# data[].attributes.body
Since the paper talks about the immune system in the role of neuroinflammation and gut inflammation, more data on particular immune cells can further validate the study's conclusion.

Potential studies related to other models of PD, to see if there is a standardized improvement to different extremes of PD.

The study may study long-term effects of FMT on PD symptoms.

The study may potentially explore other PD-related symptoms, may that be psychological, behavioral, etc.

--> To ultimately assess how it would improve the quality of life.

Moreover, the interplay of certain bacterial species is another avenue for researchers to investigate. Researchers may explore their underline role before or after treatment.

Furthermore, researchers may also begin to investigate its potential use in clinical trials.

# data[].attributes.headline
Unveiling the Gut-Brain Connection: Microbiota and Parkinson's Disease

# data[].attributes.subject
Unveiling the Gut-Brain Connection: Microbiota and Parkinson's Disease

# data[].attributes.body
Allison Tran, Momiji (Momo) Uji, Tra Pham, Michelle Lee

Zhao, Z., Ning, J., Bao, Xq. et al. Fecal microbiota transplantation protects rotenone-induced Parkinson’s disease mice via suppressing inflammation mediated by the lipopolysaccharide-TLR4 signaling pathway through the microbiota-gut-brain axis. Microbiome 9, 226 (2021).

# data[].attributes.body
Parkinson’s Disease (PD) is a neurodegenerative disorder that primarily displays motor deficits that gradually develop, as well as gastrointestinal dysbiosis. PD occurs when the neurons in the brain responsible for producing dopamine, which is a chemical messenger that controls movement die or become impaired.

# data[].attributes.body
Common motor deficit symptoms include:

Resting tremors: typically starting in a limb

Bradykinesia: slowness of movement

Postural instability: impaired balance and coordination

Some premotor GI dysfunctions are:

Constipation

Dysphagia - difficulty in swallowing. It can occur at any stage such as the mouth, throat, or esophagus. Can range from mild to severe problems in eating, drinking, and taking medications.

Nausea

Vomiting

Weight loss

# data[].attributes.headline
As disease progresses... symptoms worsen. 

# data[].attributes.subject
As disease progresses... symptoms worsen. 

# data[].attributes.body
Currently, there is no cure to PD however there are several treatments available aimed to help manage its symptoms and improve the quality of life. This can be through:

1. Medications.

Levodopa which is used to manage motor symptoms of PD. It is converted into dopamine in the brain to help alleviate symptoms.

Other medications include dopamine agonists, which help mimic the effects of dopamine in the brain. MAO-B inhibitors or COMT inhibitors.

2. Deep Brain Stimulation.

This involves the surgical implantation of electrode in specific areas of the brain. These electrodes deliver electrical impulses to targeted regions of the brain.

3. Physical therapy such as exercise.

Dietary adjustments such as an increase in fiber intake.

Ongoing research aims to better understand its underlying mechanisms and develop more effective treatments.

# data[].attributes.headline
What is the connection of the microbiota to PD? 

# data[].attributes.subject
What is the connection of the microbiota to PD? 

# data[].attributes.body
It has been increasingly evident that the gut microbiota affects the communication between the gut and the brain in PD pathogenesis, also known as the microbiota-gut-brain axis. The presentation of GI dysfunctions which precede the motor symptoms of PD patients, show that the alterations of the microbiota community on the communications of the brain and gut are also involved in the development of PD.

Many pathological alterations of microbial taxon abundances have been reported in PD patients such as:

Elevated abundances in Akkermansia, Bifidobacterium, and Lactobacillus.

Decreased levels of Blautia and Faecalibacterium.

Infection of helicobacter pylori (Hp) has been reported to be associated with PD.

# data[].attributes.headline
What is the comparison to healthy individuals?

# data[].attributes.subject
What is the comparison to healthy individuals?

# data[].attributes.body
In healthy individuals, stable gut microbiota compositions play a crucial to sustaining the balance of the intestinal barrier integrity and inflammation, thus positively regulating brain development and behaviour through the microbiota-gut-brain axis.

# data[].attributes.body
Recent studies have approached re-establishing a normal microbiota community through fecal microbiota transplantation (FMT) which has been shown to exert beneficial effects.

Healthy mice receiving gut microbiota transplants from PD disease donors showed motor dysfunctions in some research. Collectively, these reports suggest that gut microbiota dysbiosis plays a pivotal role in the pathogenesis of PD.

