





































Berkeley
Pharma Tech
Journal of Medicine

Correspondence: 
ygayoung@umich.edu

Keywords:
Alzheimer's Disease (AD)           
AD pathology                 
MicroRNAs (miRNAs)       
Amyloid cascade hypothesis 
Amyloid beta (Aβ) plaques       
Tau Hypothesis        
Neurofibrillary tangles (NFT)

Submitted: October 5, 2022 

Accepted: November 21, 2022

Published: December 28, 2022

Full Open Access

Creative Commons Attribution 
License 4.0

Abstract
Alzheimer’s disease (AD) is a progressive, neurodegenerative disease and is the most common 
cause of dementia. The disease pathology of AD is marked by the accumulation of Beta-
amyloid (Aβ) plaques and deposition of phosphorylated tau NFTs in the brain. Currently, 
the therapeutic approaches to AD are solely palliative in nature and thus can do little to stop 
or reverse the disease pathology once it has begun. MicroRNAs (miRNAs) are a class of 
noncoding nucleotides that are critically involved in the regulation of various post-
transcription mRNA processes, such as synapse plasticity and neuron differentiation. Owing 
to the multifactorial nature of AD, miRNAs have garnered much attention in the research 
field due to their concomitant dysregulation and appearance in several AD 
pathophysiological processes. This review paper offers insight into the potential use of 
miRNAs as a therapeutic target and diagnostic marker in AD.

MicroRNAs as a Diagnostic Marker and a 
Therapeutic Target for Alzheimer’s Disease
By: William Ugorji, Gayoung Yang and Prakruti Jajoo



Berkeley Pharma Tech Journal of Medicine | 49 

1. Introduction
Alzheimer’s disease (AD) is the leading cause of dementia in the world, with 
a disease burden exceeding more than 5.5 million individuals in the United 
States and up to 80% of all dementia diagnoses overall1. The two clinical 
hallmark pathologies of the disease are the Beta-amyloid (Aβ) plaque and 
deposition of neurofibrillary tangles (NFTs) of hyperphosphorylated tau 
hypotheses. The Beta-amyloid hypothesis suggests that an accumulation of 
amyloid plaques in the brain triggers a cascade of pathological events that 
ultimately lead to the clinical presentation of the disease1. Isoforms of the Aβ 
peptide are implicated in the beta-amyloid hypothesis, and Aβ38, Aβ40, and 
Aβ42 exhibit the greatest tendency to cluster and produce the neuronal 
oligomers that trigger the amyloid cascade1. Within this cascade, various 
biological stressors, such as localized inflammation, glutamate production, 
and oxidation, are involved. Conversely, the Tau hypothesis entails the 
process of hyperphosphorylated tau decoupling from their normal 
microtubule function to form NFTs that disrupt normal neuronal function 
and transport. While the Beta-amyloid and Tau hypothesis were initially 
regarded as two distinct pathophysiological pathways, recent evidence has 
given credence to the notion that both pathways act interdependently, 
resulting in the clinical presentation of AD1. 

Symptoms of cognitive impairment and memory loss are the main assessment 
criteria for AD patients, and differential diagnosis can be made through 
cerebrospinal fluid (CSF) and positron emission tomography (PET) 
analysis1. These methods, however, suffer from issues such as the high cost of 
application, invasiveness, and low specificity that combine to limit their 
accessibility and usage in routine clinical scenarios2. As such, a definitive 
diagnosis of AD can only be made through post-mortem tissue analysis of 
suspected AD patients. 

The current treatment landscape for AD primarily involves palliative 
therapeutic approaches, such as cholinesterase inhibitors and N-methyl D-
aspartate (NMDA) antagonists like memantine. Cholinesterase inhibitors 
include drug classes like donepezil and galantamine and work by stopping the 
degradation of acetylcholine molecules in the brain3. Cholinesterase 
inhibitors are typically prescribed for AD patients in the mild, moderate, or 



 

Berkeley Pharma Tech Journal of Medicine | 50 

severe dementia stages based on the mini-mental state examination score 
(MMSE)4. NMDA antagonists function by regulating glutamate action in 
the brain3. While the current pharmacological approaches for AD can 
enhance patient quality of life, they are unable to alter disease progression or 
overall life expectancy for individuals with AD. As such, there exists a great 
need to develop a non-invasive, cost-effective approach to provide robust 
early diagnosis and treatment options for this condition in the medical 
community. 
  
