





































Berkeley
Pharma Tech
Journal of Medicine

Correspondence: 

venkatarepaka@gmail.com

Keywords:
Lewy body dementia
alpha-synuclein
neurodegenerative disorders
acetylcholine pathways          

dopamine pathways

Submitted: September 12, 2022     

Accepted: November 28, 2022

Published: December 28, 2022

Full Open Access

Creative Commons Attribution 
License 4.0

Abstract
Lewy Body Dementia (LBD) is a neurodegenerative disorder in which the brain has 
abundant misfolded alpha-synuclein proteins. While LBD has similar symptoms to 
other degenerative neurological disorders, such as Alzheimer’s disease (AD) and 
Parkinson’s disease (PD), they are not the same medical diagnosis. LBD is 
characterized by all the motor deficit symptoms of Parkinson's disease (PD), but the 
opposite cannot be said, as PD is more complex and has more underlying symptoms. 
Clinical trials and in vivo experiments have shown that specific genes related to these 
misfolded proteins are potentially good genetic treatment and therapeutic targets. This 
review article seeks to provide an overview of the current state of novel therapeutic, 
genetic strategies to reduce the effects of Lewy Body Dementia.

Novel Genetic Therapeutic Strategies for 
Lewy Body Dementia
By: Venkata Repaka, Carlota Sagarduy and Gatik Trivedi



 

Berkeley Pharma Tech Journal of Medicine | 2 

1. Introduction 

There are three main goals we would like to achieve with this review paper. 
The first is to lay out a list of possible and current treatments available for 
Lewy Body Dementia (LBD) to reduce its effects. Next, we aim to 
understand how LBD can affect other conditions, such as Parkinson’s 
Disease (PD) and Alzheimer’s Disease (AD), and the connection between 
such diseases. Lastly, we seek to understand the molecular mechanism of the 
initiation of LBD. 
 
Due to limited research and investigation on the topic, there is currently no 
cure for LBD. Because of the related symptoms among LBD, AD, and PD, 
some medications used to treat AD and PD can be used for LBD. One 
medication is an FDA-approved drug to treat AD called rivastigmine 
(Exelon). It is a reversible cholinesterase inhibitor that acts on a chemical in 
the brain critical for memory formation and cognitive thinking1,2. This is a 
reversible cholinesterase inhibitor that is known chemically as (S)- 3- [1-
(dimethylamino) ethyl]phenyl ethyl methyl carbamate3. Another 
medication, carbidopa-levodopa, is used to treat PD and could be used for 
LBD movement-related treatment1,2. Levodopa is the precursor of dopamine 
and can cross the blood-brain barrier to create more dopamine in dopamine-
deficient areas in the brain4. 

 

Some clinical features of LBD include visual hallucinations and 
Parkinsonism. Recurrent, complex visual hallucinations occur in up to 80% 
of patients with LBD and are a frequent clinical signpost to diagnosis5. They 
are typically well-formed, featuring people, children, or animals, sometimes 
accompanied by related phenomena including passage hallucinations, sense 
of presence, and visual illusions. Spontaneous parkinsonian features are 
common in LBD, eventually occurring in over 85% (Parkinsonism in 
Parkinson's disease (PD) is defined as bradykinesia in combination with rest 
tremor, rigidity, or both)5. 
 
LBD is defined as a progressive disease in which symptoms worsen as one 
ages. 1,2 Hallucinations are common in the early stages of LBD, as are 
restlessness, acting out dreams during sleep (called REM sleep disorder), and 



 

Berkeley Pharma Tech Journal of Medicine | 3 

movement difficulties5. Others may develop urinary urgency and 
incontinence. Unlike AD, memory is usually still fairly intact in the early 
stages. However, confusion and some mild cognitive changes may be present. 
As LBD progresses, symptoms develop and more strongly resemble 
Parkinson's disease5. These symptoms include increased problems with 
motor functions, difficulty with speech, swallowing problems, and greater 
paranoia and delusions6. Cognition also continues to decline, with shorter 
attention and significant periods of confusion occurring. In the later stages 
of LBD, extreme muscle rigidity and sensitivity to touch develops. Patients 
need assistance with almost all activities of daily living. Speech is often very 
difficult and may be whispered. Some LBD patients stop talking altogether7. 
 