# data[].attributes.headline
What is fecal microbiota transplantation (FMT)? 

# data[].attributes.subject
What is fecal microbiota transplantation (FMT)? 

# data[].attributes.body
Fecal microbiota transplantation (FMT) is targeted at the gut microbiota dysbiosis and has been emerging as a promising therapy in various diseases such as CDI (Clostridium Difficile Infection) and metabolic syndrome. It is a process of introducing normal fecal microbiota from healthy donors into the GI tracts of patients to re-establish a stable gut microbial environment, which may reduce symptoms of disorders by regulating the gut microbiota-associated pathways.

# data[].attributes.body
Reported that FMT treatment has shown beneficial effects in several neurological disorders like autism and multiple sclerosis (MS). One case reported that FMT can protect the GI dysfunctions and motor disorders in PD patients.

Sun et al. showed that FMT administration alleviated the MPTP-induced PD mouse model by reducing gut microbiota dysbiosis and neuroinflammation.

# data[].attributes.body
Zhao et al. aim to investigate how FMT can induce protective effects on PD and to explore its underlying mechanisms such as the involvement in the gut microbiota dysbiosis in PD pathogenesis via the microbiota-gut-brain axis.

# data[].attributes.body
This is through establishing a chronic PD mouse model by rotenone and then treating the mice with FMT.

Using a chronic rotenone-induced PD mouse model to assess whether FMT treatment can protect PD and to elucidate the underlying mechanisms as well as explore the potential role of the microbiota-gut-axis in PD pathogenesis.

# data[].attributes.body
A classic insecticide that has shown great ability to mimic clinical and pathological manifestations of PD.

Many studies have proven that the pathogenesis of the chronic rotenone-induced PD mouse is closely related to gut microbiota dysbiosis

# data[].attributes.body
They hypothesize that the gut microbiota dysbiosis induced by rotenone plays a significant role in the genesis of PD and that FMT administration can prevent GI dysfunctions and motor impairments by restoring the gut microbiota in PD mice.

# data[].attributes.headline
What happens during the development of PD?

# data[].attributes.subject
What happens during the development of PD?

# data[].attributes.body
During development, gut microbiota dysbiosis can trigger inflammation of the intestines as well as the brain through the microbiota-gut-brain axis. As a result, the inflammation in the GI tract associated with the imbalance of the gut can lead to damaged barriers - known as leaky gut.

This increases the permeability of the blood-brain barrier, allowing for harmful substances to enter the bloodstream to the brain such as LPS and inflammatory cytokines. As a result, neuroinflammation and cell death of dopaminergic neurons occurs in the substantia nigra (SN) leading to PD. During the whole process, LPS activates immune cells both in the SN and intestinal tracts by interacting with toll-like receptors (TLR4) on their surfaces.

The dopamingeric neuronal death in the SN and the aggregation of alpha-synuclein in the remaining neurons are two dominants pathological hallmarks of PD which contribute to the occurrence of motor symptoms in PD patients.

# data[].attributes.headline
FMT alleviates motor symptoms and GI dysfunctions in rotenone mice 

# data[].attributes.subject
FMT alleviates motor symptoms and GI dysfunctions in rotenone mice 

# data[].attributes.body
Motor deficits are characteristic of PD; rotenone mice performed worse on motor tests like the rota-rod, grip test, and pole tests, which test for motor functions and coordination, sensorimotor integration, and muscle force of limbs and balance. However, after FMT administration, the rotenone mice began to perform much better. These improved results also correlated with improved pellet numbers with less water content percentage, which underlines the gut-brain connection.

This set of data suggests that rotenone intoxication and PD phenotype has implications for weight loss, motor disorders, and GI dysfunctions, and that FMT can attenuate these manifestations.

# data[].attributes.headline
FMT-driven restoration of the blood brain barrier (BBB) and the intestinal barrier

# data[].attributes.subject
FMT-driven restoration of the blood brain barrier (BBB) and the intestinal barrier

# data[].attributes.body
PD is a disease that links the gut and the brain in a bidirectional axis; it is no wonder then that damage in the BBB is echoed by disruptions in the intestine! Healthy patients have well organized tight junctions to maintain stratification in the intestine, and this team sought to probe the difference when it came to their rotenone-driven PD model.

Western blots revealed that expression of the 3 major tight junction proteins, ZO-1, occludin, and claudin, were seriously impaired in the rotenone mice, but the healthy phenotype was rescued upon FMT administration. This has implications for the leaky gut phenomenon observed in PD and possibly involved in its pathogenesis, and the wider physical manifestations of PD as well as the neuroinflammation that can occur.