MicroRNAs (miRNAs) are a class of small, non-coding RNA molecules that 
have the potential to act as therapeutic agents and biomarkers in AD. 
Ranging approximately 22 nucleotides in length, miRNAs work on the post-
transcriptional level of mRNAs and are involved in the regulation of nearly 
every cell and protein-coding process in the body5. A few of the regulatory 
facets that miRNAs act on include cellular differentiation, proliferation, as 
well as programmed cell-death mechanisms like apoptosis6. A single miRNA 
can alter up to 200 mRNAs and multiple genes, thus making them 
increasingly valuable targets for research into how changes in their expression 
levels contribute to disease states such as AD or cancer5. MiRNAs specifically 
function by attaching and binding to the 3’ untranslated region (UTR) of 
their associated mRNAs, in which the complementarity between the 
miRNA and its target eventually results in the degradation of the mRNA 
targets7. Current research shows that approximately 70% of identified 
miRNAs have expression patterns in the brain, which further highlights the 
dynamic potential of miRNA processes in healthy brain function and 
diseased states7. Within the brain and nervous system environment, miRNAs 
are particularly involved in regulating synapse plasticity, dendritic spine 
morphology, and neurite outgrowth, thus contributing to the modulation of 
the cognitive and memory functions typically lost in AD pathology through 
acting upon protein synthesis in synapses8. 
  
MiRNAs are predominantly found in circulatory biofluids, such as blood 
serum and plasma9. Due to its proliferation in the blood serum, miRNA has 
wide potential to be a cost-effective and less invasive diagnostic approach for 
AD. In this review, we focus on exploring the most recent advances in the 



 

Berkeley Pharma Tech Journal of Medicine | 51 

research and development of miRNAs involvement in AD, which has broad 
therapeutic and diagnostic potential that remain to be unlocked. 
  

2. Pathophysiology of Alzheimer’s Disease 
2.1. Amyloid plaques 

Amyloid pathogenesis starts with altered cleavage of Aβ peptide from the 
internal transmembrane protein amyloid precursor protein (APP) by the 
alpha, beta, and gamma secretase10. Two main types of Aβ polymers are 
involved in plaque formation and induced neurotoxicity. Aβ40 is more 
abundant and less neurotoxic than Aβ42, which is highly insoluble and 
neurotoxic. Aβ40/Aβ42 aggregation blocks ion channels, alters calcium 
homeostasis, increases mitochondrial oxidative stress, and diminishes energy 
metabolism and glucose regulation, which promotes neuronal cell death11. 
Under normal conditions, proteolysis of APP by either alpha or β-secretases 
(BACE1) cleaves off small nontoxic fragments. However, altered cleavage of 
APP by β followed by γ-secretases results in 42 amino acid peptides (Aβ42) 
which then aggregate to form oligomers that diffuse into synaptic clefts and 
interfere with synaptic signaling. Increased level of Aβ42 leads to the 
polymerization of insoluble amyloid fibrils that causes neuronal 
toxicity10,11,12. Accumulation of these amyloid plaques initially occurs in the 
basal, temporal, and orbitofrontal neocortex region of the brain and later 
progresses throughout the hippocampus, amygdala, and cerebral cortex12. 
  
Sustained elevation and continuous aggregation of dense amyloid plaques 
can stimulate a chronic response of the innate immune system by inducing 
astrocytes and microglia recruitment surrounding the plaques. This results 
in the increased level of local inflammatory response due to the elevated 
release of inflammation related mediators, such as complement factors, 
eicosanoids, chemokines, and proinflammatory cytokines, which can disrupt 
microglial clearance of amyloid plaques, while also increasing microglia 
mediated neuronal death, damage to axons and dendrites, synaptic loss, and 
neurotoxicity10,11. Consequently, these neuronal dysfunction inhibits cell 
synaptic communication, contributing greatly to AD pathogenesis. 
 
  
 



 

Berkeley Pharma Tech Journal of Medicine | 52 

2.2. Neurofibrillary Tangles (NFTs) 
Tau protein, encoded by the microtubule associated protein tau (MAPT) 
gene, is a microtubule-associated protein that can form insoluble filaments 
that accumulate as NFTs. Tau protein facilitates the maintenance of 
neuronal structure and function. In Alzheimer’s, the abundance of Aβ 
plaques in the cell causes the Tau protein to become hyperphosphorylated, 
leading to oligomerization. Consequently, the loss of its affinity for tubulin 
leads to dissociation of tubule subunits that eventually fall apart and form 
large fragments of tau filaments that can aggregate into NFTs. NFTs are 
straight, fibrillary, and highly insoluble patches in the neuronal cytoplasm 
that are composed of paired helical fragments (PHFs) of tau fibrils 
approximately 20 nm in diameter. They spread throughout the brain as AD 
progresses, beginning near the entorhinal cortex, leading to abnormal loss of 
communication between neurons and signal processing and finally 
apoptosis, cell death, in neurons. In addition, the transfer of 
hyperphosphorylated tau proteins diffuse to surrounding cells and cause 
damage to neuronal function, contributing to the onset of AD. Genomic 
studies of brain tissues of AD patients have found significant 
downregulation of miRNA-124 and miR-425-5p, which under normal 
conditions inhibit the abnormal hyperphosphorylation of Tau protein. On 
the other hand, a significant upregulation of miR-132 and miR-125b in AD 
patients has been found to induce Tau protein phosphorylation and 
neuronal apoptosis. 
  