Both LBD and PD are quite similar and have overlapping characteristics, but 
there are specific key differences that can differentiate LBD and PD in the 
spectrum1,2. There is a frequent coexistence of the pathology of amyloid 
plaques and neurofibrillary tangles in LBD compared with Parkinson's 
disease dementia. Amyloid plaque are misfolded proteins in the synaptic 
clefts of neurons. This would effectively block the transmission of 
neurotransmitters from neuron to neuron. Additionally, the accumulation 
of the protein tau within neurons are called neurofibrillary tangles. The tau 
protein works to help the neuron’s microtubules which help guide nutrients 
and vitamins move in the neuron. Particularly, because tau proteins are 
‘sticky’ in character they will bind to each other while they are connected to 
microtubules and create tangles of the microtubules inside neurons. This can 
harm the synaptic communication and internal cell communication of the 
neuron31. Alzheimer’s differs from LBD clinically because of its unique 
cognitive profile and its lack of parkinsonian features except in the late 
stages2. 

 

This paper provides an overview of novel therapeutic genetic strategies to 
reduce the effect of LBD by targeting topics of epigenetics, cognitive 
enhancers, non-coding RNAs, micronutrients, making alterations of central 
cholinergic (ACh) and dopaminergic (DA) systems, and looking at current 
drugs and treatments. This review will also be discussing how factors such as 
age, diet, and underlying health conditions can affect the intensity of Lewy 
Body Dementia in a patient. 



 

Berkeley Pharma Tech Journal of Medicine | 4 

 

2.  Molecular Components of LBD 
While there are many molecular pathways of LBD, research has shown that 
alpha-synuclein(AS)-positive inclusions are the main indicator of Lewy 
Body8,9, causing the impairment of protein degradation pathways, including 
both the ubiquitin-proteasome system and the autophagy-lysosome 
pathway. The ubiquitin-proteasome pathway (UPP) is the main pathway 
that destroys unneeded proteins and eliminates misfolded or misguided 
proteins that are in the wrong locations within the cell with the use of a 
protease or proteasome32.  This mechanism works through the formation of 
a polyubiquitinated protein, which serves as a recognition signal for the 
eventual action of the proteasome to degrade the proteins into peptides, as 
shown in Figure 1. This is an important mechanism as this can decrease the 
number of unnecessary proteins and debris in the body that is unneeded. 
Defects in the UPP can be detrimental to the homeostasis of the amounts of 
tau protein in the neuron. A possibility of the amount of extra tau protein in 
the neuron can be due to a mishap of the UPP. 
 
 
 
 
 
 
 
 
 
 
 



 

Berkeley Pharma Tech Journal of Medicine | 5 

 
Figure 1. The ubiquitin-proteasome pathway (UPP). Ubiquitin, a 76 amino acid 
protein, marks the molecule to be degraded by attaching itself to a substrate protein. In this 
process, E1–the ubiquitin-activating enzyme, E2–the ubiquitin-conjugating enzyme, and E3–
the ubiquitin-protein ligase, cause a cascade of reactions, the result of which is the linkage of one 
molecule of ubiquitin to the protein (mono-ubiquitination). Polyubiquitination occurs when 
additional molecules attach to the seven lysine residues or the N-terminus of the ubiquitin 
molecule to form a chain. Polyubiquitination is the recognition signal for the proteasome to 
degrade the target protein into peptides. 

 
The autophagy-lysosome pathway is another important catabolic pathway 
that regulates the quality and the number of proteins made within the body’s 
cells. There are three common mechanisms of lysosomal autophagy which 
are macroautophagy, microautophagy, and chaperon-protein mediated 
autophagy. Macroautophagy is where an autophagosome is created 
containing the surplus amount of protein and a lysosome will bind to the 
organelle-like structure to degrade the particles within it. All these pathways 
separately are important to degrade an excess number of large proteins. In the 
case of smaller proteins, a bigger lysosome will use phagocytosis to degrade 
the need proteins. Similarly, chaperon -mediated pathway will utilize a longer 
way to degrade proteins including another chaperon protein which connects 
the excess amount of protein to a channel that leads to the lysosome. This 
lysosomal pathway uses a lysosome to engulf the autophagosome and destroy 
its contents with enzymes33. These pathways then will degrade the neurons 
present in the brain. 
 



 

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Figure 2. The three different autophagy-lysosome pathways–macroautophagy, 
microautophagy, and chaperone-mediated autophagy. 
 