# data[].attributes.headline
FMT attenuates TLR/MyD88/NF-KB signaling in the SN and the colon of rotenone mice

# data[].attributes.subject
FMT attenuates TLR/MyD88/NF-KB signaling in the SN and the colon of rotenone mice

# data[].attributes.body
Western blot, qPCR, and immunofluorescence in the colon and SN also revealed enhanced expression of TLR4 in the rotenone group. When FMT was administered, the levels dropped drastically, pointing to the attenuating effects of FMT when it comes to inflammation and deactivation of the TLR4 pathway.

# data[].attributes.body
All of the above results - from the loss of tight junctions, to the histopathological manifestations, to the evidence of neuroinflammation and dopaminergic cell death - all points to the bidirectional pathology of PD.

There are many reports linking gut microbiota dysbiosis in PD models that also suggest its role in the development of the neurodegenerative disorder. These results serve as compelling evidence to strengthen the connection between the gut and its microbiota and the brain, suggesting that FMT has the potential to be powerful tool to attenuate dysbiosis and PD.

# data[].attributes.body
45 male mice were randomly assigned to a control or model group. The model group (n=30) received Rotenone administration whereas the control group (n=15) received vehicle.

This model allows researchers to study the progression of PD-like symptoms and investigate potential treatments or interventions.

The model group was then further divided into the rotenone (n=15) and the FMT group (n=15). Fecal samples from the control group were used for FMT.

# data[].attributes.headline
Schematic illustration of the animal experimental design timeline

# data[].attributes.subject
Schematic illustration of the animal experimental design timeline

# data[].attributes.body
The model group received rotenone orally for 4 weeks to induce PD, while the control group received the vehicle.

After 4 weeks, the model group was divided into the FMT or rotenone group.

During week 5 and 6, the mice in the FMT group were treated with FMT once per day.

The control group and the rotenone group mice received vehicle administration once a day during this time.

GI function tests and behavioral tests were performed at week 6. Then all the mice were sacrificed for further analysis.

# data[].attributes.headline
Overview of the methods used in the study

# data[].attributes.subject
Overview of the methods used in the study

# data[].attributes.attachment_caption
Video explaining how TEM works (Physics channel, 2017)

# data[].attributes.body
Thinly sliced sections of the brain and colon tissues were observed under a transmission electron microscope to examine and detect structures of the gut and brain barriers and its associated changes (microvilli density, paracellular gap and TJ characteristics etc)

# data[].attributes.headline
Does FMT restore BBB and intestinal barrier in the rotenone-induced group? 

# data[].attributes.subject
Does FMT restore BBB and intestinal barrier in the rotenone-induced group? 

# data[].attributes.attachment_caption
1. (Biomol GmbH - Life Science Shop, n.d.)  2. (Liu et al., 2012) 

# data[].attributes.body
Western Blot was also used to analyze the changes in expression of 3 major tight junction proteins of the Blood Brain Barrier (BBB) which were ZO-1, occludin and claudin between the rotenone group and FMT group.

# data[].attributes.headline
How does FMT treatment protect against GI dysfunction and motor deficits? 

# data[].attributes.subject
How does FMT treatment protect against GI dysfunction and motor deficits? 

# data[].attributes.body
Using immunofluorescence, they detected the activation of glial cells. GFAP was used as the marker of astrocytes and Iba-1 was used as a marker of microglia.

They then used these secondary antibodies to detect those primary antibodies.

# data[].attributes.body
It has been reported that during PD development the activation of microglial cells and astrocytes may contribute to neuroinflammation and neuronal death in the SN so they wanted to see if FMT treatment protected motor deficits through attenuation of these cells.

# data[].attributes.headline
Evaluating immune infiltration and epithelium impairment in the colon

# data[].attributes.subject
Evaluating immune infiltration and epithelium impairment in the colon

# data[].attributes.attachment_caption
Illustration of the H&E staining methods used in histology (Ling, 2021). 

# data[].attributes.body
This was done to visually see how many inflammatory cells were present or lesions/erosions were present.