Moreover, miRNAs could promote the progression of AD by promoting 
phosphorylation of the Tau protein. miR-483–5p, miR-125b-5p and miR-
23b indirectly regulates Tau phosphorylation by targeting extracellular 
signal-regulated kinases 1 and 2(ERK1/2), protein phosphatase 
methylesterase-1 (PME-1) and N-acetylglucosaminyltransferase III (GNT-
III) signaling pathways, respectively13. Amyloid pathology appears to precede 
that of tau, with NFTs only being found in regions where amyloid was 
already present, but both Aβ plaques and neurofibrillary tau tangles are 
significant factors of the pathogenesis of AD that lead to synapse loss and 
neuronal atrophy, especially throughout the hippocampus and cerebral 
cortex11, 12. 
  



 

Berkeley Pharma Tech Journal of Medicine | 53 

2.3. Microglial Activation 
Microglia are macrophages that reside in the CNS and play a significant role 
in maintaining neuronal plasticity, synapse remodeling, phagocytosis, and 
clearance of Aβ plaques in healthy individuals. The binding of microglia to 
extracellular Aβ plaques via cell-surface receptors such as SCARA1, CD36, 
CD14, α6β1 integrin, CD47, and Toll-like receptors (TLRs), a class of 
pattern recognition receptors (PRRs) that ignites innate immune response, 
initiates the endocytosis of Aβ oligomers and NFTs for degradation by 
microglial proteases such as neurolysin and insulin-degrading enzymes11. 
However, under pathological conditions, the phagocytotic functioning of 
the Aβ oligomers by the microglia is weakened, and overexpressed Aβ 
plaques and NFTs can lead to microglial activation around the plaque areas 
and release inflammatory factors such as IL-1β and TNF-α, which aggravate 
neuronal damage and exacerbate AD pathology by giving rise to increased 
synaptic damage, oxidative stress, and neuroinflammation7. Furthermore, 
insufficient Aβ plaque clearance is observed due to elevated levels of localized 
cytokine concentrations that downregulate the expression of Aβ 
phagocytosis receptors, thus decreasing Aβ clearance13. Moreover, 
proliferation and activation of microglia in the brain can affect insulin 
receptor substrate 1 (IRS-1) and block intracellular insulin signaling, which 
has an important role in neural health11. 
  

3. Genetic basis 
The role of genetics in AD pathogenesis accounts for about 70% of the AD 
cases. Most cases of early onset AD (EOAD) are known to be inherited in an 
autosomal dominant pattern and mutations in the dominant genes including 
Amyloid precursor protein (APP), Presenilin-1 (PSEN-1), Presenilin-2 
(PSEN-2)14, apolipoprotein E (ApoE), Clusterin (CLU), Bridging Integrator 
1 (BIN1), and TREM215. 

  
3.1. APP 

APP is a transmembrane protein cleaved by α-, β-, and γ-secretase that releases 
Aβ and other proteins and is encoded by the APP gene on chromosome 21. 
Twenty-five out of thirty mutations have been found in the APP gene to be 
related to AD, along with the elevated level of insoluble Aβ aggregates. 
KM670/671NL mutation in mouse models has shown an increasing level of 



 

Berkeley Pharma Tech Journal of Medicine | 54 

amyloid plaques in the hippocampus and cortex. A673V, D678H, D678N, 
E682K, and K687N mutations have shown cortical atrophy, and E682K has 
shown hippocampal atrophy15. Moreover, A673V mutations have shown a 
presence of NFTs and Aβ, activation of microglia and astrocytes, and 
neuronal loss. Other mutations such as T714I, V715A, V715M, V717I, 
V717L, L723P, K724N, and I716V affect the γ-secretase cleavage site, 
increasing the Aβ42/Aβ40 ratio. E693G, E693K, D694N, and A692G 
mutations affect the α-secretase cleavage site, causing polymorphic aggregates 
that can disrupt bilayer integrity. Meanwhile, one protective mutation 
(A673T) has been identified, which protects against AD by decreasing Aβ, 
Aβ40, and Aβ42 secretion15. 
  