Alpha-synuclein also is a major component of the filamentous glial cell 
inclusions (GCIs) that are abundant in the white matter oligodendroglial 
cells of multiple system atrophy (MSA) brains. Accumulation of alpha-
synuclein into filamentous inclusions could play a mechanistic role in the 
pathogenesis of several progressive neurological disorders, such as 
Parkinson’s disease, LBD, Familial Alzheimer's disease, Lewy body disease 
variant of Alzheimer’s disease, sporadic Alzheimer's disease, and multiple 
system atrophy10. This path is obscure, but UPP and autosomal-lysosomal 
pathways are the commonly known pathways that LBD is categorized into. 
LBD specifically affects the thalamus structurally and functionally8,9. 
 
Additionally, a study suspected there are five specific important and targeted 
genes from LBD patients: BIN1 and TMEM175, SNCA, APOE, and GBA- 
510. This was done by uncovering participant samples from 44 different 
European ancestry banks; specifically, 17 in Europe and 27 across North 
America. When the sequences from LBD patients and control patients were 
compared, they found 5 consistent different genes that were among the LBD 
patients. To confirm their results and conclusions, the researchers also 
compared those 5 genes to another 970 LBD patients with a new control set 
of 8,928 control subjects10. 



 

Berkeley Pharma Tech Journal of Medicine | 7 

Figure 3. The 5 genes GBA, BIN1, TMEM175, SNCA, and APOE on their 
respective chromosomes. 
 

Widespread mitochondrial dysfunction is very closely related to disease 
development as well. The impairment of protein degradation pathways, 
including both the ubiquitin-proteasome system and the autophagy-
lysosome pathway, also plays an important role during the development of 
Lewy body diseases11. Differential expression changes of isoforms 
corresponding to genes primarily involved in Lewy body formation point to 
alternative splicing as another important mechanism in the development of 
dementia with Lewy bodies11. 
 

3.  Epigenetics 
Parkinson's disease and dementia with Lewy bodies are deemed similar based 
on a neurological overlap between them. Both PD and LBD are distinguished 
by an abnormal accumulation and deposition of misfolded and aggregated 
alpha-synuclein which gives rise to Lewy bodies and Lewy neurites. 
 
The diversity and complexity of LBD make them complex multifactorial 
disorders. Thus, many LBD cases originate from the interaction of multiple 
genetic and environmental, epigenetic factors. There are many genes of 
interest that are involved in LBD, one of them being SNCA, which is a rare 
gene involved in LBD. It has two distinct profiles within its locus, one 
pertaining to PD, located in the 3’ SNCA portion, and the other to LBD, 
located in the 5’ SNCA portion12. SNCA was the first and is one of the most 
studied genes identified as an LBD-causing gene. SNCB, like SNCA, has 
been detected in some LBD cases. 



 

Berkeley Pharma Tech Journal of Medicine | 8 

 
The b-syn, from the synuclein family, has shown to be a regulator of the a-
syn aggregation. Common variants, like rare variants, that could increase the 
risk of developing LBD have been found to be located in genes associated 
with PD or AD. One of these well recognized risk variants is the allele ε4 of 
the apolipoprotein E gene (APOE). APOE poses a risk in LBD patients 
because the allele ε4 accumulates and accelerates the disease which leads to a 
shorter lifespan for the patient13. On the other hand, APOEε2 has been 
shown to have protective effects against the development of LBD12. 

Epigenetics regulate gene expression through methods that are independent 
of the primary DNA sequence, even though they can be heritable. Without 
altering the DNA sequence, epigenetic mechanisms moderate reversible 
changes in gene expression and cell phenotype. 
 
There are two major mechanisms pertaining to epigenetics modifications, 
shown in Figure 4. The first is DNA methylation, a biochemical process by 
which a methyl group is added to DNA, thereby modifying the function of 
the gene. It occurs at cytosines located 5’ to guanine (CpG), and it is 
mediated by methyltransferases. In the promoter regions, DNA methylation 
can either repress gene expression, hypermethylated CpG, or increase gene 
expression, hypomethylated CpG. This mechanism plays a big role in aging 
and development.  
 
The second mechanism is Histone tail modification which either loosens or 
encompasses the tail to turn a gene “off” or “on” or deactivate or activate a 
gene, respectively. The proteic part of chromatin is referred to the histones 
which allow the compaction of DNA. These two mechanisms have a 
fundamental part in learning and memory processes because they are 
dynamically controlled in neurons. Epigenetic mechanisms mediate gene-
environment interactions because they can often be provoked by 
environmental risk factors. This emphasized the importance of certain 
factors in patients with LBD, such as diet, physical activity, and lifestyle13. 
 



 

Berkeley Pharma Tech Journal of Medicine | 9 

 
Figure 4. The process of the epigenetic mechanisms. The effects of the environment and 
genetics may have an influence on changes in gene expression and cell behavior.  