These stains are the most widely used histological stain because of its comparative simplicity and ability to demonstrate clearly an enormous number of different tissue structures

# data[].attributes.headline
Validating the hypothesis and evaluating the effects of FMT administration

# data[].attributes.subject
Validating the hypothesis and evaluating the effects of FMT administration

# data[].attributes.body
"Disrupted barriers can lead to the leakage of pathogenic LPS and LBP, thus activating the TLR4 pathway both in SN and the colon"

# data[].attributes.body
They compared the serum levels of pathogenic LPS and LBP molecules in the circulation between the different groups using ELISA

# data[].attributes.body
H&E staining in the colon reveals the loss of organization, immune infiltration, and epithelium impairment. They also assigned histological scores, which are remarkably higher in the rotenone group. This ties significantly into the leaky gut pathology associated with PD!

# data[].attributes.headline
Does FMT treatment alleviate motor symptoms of PD mouse models? 

# data[].attributes.subject
Does FMT treatment alleviate motor symptoms of PD mouse models? 

# data[].attributes.headline
LPS Endotoxin and LBP presence in places where they should not be: rotenone-model vs FMT vs control! 

# data[].attributes.subject
LPS Endotoxin and LBP presence in places where they should not be: rotenone-model vs FMT vs control! 

# data[].attributes.body
This set of figures demonstrates the elevation of LPS in the SN of the rotenone group compared to the control, which is significantly decreased in the FMT group. This pattern is the same in the colon, where FMT significantly inhibits the levels of LPS.

Increased LPS and LBP leads to more inflammation because they trigger the immune system via the TLR4 and MyD88 inflammatory pathways. In the FMT mice however there is overall less LPS and LBP, which points to the link between the richness of the microbiota and the decrease in inflammation, or at least the attenuation of these inflammatory molecules. This has important implications for the level of inflammation in the brain that can subsequently occur, as these inflammatory molecules may traffic to the brain via the circulatory system due to the loss of barrier integrity in the gut and in the BBB.

# data[].attributes.headline
A brief look into the histopathology of PD in rotenone vs FMT vs control mice 

# data[].attributes.subject
A brief look into the histopathology of PD in rotenone vs FMT vs control mice 

# data[].attributes.body
Histologically, PD is marked by death of dopaminergic neurons and the accumulation of alpha-synuclein. This study carried out immunofluorescence and western blotting in tissue samples of the substantia nigra (SN) and the colon to look at the effects in rotenone and FMT models, and found that there was much loss of dopaminergic neurons in the SN of rotenone mice, and increased a-syn expression in the midbrain. We can also see that FMT also markedly reduces the levels of a-syn in the brain.

Colon histology is included here due to the bidirectional pathology of PD: what happens in the brain should also be echoed in the colon. We see immune infiltration in the area marked by the black arrow in the rotenone mice, and a fuzzy lack of organization in the tissues...

# data[].attributes.headline
Markers of Microglial and Astrocytic Activity indicate overactivity in rotenone mice

# data[].attributes.subject
Markers of Microglial and Astrocytic Activity indicate overactivity in rotenone mice

# data[].attributes.body
Perhaps this inflammation and dopaminergic cell death is linked to the high activity of microglial cells and astrocytes in the brain, which is what the current literature reports: this study also looked at the co-occurrence of glial cells. Using immunofluorescence they found that both GFAP+ and Iba-1+ microglia and astrocytes were present in rotenone mice, but significantly decreased in FMT mice, which points to their role in the neuroinflammation typical of PD - as well as the protective, inflammation-attenuating effects of FMT.

# data[].attributes.attachment_link.title
rotenone markers microgli and astrocyt.PNG

# data[].attributes.body
Motor function was assessed using these 4 test:

1. Rota-Rod Test: assesses balance, coordination, and motor skill learning as mice balance on a rotating rod. Their latency to fall is recorded (Xhako, n.d.)

2. Pole Test: evaluates motor coordination, bradykinesia (slowness of movement), and balance. It involves measuring the time it takes for a mouse to turn downward and descend a pole (Brenner, 2015)

3. Adhesive Removal Test: assesses sensorimotor deficits, including tactile sensory function and motor coordination. It involves measuring the time it takes for a mouse to remove adhesive tape applied to its paw. (Hines & Haydon, 2013)

4. Grip Strength Test: measures the maximal force applied by a mouse using its forelimbs to assess muscle strength (Augusta University, 2023).

These tests were likely chosen for this experiment because they provide a comprehensive evaluation of different aspects of motor function that manifest PD like balance and coordination.