3.2. PSEN1 and PSEN2 
Presenilin genes (PSEN1 and PSEN2) are part of the γ-secretase family and 
were also found to be mutated in AD14. It has been found that AD patients 
may be predisposed to PSEN1 mutation leading to familial AD at a young 
age. Mutation in the PSEN1 gene is more common, with more than 200 
mutations identified. On the other hand, a rare form with less than 40 
mutations was identified in the PSEN2 gene, causing an increased level of 
toxic forms of amyloid Aβ42 as opposed to non-toxic Aβ40, aggravating AD 
pathology. PSEN1 plays an important role in the production of Aβ from 
APP by activating γ-secretase. Knockout studies of PSEN1 in mice models 
showed synaptic dysfunction and memory impairment. On the other hand, 
PSEN-2 mutations might have a critical effect on the Aβ 42/40 ratio, causing 
familial AD in the presence of normal PSEN-1 alleles, but some of the PSEN-
2 mutations are rare polymorphisms and are not pathogenic mutations and 
plays a relatively minor role in Aβ production15. 

  
3.3. APOE4 

ApoE protein is a glycoprotein expressed highly in the liver and brain 
astrocytes and some microglia. It serves as a receptor-mediated endocytosis 
ligand for lipoprotein particles like cholesterol, which is essential for myelin 
production and normal brain function. The ApoE gene located on 
chromosome 19 has three isoforms, ApoE2, ApoE3, and ApoE4, which 
cause changes in the coding sequence15. The APOE4 variant is the most 
significant genetic risk factor for sporadic Alzheimer’s disease (sAD). APOE4 



 

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has a multidimensional impact on the pathogenesis of AD, including 
dysregulation of lipids and lipoproteins, such as APOE plasma levels13. The 
ApoEε4 allele is a strong risk factor for both early onset AD (EOAD) and late 
onset AD (LOAD) compared to ApoEε2 and ApoEε3 alleles, which are 
associated with lower risk and protective effect, respectively. ApoEε4 plays 
an important role in Aβ deposition as a senile plaque and causes cerebral 
amyloid angiopathy (CAA), which is known as a marker for AD. ApoEε4 
was also shown to be associated with vascular damage in the brain, which 
leads to AD pathogenesis15. 
  

3.4. CLU and BIN1 
Clusterin (CLU) and Bridging Integrator 1 (BIN1) genes are novel risk 
factors for LOAD. CLU gene is reported to be located on chromosome 8. 
Under normal conditions, CLU plays a protective role by interacting with 
Aβ and promoting its clearance or a neurotoxic role by reducing Aβ 
clearance. However, in AD patients, CLU is upregulated in the cortex and 
hippocampus. The Aβ ratio values determine whether the CLU role is 
neuroprotective or neurotoxic. BIN1 is a Bin-Amphiphysin-Rvs (BAR) 
adaptor protein that is involved in the production of membrane curvature 
and other endocytosis cellular functions. BIN1 has several isoforms—some 
are found in the brain, where they interact with different proteins such as 
clathrin, synaptojanin, and amphiphysin 1, and others in which they regulate 
synaptic vesicle endocytosis. Recently, BIN1 was recognized as the second 
most important risk factor for LOAD after ApoE, where it plays a role in Aβ 
production and as a tau and NFT pathology modulator15. 

  
3.5. TREM2 

TREM2 is a transmembrane receptor expressed in cells of the myeloid 
lineage. It facilitates mediating phagocytic clearance of neuronal debris and 
binds anionic carbohydrates, bacterial products, and phospholipids to 
transmit intracellular signals through the associated transmembrane adaptor 
DAP1255 and further phosphorylation of downstream mediators. In AD, a 
rare mutation of TREM2 (R47H) has been reported that plays a potent role 
in aggravating the risk of developing AD. This mutation leads to an inability 
of the receptors to clear Aβ from the CNS, contributing to Aβ accumulation 
and further intensification of pathogenesis in AD patients16. 



 

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4. miRNA usage in the treatment of AD 
As a result of their ability to post-transcriptionally regulate many of the genes 
involved in AD, miRNAs have emerged as a valuable potential therapeutic 
agent for the treatment of AD. Various miRNAs have been shown to be 
integral to the production and regulation of amyloid-beta, and thus 
modification of miRNA expression levels could attenuate facets of AD 
pathology16. Therapeutic approaches to AD utilizing miRNAs generally 
function through two pathways. MiRNAs expression levels may be restored 
to their normal baseline magnitude or be upregulated through the in vivo 
transfection of miRNA oligonucleotide that mimics endogenous miRNA 
functions. Alternatively, harmful miRNAs in AD can be downregulated 
through the administration of complementary antisense oligonucleotides17. 
  
Subsequently, the most recent studies in the field have demonstrated 
promising results of miRNAs facilitating neuroprotectant and ameliorating 
cognitive deficits through investigations using in vivo AD animal models and 
in vitro cell cultures17.  In one study, upregulation of the miR-23b-3p 
molecule via in vitro transfection reduced hyperphosphorylated tau clusters 
and inhibited levels of neuronal apoptosis in Swedish mutant amyloid-
precursor protein (APPswe) cells via inhibiting the upstream expression of 
glycogen synthase kinase-3 (GSK-3) apoptotic pathway18. This is significant 
since miR-23-b-3p has clinical diagnostic potential due to it being greatly 
downregulated in the blood plasma of AD patients when compared to 
healthy controls, and further investigations revealed a positive correlation 
between increased miR-23b-3p and improved measures of cognitive 
function for individuals with AD18. 
  