LBD studies have mostly been focused on genetics rather than epigenetics; 
however, epigenetic mechanisms and regulation have proved to play an 
important role in the pathophysiology of the disease and genome. Even 
though there are scarce studies on epigenetics in LBD, there is evidence of an 
overlap of APOE and SNCA from their genetic and epigenetic regulation 
(Figure 5)13. Transcriptomic and proteomic studies analyzing the genetic 
pathway have shown clinical and neurological correlates to the disorder 
through the synaptic function, lysosomal processing, and circadian 
rhythm13. The origin of the cause of these changes has not yet been 
determined. There are a few limitations in the evidence that exists including 
small sample sizes, tissue specificity, and lack of information. As more 
technologies are developed, more will be discovered regarding this topic. 



 

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Figure 5. Genetic Association and Epigenetic Association in LBD. This figure shows 
the different genes involved in LBD and how they are associated with genetics or epigenetics. 
As seen, APOE and SNCA have both genetic and epigenetic associations. 

 
With the appropriate information, epigenetics are an important tool and 
strategy that can be used to battle a variety of different diseases. There are 
tactics that would delay the onset and progression of neurodegenerative 
diseases, such as LBD. One of these tactics includes targeting the 
epigenome14. This can be done using small drugs, such as HDACi, that are 
able to cross the blood brain barrier14. Even though studies are scarce and 
there are concerns with using this type of drug, there are potential targets for 
drug development that could have a promising result for potential epigenetic 
preventive factors for neurodegeneration. As more is discovered about this 
disease, epigenetics will serve as a fundamental factor in either delaying the 
onset or helping in the stratification and improvement of the diagnosis. 
 

4.  Cognitive Enhancers 
Cognitive enhancers, also called nootropics, are neuroprotective or extremely 
nontoxic in consideration to neurodegenerative diseases like LBD. 
Nootropics can be naturally found or synthetically made which can enhance 
attentional control and memory. There are various mechanisms by which 
nootropics acts, which are as follows: 1) increasing circulation to the brain, 
2) providing precursors to neurotransmitters (chemical messengers in the 



 

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brain), 3) improving neuron function, 4) preventing free radical and 
oxidative damage to brain cells, and 5) providing usable energy to the brain15. 
 
Nootropics exist in three main categories: supplements, racetams, and 
stimulants. Supplements or dietary sources of nootropics are mainly natural 
and can be found in fruits and vegetables. Natural nootropics come in the 
form of vitamins like Omega-3, iron, antioxidants, amino acids, and caffeine. 
Racetams are positive allosteric modulators of AMPA receptors in the brain 
and include piracetam and nefiracetam. Racetams are categorized and 
claimed as “pharmacologically safe” drugs15. The amnesia reversal effect with 
racetams is compared with scopolamine, electroconvulsive shock, and 
hypoxia, which are more invasive strategies considering the safe nature of 
racetams16. Specifically, nefiracetam has been proven to have more affinity 
for muscarinic receptors at the nanomolar range than other aniracetam and 
nebracetam. Most racetams are safe but can cause adverse reactions to males 
than women if used incorrectly or in excessive amounts15. Lastly, stimulants 
are another type of smart drug under nootropics that enhance productivity 
in the brain. Some examples include methylphenidate and amphetamines 
and are specifically known to improve ADHD symptoms in patients with 
ADHD15. Amphetamine salts contained primarily of dextroamphetamine 
(d-AMP) are known by the trade name Adderall that help patients with 
ADHD17. Unlike racetams, stimulants can enhance cognitive abilities in 
impaired or unprescribed patients without causing adverse effects. Similar to 
racetams, they can be found in natural and synthetic forms that affect 
neurotransmitter levels, neurogenesis, and blood flow to the brain17. Some 
stimulants are known to improve symptoms of LBD and reverse the 
progression of dementia. Additional categories of nootropics include 
dopaminergics, specifically work to raise levels of dopamine, and 
serotonergics, specifically work to raise levels of serotonin, which can also 
raise treatments to reverse symptoms of LBD15. 
 

