory, which interfere with daily activities and other
cognitive �elds—this is linked through a reduction in brain volume of such
individuals.2 The risk of AD increases with age, which doubles about every
�ve years above the age of 65. With increasing age, the hippocampus’
cognitive function declines, a common trait of neurodegenerative disorders
and AD. Patients with AD tend to live within 5–12 years of the onset of
AD symptoms due to declining performance of basic functions and brain
incompatibilities.3 The hippocampus serves as the main part of the brain
responsible for memory. The cerebral cortex and hippocampus are closely
associated with cognitive function and neurogenesis (neuronal formation)
in the brain.4 Reduction of brain mass is often indicated through neural
death and synapse degradation of the hippocampus. It has been commonly
noted that hippocampal degeneration is an indication of AD.2

Diagnosis of AD is characterized in the brain by an increase in the buildup
of proteins between neurons.5 AD can be examined through chronic
neuroin�ammation with neuronal loss of the extracellular senile plaques
(SPs), amyloid-β peptide (Aβ) deposits, and tau proteins that form
neuro�brillary tangles (NFTs), which lead to extensive metabolic
dysfunctions. NFTs (abnormal production of tau protein neurons)
contribute to neural death, inducing progressive deterioration of memory
and cognitive ability.6 In AD, degeneration occurs with the accumulation of
β-amyloid (Aβ) and tau proteins in the brain. Senile plaques of protein
fragments beta-amyloid (Aβ) induce the build-up of tau proteins leading to
AD patients’ nerve cells shrinking and dying, spreading to the entire brain.
Neural networks of AD patients are impaired due to a lack of the
transmitter acetylcholine, which plays an important role in intercellular
signaling.7,8

In the gene encoding Aβ precursor protein (APP), mutations of this gene
can cause hereditary cerebral hemorrhage, leading to Aβ build-up.9

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Hereditary cerebral hemorrhage with amyloidosis (Aβ buildup) showed that
APP mutations could cause an abnormal amyloid deposition, albeit mainly
outside the brain parenchyma.10 Altered APP processing and Aβ
accumulation predate tau. The mechanism for the aggregation of AD is
characterized by the “amyloid cascade hypothesis” (Figure 1). According to
this hypothesis, the extracellular deposition of Aβ is a critical and central
event in the disease's progression, leading to the formation of neuro�brillary
tangles, causing neuroin�ammation, cell death, and dementia.11,12

Abnormal processes or mutations of processing APP and Aβ peptides hold
signi�cant development for AD. Yet, it is suggested that targeting APP
processing to treat AD can result in tumor development.13 The
accumulation of Aβ peptides and tau are caused by disturbances of
homeostasis from APP degradation. The clinical manifestations of AD are
progressive and clinical trials are still ongoing.

Figure 1: Summary sequence of events of AD development via the amyloid cascade 
hypothesis, presenting the signi�cance of Aβ plaque buildup in AD symptoms. As 
previously discussed, APP genes encode amyloid precursor proteins that are the main 
building block of Aβ plaques. PS1 and PS2 genes express presenilin-1 and presenilin-2 
proteins respectively. Mutations in the aforementioned genes lead to exempli�ed Aβ plaque 
production, leading to neuronal cell dysfunction and death.

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Stem cells are immature cells with self-renewal capabilities and the ability to
di�erentiate into various cell types. Stem cell transplantation can mobilize
endogenous stem cells in adult brains and provides a promising form of
therapy for other neurodegenerative diseases, such as Parkinson's
Disease.14,15 For cells to be labeled as stem cells, they must have unlimited
self-renewal and encompass specialized cell types.16 Pluripotent stem cells
are common regeneration approaches in their abilities to di�erentiate into
all cell types, which naturally don’t last before di�erentiating to a specialized
stem cell.16 They di�erentiate into cells of all germ layers, making these
types of cells e�ective for stem cell therapies through autologous or
allogeneic transplantation.17, 18 In this instance, stem cells can repair neural
damage through cell division, which the most common approach to stem
cell therapy.

2. Discussion

AD develops as a process of many factors by high neuropathological
diversi�cations. Therapeutic stem cells can di�erentiate into other body
cells, which brings a promising approach to stimulating neurogenesis
circuitry. To develop stem cell therapy, a suitable cell source must be
determined. During literature searches, common stem cell types were noted:
brain-derived neural stem cells (NSCs), mesenchymal stem cells (MSCs),
and embryonic stem cells (ESCs) (Figure 2).