The miRNA-200 family has also been shown to play an innate defensive role 
against Aβ-induced neurotoxicity. A study conducted by Higaki et. al. 
demonstrated that administration of members of the miRNA-200 family – 
such as miR-200b/c – showcased reduced Aβ in cellular mediums and in vivo 
amelioration of Aβ-induced cognitive impairments in Tg2576 mouse 
models, thus leading to restoration of spatial memory performance in the 
Barnes maze test19. Aβ has been shown to degrade the neuronal memory 
centers and synapses that act upon the hippocampus and frontal cortex 
tissue, making the miR-200 family a potential therapeutic target due to their 



 

Berkeley Pharma Tech Journal of Medicine | 57 

ability to alter S6k1 levels and modulate extracellular insulin signaling in the 
brain19. Similarly, another study conducted by An et. al demonstrated the 
differential expression of miR-124 in AD compared to healthy control 
populations17. miR-124 was revealed to interact with the Beta-site Amyloid 
precursor protein Cleaving Enzyme 1 (BACE1) network in AD, which is 
prominently involved in AD via functioning in the production of Aβ from 
APP20. It was found that miR-124 expression was downregulated in AD 
models while BACE1 was simultaneously overexpressed20. Subsequently, 
miR-124 is a potential novel therapeutic target as its administration via 
transfected mimics could be utilized to regulate and inhibit expression of 
BACE1 mRNAs and proteins in affected AD tissues, resulting in lowered 
Aβ and NFT burden20. 
  
Many other miRNAs are upregulated in AD pathogenesis and contribute to 
neurotoxicity, and thus therapeutic approaches that leverage under-
expressing these classes of miRNAs could potentially alleviate the negative 
effects on neurons posed by AD. Through an analysis study on SH-SY5Y cell 
cultures, it was shown that the pathogenesis of AD triggers dysregulation of 
miRNA-146a, causing significant overexpression of these miRNAs in the 
brain that results in the disruption of the phosphatase PTEN, thus causing 
increased hyperphosphorylation of tau protein and NFT cluster formation21. 
The effects of miRNA-146a overexpression were most pronounced in the 
brain regions that are generally most susceptible to tau aggregation in AD and 
other related dementias – most notably in the hippocampus and temporal 
cortices, which are fundamental to learning and memory formation21. In this 
same study, the 5xFAD transgenic mice model reacted positively to the 
downregulation of miRNA-146a via a series of miRNA-146a antagomir 
injections, ultimately showing a restoration of endogenous frequencies of 
phosphatase PTEN and a rescue of function in hippocampal memory and 
neural pathways21. While miRNAs have traditionally been downregulated in 
AD pathology, the overexpression of miR-146a has been experimentally 
shown to be intricately involved in the tau pathology of AD, thus making the 
selective inhibition of this miRNA molecule a viable target for an in vivo 
therapeutic of the disease. A more extensive list of identified miRNAs and 
their pathophysiologic targets in AD are displayed below in Table 1. 
  



 

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The clinical application of miRNA in AD can be achieved through diverse 
pathways and delivery methods. Studies have shown that naturally occurring 
compounds like resveratrol can act upon and regulate specific miRNAs in 
the body and, therefore, can be attuned to modulate miRNA expression 
levels in vivo22. Conversely, certain anti-inflammatory therapeutics can 
exhibit regulatory-like control on the expression of certain miRNA 
molecules, thus providing a treatment option for AD that functions via 
miRNA modulation23. Other innovative and emerging approaches involve 
using exosome vesicles as a targeted vehicle to effectively cross the blood-
brain barrier and deliver miRNA into localized regions for the greatest 
benefit in the diseased brain23. 
  

miRNA Target/Pathologic Process 

miR-126 Involved in BACE1 expression; overexpression 
suppresses BACE1 while under expression increases 
BACE1 proliferation 

miR-146 Observed to have higher levels of expression in MCI  
patients that later manifested with AD; is also associated 
with APOE4 protein expression 

miR-26b Shown to increase tau phosphorylation and neuronal 
apoptosis 

miR-181a Associated with an increased Aβ concentration in 
cerebrospinal fluid 

miR-200b Under expressed in experiments with APP/PS1 
transgenic mice & positively reduced APP expression 

miR-339-5p Targets & inhibits BACE1; expression levels were shown 
to be reduced in AD patients 

miR-16-5p & 
miR-708-5p 

Differentially expressed molecule in the cerebrospinal 
fluid cells of AD patients; potential biomarker 