One clinical trial study of nootropics has been done on patients with AD. 
Researchers were particularly interested in comparing the effects of specific 
nootropics that affected behavioral and psychological symptoms of 
dementia which is how LBD can also be affected in the study. Specifically, 
the study looked at cholinesterase inhibitors and memantine or a N-methyl-



 

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D-aspartic acid (NMDA) receptor antagonist. Cholinesterase inhibitors of 
donepezil and rivastigmine increase the concentration of acetylcholine at the 
neurotransmitter sites.  The other cholinesterase inhibitor tested was 
Galantamine which is a double action that not only increases acetylcholine 
at neurotransmitter sites like donepezil and rivastigmine, but also acts by 
modulating activity at nicotinic receptors. Memantine is a NMDA receptor 
antagonist modulates glutamate in the glutamic system of the brain. The 
study had selected patients with AD and had given a placebo to some patients 
and others received a cognitive enhancer. Observations were made with the 
efficacy and reversal of dementia in these patients. This clinical trial has 
potential to show that more than 100,000 patients are eligible for cognitive 
enhancers in Canada alone as 30% of the AD patients have moderate 
dementia. These medications have been approved for the treatment of 
Alzheimer’s disease in many countries as well18. 

 

Another facet to consider is the administration of such effective nootropics. 
In a clinical trial led by Dr. Murat Emre from Istanbul and published in the 
prestigious New England Journal of Medicine in 2005 had shown that 
rivastigmine, as previously mentioned, a cholinesterase inhibitor that 
enhances ACh concentration in neurotransmitter sites was effective in 
Parkinson’s disease (PDD). Although this drug is not approved for LBD 
patients in the Dr. Emre’s trial19. However, many doctors and providers 
consider both disorders to have similar enough symptoms for the 
rivastigmine medication to be effective in both conditions. In this study both 
the patch, developed and approved for use in 2007, and the pill of 
rivastigmine were given along with the placebo to patients with PDD. The 
patch and pill of rivastigmine were proven to be more effective than the 
placebo and showed the same effectivity. However, one trial of Dr. Emre’s 
study declared the patch was more effective than the pill of rivastigmine 
mainly because of the lower recurrence of side effects of nausea and vomiting 
in the patch than in the pill. Because medications were taken by the skin in 
comparison to the mouth, GI issues decreased in patients who used the 
patch19. 
 

5.  Non-coding RNAs 
As previously described, LBD is very complex and has become an increasing 



 

Berkeley Pharma Tech Journal of Medicine | 13 

demand on global health care systems. Because it is so complex, there are 
many factors that need to be researched to create possible therapies or 
treatments. Non-coding RNAs (ncRNAs) are RNA sequences that cannot 
be translated into proteins. There is a vast variety of different ncRNA 
families; however, the two most valuable to this topic are the miRNA and 
lncRNA families. These two families have the capacity to provoke gene 
regulation across cellular physiological pathways. Since miRNAs and 
lncRNAs influence disease pathways, it is important to research ncRNAs for 
possible therapies and for more information on the pathogenesis20. miRNA 
and lncRNA families have different influences on dementia20. miRNA, short 
for microRNA, refers to a small single stranded ncRNA molecule. It 
comprises 22 nucleotides and functions in RNA silencing and post-
transcriptional regulation of gene expression. miRNA inhibits the 
translation of proteins coded by mRNA transcript by acting as a physical 
obstruction for ribosomal action. There are many studies attributing and 
demonstrating the effects of miRNA defects on multiple forms of dementia, 
however because LBD has not been deeply studied there are no details on the 
influence of miRNA on LBD21. Specifically, lncRNA, short for long non-
coding RNA, refers to a single RNA sequence composed of at least 200 
nucleotides. lncRNA regulates gene expression in several levels such as 
epigenetics and transcriptional levels. Most lncRNAs are detrimental to 
pathways in neurodegenerative diseases21. Just as in miRNA, there are no 
studies on the specific effect of lncRNAs on LBD. 

 

As stated previously, small molecule drugs show potential for the future of 
this disease. One of the few studies that has been done using ncRNAs is the 
use of small molecule drugs targeting ncRNAs as treatments for dementias22. 

ncRNAs could function as therapeutic targets because they are enriched in 
the central nervous system. A small molecule can bind to ncRNA, changing 
its conformation, to regulate it. There has been extensive work in developing 
oligonucleotides to target mRNAs and ncRNAs, however there are many 
obstacles that have not yet been researched which block the entry, specifically 
in the blood brain barrier. Another tactic that needs further studying is the 
use of gene therapy. Using gene therapy with viral vectors can edit ncRNAs 
and can allow for more durable ncRNA modulation. However, this also 



 

Berkeley Pharma Tech Journal of Medicine | 14 

comes with obstacles regarding the delivery and expression of the target 
genes, making the therapy ineffective. 
 