Figure 2: The most common stem cell types are brain-derived neural stem cells (NSCs),
mesenchymal stem cells (MSCs), or embryonic stem cells (ESCs). Transplantation of these

Berkeley Pharma Tech Journal of Medicine | 4

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104807/


cells has been investigated as a prospective therapeutic approach for neurodegenerative
disease, including cases with AD.35

2.1 Neural Stem Cells

NSCs are multipotent and self-renewing cells capable of di�erentiating
neurons in the brain’s hippocampus.13 AD generates approximately half the
rate of neurogenesis compared to normally aging individuals. NSCs can
ameliorate AD symptoms by regenerating lost or damaged cells.6

Mechanisms of improved cognition involving enhanced hippocampal
synaptic density are mediated through brain-derived neurotrophic factors
(BDNF). Several studies found that the transplantations of NSCs lead to
di�erentiation into neural types, promoting hippocampal neurogenesis and
elevating BDNF levels. In mouse models, NSC transplantation rescued
cognitive performance in AD mice.7 Ager, Davis, Agazaryan, Benavente,
Poon, La Ferla, and Blurton-Jones found that with human cells and models,
human NSCs can improve cognition of AD pathogenesis and hippocampal
neural loss.20 Studies showcased that NSC injections rescued cognitive
functions in transgenic mice, exhibiting advanced AD pathology.
NSC-derived cells elevated hippocampal BDNF, which led to the increased
synaptic density of the hippocampus and restored cognition abilities.21

Figure 3: Modi�ed from Chang, Kim, Joo, Ha, and Suh,3 the amyloid cascade hypothesis
illustrates the accumulation of Aβ derived components of AD, including neuronal and
synaptic loss, neuro�brillary, and cognitive dysfunction (blue arrows). While drugs target
the initial accumulation of Aβ, stem-cell-based therapies intervene at all stages. Stem cell

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therapies could treat AD by targeting AD pathogenesis. NSC (green arrows) provides
synaptic plasticity and neurotrophic activity.

2.2 Mesenchymal Stem Cells

MSCs can regenerate and di�erentiate under appropriate conditions, such
as standard cultured solutions.4,23 In particular, MSCs can be isolated from
brain regions. A recurring cell in literature reviews was found to be human
umbilical cord blood-derived MSCs (hUCB-MCSs) and bone
marrow-derived MSCs (BM-MCSs). Hippocampal transplantation of
(hUCB-MCSs) showed rescuing of memory de�cits and cognitive abilities
in AD mice by reducing neuronal apoptosis, which increased brain
volume.24-27 BM-MCSs were transplanted in theAPP mouse model of AD, ,
resulting in a reduction in microglial numbers without altering amyloid
plaques, the baseline of the development of AD.27 Yet, some studies also
show a signi�cant decrease in amyloid plaques after two months of
injection.28 Transplantation of huCB-MSCs and BM-MCSs into the
hippocampus through multiple studies has shown to be feasible, safe, and
tolerated to improve cognitive function and lower amyloid plaques in the
brain.4,29

2.3 Embryonic Stem Cells

ESCs from inner masses of blastocysts have shown to be pluripotent and
thus capable of cell di�erentiation and self-renewal into primary germ
layers.2,6 For cell replacement therapies, ESCs provide
pluripotency-regulated neural lines. Several reports have explored ESC’s
roles in mitigating AD in rodent models. Here, ESC progenitor and
cultural cells transplanted into the hippocampus of rat models
di�erentiated neuron cells, increased synapse regulation, and improved
memory de�cits of AD pathologies.26 Neuron-derived ESCs also
di�erentiated into mature cholinergic neurons and restored the cognitive
performance of AD transgenic mice.16,28 Nevertheless, there are
controversial issues with ESCs, such as immune system rejection, ethical
concerns, and risks of teratoma (a germ cell tumor) upon transplantation.6,30

Due to the low number of literature papers on ESCs, more research should
be conducted to explore the role and e�ects of AD as an alleviating factor.

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Table 1: Summary of AD model results of stem cell therapy.

3. Limitations and Future Research

Clinical �ndings have advanced in recent decades, generating promising 
results in stem cell technology. Yet, technological challenges remain on stem 
cell therapy use in AD. Even with the possibility of regenerative medicine, 
the future of stem cell therapy for regeneration remains unclear. Research 
concerning stem cell therapy and AD analysis are based on animal models, 
which may not demonstrate favorable results in humans.14,36,37 Stem cell 
therapy results in di�erent cognitive e�ects based on animal models 
transfected with AD, proving that it can improve learning and memory 
de�cits.18,29,32 . The current AD research primarily used transgenic mice 
models to reveal cellular alterations through disease progression. These 
�ndings support the amyloid cascade theory of the accumulation of tau 
NFTs causing neurodegeneration.30 Yet, the progressive nature of AD 
requires longitudinal studies to assess the lasting e�ects and safety of pro�le 
treatments.