 

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miR-93-5p Differentially expressed molecule in the cerebrospinal 
fluid cells of AD patients; potential biomarker 

 Table 1: List of the relevant miRNAs & the corresponding nervous system targets 

  

5. MiRNAs functioning as predictive biomarkers of AD 
5.1. Amyloid Cascade Hypothesis 

There is evidence that Aβ and its imbalance between production and 
destruction is a leading cause of AD, as it causes a cascade of events in the 
bodily systems24,25. APP is cleaved by the BACE-1 gene first to produce the 
Aβ protein25, 26. Some proteases are meant to clear the Aβ in the system 
through proteolytic degradation and receptor-modulated endocytosis24. 
When this process is not done at an adequate rate, the Aβ protein can build 
up in the blood plasma or CSF. Some forms of this protein are toxic and are 
known to cause neurotoxicity, neuron apoptosis, inflammation, and 
synaptic loss, which all play a role in AD24,25,27. The buildup of Aβ protein is 
deposited as plaque in the systems of the brain and CNS, which in turn 
causes increased production of proinflammatory cytokines. These cause the 
degeneration of glial cells and their tissue, which causes and progresses 
Alzheimer’s25. 
  

5.2. Other miRNA in pathogenesis of AD 
Astrocytes regulate ion homeostasis in the brain, and therefore, support 
neuronal function. Additionally, astrocytes have been shown to release 
cytokines which play a crucial role in disease progression and creation25. 
miRNA is an important immunoregulator, and an imbalance in the 
expression of specific miRNAs can cause certain proteins or cytokines to be 
over or under-produced. For instance, an excess of inflammatory cytokines 
causes the nearby neural cells and neurons to die25. This process, along with 
the Amyloid Cascade Hypothesis, has shown that although AD cannot be 
pinpointed to one specific trigger or cause, the levels of particular miRNA 
play a role in the existence, pathogenesis, and pathophysiology of AD. 
  

5.3. Specific miRNAs as biomarkers 
There are many studies that show patterns in the levels of expression of 
specific miRNA segments that relate to AD26. In the serum of AD patients, 
segments such as miR-149, miR-34a-5p, miR-125b-5p, miR-15b, miR-16, 



 

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miR-124, miR-29c and miR-374b-5p were all found in reduced quantities 
when compared to healthy individuals27. Out of these, miR-149, miR-34a-
5p, miR-16, miR-29c and miR-374b-5p were found to directly target BACE-
127. This relates to the upregulation of BACE-1 found in AD patients, which 
in turn cleaves the APP and promotes the production of Aβ proteins. There 
were other miRNAs, such as miR-146a and miR-181a, which were found in 
higher concentrations in AD patients, more specifically in patients who 
initially had mild cognitive impairment (MCI) and later progressed into 
AD21. In different parts of the body, the expression levels of different 
miRNAs were shown to have similar patterns. The downregulation of miR-
132/212 and miR-335–5p in the brain tissues were found in AD patients, 
which caused a higher production of Aβ and more plaque buildup in the 
brain, causing symptoms consistent with the disease26. Generally, miRNA 
has shown to be strongly related to the pathophysiology of Alzheimer’s and 
plays a direct role in many of the genes of interest. 
  

6. Genes/factors of interest 
6.1. APP 

Studies have indicated that an increased APP level due to genomic locus 
duplication or mutation in the APP regulatory sequences can result in the 
development of early-onset dementias, including AD. APP regulation is of 
special interest as it provides valuable insight into the genetic basis of AD and 
its novel therapeutics. A study that tested the regulatory effect of miRNAs 
on the level of APP gene expression demonstrated that complementary 
binding between miRNAs hsa-mir-106a and hsa-mir-520c and their 
predicted target sequences within the 3' UTR of APP genes results in 
repression of reporter gene expression, and that over-expression of these 
miRNAs resulted in translational repression of APP mRNA and 
significantly reduced APP protein levels in human cell lines. These results 
were the first to experimentally demonstrate the post-transcriptional 
regulatory role of miRNA in the levels of human APP28. On the other hand, 
another study has demonstrated the activity of miR-346, which requires the 
chelation of an intracellular iron Fe, that targets the APP mRNA 5′-UTR to 
upregulate APP translation and Aβ production. It has also been found that 
miR-346 levels are altered in late-Braak stage AD. As a result, miR-346 leads 
to the upregulation of APP in the CNS, and participate in maintaining APP 



 

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regulation of Fe, which is disrupted in the late stages of AD29. Substantial 
progress towards understanding the role of miRNA-induced alterations in 
the APP gene expression and Aβ production levels and the multifaceted 
biological involvement of miRNAs in APP metabolism is of interest to 
current research underlying the pathophysiology of AD28,29. 
  