More research and knowledge could lead to identifying novel diagnostic 
procedures and/or drug targets. While these possible therapies or drugs may 
not be able to cure a patient, they can help with the control of the patient’s 
mental condition, disease progression, and cognitive decline. 
 

6.  Other Factors in Effect 
6.1 Inflammation 

 

As LBD and AD have similar symptoms and neuroinflammatory 
mechanisms involving the activation of microglia, overexpression of 
interleukin-1 and other inflammatory mediators, and inflammatory toxicity 
to neurons. The activation of microglia are also resultants from the 
overexpression with α-synuclein-containing neurons and glia in PD. These 
connections are also associated with the microglial associations with 
neurofibrillary tangle-containing neurons in AD. It is shown that there is a 
reciprocal induction between α-synuclein and injured neurons on one hand 
and activated microglia and cytokine overexpression with in vivo and in vitro 
experiments. This mechanism of inflammation can lead to more injured 
neurons which can activate microglia and cause a cycle of inflammation 
beneficial to the neuron which can cause neuronal death. This concept can 
show the progression and overlap between both AD and LBD25. 

 

6.2 Risk Factors 

There are several factors that contribute to a person's risk for developing 
LBD. A history of high caffeine intake, for example, is associated with a lower 
risk of LBD. Research has suggested that the benefits increase in tandem with 
the amount of caffeine a person drinks per day and may reduce the risk of 
LBD by as much as 29%26. Genetics and heredity appear to play a role in the 
risk of LBD as well. Generally, if you have a first-degree family member with 
Lewy body dementia or PD, your risk of Lewy body dementia increases. 
Additionally, for reasons not entirely clear, a history of depression and 
anxiety is linked to an increased risk of Lewy body dementia27. Metabolic 



 

Berkeley Pharma Tech Journal of Medicine | 15 

Disorders Hypertension (high blood pressure) is linked to an increased risk 
of Lewy body dementia. The incidence of hypertension among people with 
Lewy body dementia is roughly 65%. Having high blood pressure, in turn, 
increases the risk of Lewy body dementia by 60.5%. Type 2 diabetes, a form 
of diabetes strongly linked to lifestyle, is associated with a 25% increased risk 
of Lewy body dementia. High cholesterol also increases the risk of Lewy body 
dementia by roughly 25%28. 

6.3 Micronutrients 

Micronutrients are a fundamental part to healthy development, 
disease prevention, and a good lifestyle. No micronutrients, except vitamin 
D, are produced in the body therefore they must come from a person’s diet 
and intake. Micronutrients are important for healthy people but even more 
important for those who have a disease or are genetically prone to developing 
a disease23. Those who do not supply their body with sufficient nutrients can 
suffer from malnutrition, which has been found to be tied to cognitive 
function. Deficiency of nutrients, specifically vitamin B12 and folate, can 
lead to decreased cognitive function. In addition, weight loss associated with 
malnutrition will often occur prior to the onset of dementia23. As the disease 
progresses, weight loss can also progress and vice versa. While there are several 
diets that are said to prevent, or help with, cognitive decline and dementia, 
there are no studies that directly prove one diet to help with LBD24. Finding 
the correct micronutrients that could help patients who have LBD or are 
predisposed to it could have a huge impact on this area of health. 

 

7.  Conclusion 
From the progression of research of LBD in clinical trials, in vivo, and in vitro 
experiments, the potential of epigenetic therapy should be examined more 
thoroughly. Future directions of the use of deep brain stimulation29 and 
repetitive transcranial magnetic stimulation (rTMS) has shown potential in 
other neurodegenerative diseases and could be applicable to LBD30. The 
effects of epigenetics, age, diet, and inflammation within the body can 
enhance other scientists’ knowledge when designing therapies for LBD in the 
future. As this article has mentioned many current therapies and potential 
therapies it is important to note the limitations and drawbacks of the research 



 

Berkeley Pharma Tech Journal of Medicine | 16 

presented. One drawback is that many of the clinical trials are research 
alongside Alzheimer's disease and or Parkinson’s disease so there is no precise 
way to isolate LBD research and progression. Additionally, many of the 
clinical trials and experimental data found were said to be inconclusive as the 
data was little or had little to no value of measurement. Protocols on how to 
measure the data obtained in experimental trials are still being researched 
upon. To combat these terms, this article took a holistic review of each article 
and applied most information back to LBD with reason. Nevertheless, the 
research presented is to enhance the knowledge of other scientists researching 
LBD therapies to give a foundation about the current and probable therapies 
available. 

Conflicts of Interest 

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



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