Regarding the high aggregate quantities of Aβ plaques and tau in the brain 
of patients or experimental models with AD, , transplanted cells can 
typically generate nonneuronal cells or unexpectedly die based on speci�c 
environments. This approach does not aid the therapeutic approach, 
creating a possible discrepancy with the results of experiments.7,38 A study

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by Bae, Jin, Lee, Richardson, and Carter indicated a drastic decrease in Aβ
plaques in the brain’s hippocampus region after two months.27 On the
other hand, Naaldijk, Jaeger, Fabian, Leovsky, Bluher, Rudolph, and
Stolzing found no di�erence in terms of Aβ plaque concentration but noted
improvements in cognitive functions in AD models.39 Based on recurring
inconsistent results, further research on stem cell therapy is necessary to
produce a more robust conclusion. Stem cell therapy aims to promote the
regeneration of tissues with inhibition of in�ammation, reduction of
apoptosis, stimulation of angiogenesis (blood vessel formation), and cell
di�erentiation, bringing a considerable amount of attention to stem cell
therapy as a feasible way of treating AD patients.14.27 Additionally, issues
with the procedure and basis of stem cell therapy remain unresolved, such as
long-term safety of transplantation delivery systems, cell source, and donor
cell responsiveness to AD-pathogenic environments.19,40 Even so, stem cell
therapy will become an e�cient candidate for AD treatment due to
promising results in neuron regeneration.

It is important to note that rather than multiple databases, the literature
search used only three: PubMed, Google Scholar, and the National Library
of Medicine. This may have limited the information represented in this
paper, leading to fewer referenced sources and greater variability in results.
Though more current studies were implemented, eliminating those older
than 1991 allowed analysis of more recent data and research advances since
the beginning of stem cell technology. Further research would be ideal to
analyze the e�ectiveness of stem cell therapy over a longer duration and to
ensure the therapeutic does not lead to tumors through excess cell
di�erentiation.

4. Conclusion

While the cause of AD is only partially understood, hereditary genes are
thought to play a signi�cant role in determining who contracts it.
Hypotheses have tried to explain the cellular events leading to inheritance
of AD, with the focus lying on extraneous APP accumulation. However, it
has been determined that vaccines removing APP buildup do not reverse
AD in patients.31

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More clinical trials employing stem cell therapy are ongoing for AD, 
focusing on its capability to di�erentiate into neuronal and glial cells and 
alleviate AD symptoms or curation.2 This paper analyzes the speci�c stem 
cells of NSC, MSC, and ESC to foresee possible treatment for AD 
pathogens (Table 1).

In recent years, stem cells have become a promising alternative to 
conventional methods for AD research. As a multifactorial disorder, AD 
creates barriers to alleviating its adverse e�ects, particularly in the brain’s 
hippocampus. To combat such e�ects, stem cell therapy uses a multi-
targeted approach through cell di�erentiation upon transplantation. Stem 
cells have been tested for e�ective modi�cation in slowing neuronal death 
and preventing tau accumulation in WAD. Recent data from Quin, Wang, 
Zhang, Bai; and Shin, Park, Kim, Oh, Bae, Ha, and Lee indicated that 
transplantation of stem cells alleviated neuropathology and cognitive 
de�cits in several animal models with AD.32-35 No current drugs 
demonstrated an improvement in AD symptoms and e�ects.16 Research has 
provided promising results for stem cell transplantation improving memory 
and learning abilities as a potential treatment for AD.

Therefore, stem cell therapy should be considered a healthy and suitable 
regeneration of cell function to alleviate cell death and hippocampus 
damage. Experts convey that stem cell therapy for AD has bene�cial 
outcomes, displaying a clinical e�ciency of approximately 82.2%.41 Hence, 
treatments that enhance or improve cognition, especially in the presence of 
aggregate plaque and tangle pathology, are urgently needed. Stem cells are 
being actively studied for their potential to replace dead or diseased 
cells.21,42-44 Regardless of the recent breakthrough of stem cells, 
advancements in technology con�rm the therapeutic as a potential 
treatment for AD. In the future, a thorough evaluation of implanted cells 
with AD pathogens should be conducted to con�rm their successful 
therapeutic e�ects.

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	Article 1_Segal_Galley
	Segal_References