6.2. Hyperphosphorylated Tau Peptide (p-tau) 

Several functional in vivo studies have demonstrated the potential of 
microRNA-23b-3p (miR-23b-3p) in various neurologic disorders30. Study 
results support the potent involvement of miR-23b-3p as a neuroprotectant 
in AD.  Functional in vivo studies demonstrated that intracerebroventricular 
delivery of miR-23b-3p in APP/PS1 mice reduced cognitive impairment and 
p-tau levels, while upregulation of miR-23b-3p resulted in an increased level 
of p-tau, Aβ production, and neuronal apoptosis. These results thereby 
identify miR-23b-3p as a promising therapeutic target for AD30. Several 
studies have speculated the functional role of tau in promoting microtubule 
assembly, stabilization, and spacing necessary for axonal transport. 
Moreover, 6 isoforms of tau are present in the central nervous system due to 
the inclusion and exclusion of exons 2,3, and 10. Another study aimed to 
uncover the role of miRNAs in tau metabolism identified miR-16 and miR-
132 as putative endogenous regulators of neuronal p-tau and exon 10 
splicing, respectively, and mutations in tau exon 10 have been associated with 
neurodegeneration and dementia in the adulthood31. Overall, altered levels of 
miR-16 and miR-132 were associated with tau pathology in human 
neurodegenerative disorders31. 

 

6.3. Amyloid-β (Aβ) peptides and BACE-1 

AD has been associated with increased production of amyloid-β (Aβ) 
peptides and impaired function of its clearance. miRNAs targeting the key 
proteins of the amyloidogenic pathway are of interest to current research on 
AD therapeutics. A study has shown that miR-31, previously found to be 
decreased in AD patients, suggests that miR-31-mediated modulation of 
APP and BACE1 can become a therapeutic option in the treatment of AD. 
miR-31 upregulation in 17-month-old AD triple-transgenic (3xTg-AD) 
female mice simultaneously reduced APP and BACE-1 mRNA levels in the 
hippocampus, significantly ameliorated deficits in short and long-term 



 

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memory, and reduced anxiety and cognitive inflexibility. In addition, 
lentiviral-mediated miR-31 expression significantly reduced AD 
neuropathology in the mouse mode with a reduced Aβ accumulation in both 
the hippocampus and subiculum26. MiRNAs typically inhibit protein 
expression by binding to its complement mRNAs’ 3′-untranslated regions 
(3′-UTR) in a cell-specific manner. However, the mechanisms of the 
variation of miRNA activity remain unknown. Another study demonstrated 
the differing effects of treatment of miR-298 reduced native APP and 
BACE-1 translation levels in astrocytic but not in a neuron-like cell line. The 
variation in its effects on APP-3’-UTR activity and native protein levels are 
according to cell type and 3’-UTR specificity. Researchers postulated that 
naturally occurring variations in the length of APP 3’ UTR could account 
for miR-298 cell-specificity. Such novel miR-298 involvement in AD 
provides valuable insight into the clinically relevant research on tailoring 
miRNA’s effect to a specific cell type in the treatment of AD32. 
  

6.4. Apolipoprotein E (ApoE4) 

A study identified the involvement of miR-195 in ApoE4-associated 
pathology in AD disease progression. Results demonstrated that reduced 
levels of miR-195 in the AD brain correlated with early disease progression 
but not advanced stages of AD. Moreover, it has been noted that the ApoE4 
genotype accelerated miR-195 reduction, leading to increased tau pathology 
and cognitive decline33. In addition, miR-195 overexpression reduced the 
expression of its target, synaptojanin1 (synj 1), a brain PIP2-degrading 
enzyme that plays an important functional role in AD pathogenesis in mice 
models. For example, reduced synj 1 expression is associated with faster Aβ 
clearance via the lysosomal degradation pathway, ameliorating elevated tau 
hyperphosphorylation levels and rescuing ApoE4-associated neuronal 
impairment33. Ongoing research aims to uncover specific mechanisms of 
miR-195 involvement targeted at ApoE4 for future therapeutic purposes. 

  

7. Practical/Clinical Applications and Feasibility 
7.1. miRNA Benefits 

This novel therapeutic has shown promising results in research and 
laboratory environments. But how are these principles and tools translated 
and applied to the real world? The basis of the therapeutic is the molecule 



 

Berkeley Pharma Tech Journal of Medicine | 63 

miRNA. Compared to most nucleic acids, miRNA is a highly stable 
molecule, therefore “surviving” in bodily fluids, such as the CSF, when 
observing brain diseases such as AD34. This stability allows for an easier 
analysis, making it ideal for clinical settings. 
  
Furthermore, it has been shown that miRNA is better amplified in PCR 
treatments which is a very commonly used method in the scientific and 
medical field34. Another benefit of the miRNA is that they constrain 
sequences that create molecules that have been proven to be directly related 
to AD. More specifically, miRNAs are known to regulate the production of 
genes like APP and the BACE-1, which affects the production of Aβ32,34. For 
example, miR-340 can be used to alleviate AD by targeting the Aβ and miR-
342–3p was shown to be in higher concentrations in AD patients, which 
increased the stress kinase c-Jun N-terminal kinase, therefore increased the 
accumulation of Aβ34, 36. The treatment is relatively simple and noninvasive, 
making it feasible for common use in clinical settings35. Lastly, it has proven 
to be more cost-effective than the current or competing biomarkers for AD34. 
  

7.2. miRNA Uncertainty 
 A drawback or point of uncertainty in the research of miRNA as 
therapeutics for Alzheimer’s is the discrepancy between the different trials 
and projects, starting from the beginning at the root of the collection34. 
Sometimes the miRNAs are extracted from the plasma in the patient’s blood, 
and other times in the CSF. The best example is miR-342-3p, a better 
biomarker in blood, and miR-127-3p, a better biomarker in CSF34. This 
discrepancy, along with different measurements and amplifications or testing 
methods, has caused different results from various studies. However, it is 
unlikely that only one specific approach would be used. It is instead 
important to standardize each type of treatment or biomarker. Some 
approaches are not limited to difficulties in delivering and targeting these 
miRNA treatments, safety issues, and off-target effects of these treatments37. 
These miRNAs play a role in Aβ production through cascades of different 
molecules. Similarly, they have control over other molecules and proteins. So, 
by changing the levels of specific miRNAs apart from the Aβ pathway being 
changed, other molecules and pathways could have residual effects. 
  



 

Berkeley Pharma Tech Journal of Medicine | 64 

7.3. Current Use 
The idea of using miRNA has already been adapted into some clinical 
aspects. There are patents in place using the technique of miRNA as 
biomarkers and therapies. One patent that has been filed and granted claims 
to be an invention that is able to measure the level of one neurite miRNAs, 
specific miRNAs that relate to MCI, the starting stage of AD. These specific 
miRNAs include miR-7, miR-125b, miR-128, miR-132, miR-874, miR-
134, miR-323-3p, and miR-38238. Another patent in China has published a 
similar invention in which miRNA is used as a biomarker to diagnose 
Alzheimer's in patients. This invention is said to compare miRNAs such as 
miR-191, miR-15b, and miR-142-3p with healthy controls to determine if 
the given sample has the precursors for AD39. 
  

8. Future directions 
8.1. miRNA delivery 

One step for the future of this novel treatment is enhancing the delivery 
method of the miRNA therapies. miRNA therapy is very targeted; therefore, 
Alzheimer's patients would need the miRNA injected directly into the 
CNS40,41. MiRNA cannot pass through the blood-brain barrier, so 
conventional techniques would not be adequate40. The system by which the 
treatment is delivered is important as it affects how feasible and applicable it 
is in the clinical world as well as its effectiveness. 
  

8.2. miRNA studies 
Currently, there is promise in miRNA studies; however, there are limited 
clinical trials that are ongoing that study this potential therapy41. Having 
more of these studies in the future will help the understanding of this therapy 
and has the potential to make it a more conventional practice in the medical 
field for diagnosing and treating AD. There are also other issues that need to 
be addressed, such as the tolerance of the patient’s miRNA supplementation 
or inhibition41. The lag of miRNA therapies, compared to treatments of 
other common or deadly illnesses, decreases the potential of issues like this 
from being resolved. More research needs to be done to garner a holistic view 
of miRNA therapy. 
  
 



 

Berkeley Pharma Tech Journal of Medicine | 65 

9. Conclusion 
 Alzheimer’s disease (AD) is a progressive neurodegenerative disease and is 
the leading cause of dementia across the globe. AD is frequently characterized 
by the deposition of Aβ plaques and the formation of NFTs in the brain. 
Despite continued research into the disease, AD continues to be one of the 
leading causes of mortality in elderly populations globally, thus highlighting 
the need for novel and advanced therapies that can produce robust anti-AD 
effects. Current AD treatments are typically invasive, costly, and non-
curative, thus highlighting microRNAs as an attractive alternative for the 
care of AD patients. MiRNAs are associated with several neurodegenerative 
diseases and play an outsized role in the pathogenesis of AD. Several classes 
and families of miRNAs are shown to be either upregulated or under-
expressed in amyloid-beta and AD models and cell cultures, therefore making 
the targeting of the relationship between miRNAs and the protein signaling 
an important agent for the diagnostic and treatment potential of the disease. 
  

Conflicts of Interest 
The authors declare that there is no conflict of interest regarding the 
publication of this paper. 
  
 

 



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