# data[].attributes.attachment_caption
Schematic diagram of TLR4 signaling pathways.(Stojanovska et al., 2018)

# data[].attributes.headline
How does FMT administration affect the TLR4/MyD88 signalling pathway in PD?

# data[].attributes.subject
How does FMT administration affect the TLR4/MyD88 signalling pathway in PD?

# data[].attributes.body
Augusta University.(2023). Small Animal Behavior Core-Grip Strength. Augusta University. https://www.augusta.edu/research/core/sabc/test-grip-strength.php

Brenner, D. (2015). The role of the CD95 system in Parkinson’s Disease. Research Gate . https://www.researchgate.net/publication/299295188_The_role_of_the_CD95_system_in_Parkinson’s_Disease

DuPont, H. L., Suescun, J., Jiang, Z. D., Brown, E. L., Essigmann, H. T., Alexander, A. S., DuPont, A. W., Iqbal, T., Utay, N. S., Newmark, M., & Schiess, M. C. (2023). Fecal microbiota transplantation in Parkinson's disease-A randomized repeat-dose, placebo-controlled clinical pilot study. Frontiers in neurology, 14, 1104759. https://doi.org/10.3389/fneur.2023.1104759

Fan, H.-X., Sheng, S., & Zhang, F. (2022). New hope for Parkinson’s disease treatment: Targeting gut microbiota. CNS Neuroscience & Therapeutics, 28(11), 1675–1688. https://doi.org/10.1111/cns.13916

Hines, D. J., & Haydon, P. G. (2013a). Inhibition of a snare-sensitive pathway in astrocytes attenuates damage following stroke. The Journal of Neuroscience, 33(10), 4234–4240. https://doi.org/10.1523/jneurosci.5495-12.2013

Ling, J. (2021). Illustration of the H&E staining methods used in histology. Osmosis.org. Osmosis.org. Retrieved from https://www.facebook.com/OsmoseIt/photos/a.293866334077588/2253890288075173/?type=3.

Liu, W., Wang, Z., Zhang, L., Wei, X., & Li, L. (2012). Tight junction in blood‐brain barrier: An overview of structure, regulation, and Regulator Substances. CNS Neuroscience &amp; Therapeutics, 18(8), 609–615. https://doi.org/10.1111/j.1755-5949.2012.00340.x

Neuroinflammation. Neuroinflammation - Creative Diagnostics. (n.d.). https://www.creative-diagnostics.com/neuroinflammation.htm

Physics channel. (2017, July 10). Transmission electron microscope [Video]. YouTube. https://www.youtube.com/watch?v=1l09mevRfpQ&ab_channel=Physicschannel

Stojanovska, V., Miller, S. L., Hooper, S. B., & Polglase, G. R. (2018). The consequences of preterm birth and chorioamnionitis on brainstem respiratory centers: Implications for neurochemical development and altered functions by inflammation and prostaglandins. Frontiers in Cellular Neuroscience, 12. https://doi.org/10.3389/fncel.2018.00026

Sun, J., Xu, J., Ling, Y. et al. (2019) Fecal microbiota transplantation alleviated Alzheimer’s disease-like pathogenesis in APP/PS1 transgenic mice. Transl Psychiatry 9, 189. https://doi.org/10.1038/s41398-019-0525-3

Western blot. Biomol GmbH - Life Science Shop. (n.d.). https://www.biomol.com/resources/applications/western-blot/

Westhayl618. (2016). Immunofluorescence Mechanism. Wikimedia Commons. Retrieved from https://commons.wikimedia.org/wiki/File:Immunofluorescence_Mechanism_.png.

Xhako, E. (n.d.). Snapshot: What is the Rotarod Test? National Ataxia Foundation . Retrieved from https://www.ataxia.org/scasourceposts/snapshot-what-is-the-rotarod-test/.

Zhao, Z., Ning, J., Bao, X. Q., Shang, M., Ma, J., Li, G., & Zhang, D. (2021). Fecal microbiota transplantation protects rotenone-induced Parkinson's disease mice via suppressing inflammation mediated by the lipopolysaccharide-TLR4 signaling pathway through the microbiota-gut-brain axis. Microbiome, 9(1), 226. https://doi.org/10.1186/s40168-021-01107-9

# data[].attributes.body
Introduction: Allison Tran

Methods: Momiji (Momo) Uji

Results: Michelle Lee

Discussion & Outlook: Tra Pham

# data[].attributes.headline
Major Clinical Points (Zhao et al., 2021)

# data[].attributes.subject
Major Clinical Points (Zhao et al., 2021)

# data[].attributes.body
1. Results show the reduction in inflammation by decreasing LPS levels to suppress the TLR4/MyD88 /NF-kB signaling pathway.

2. It is observed that FMT can maintain gut epithelial permeability by restoring tight junctions.

3. The leakiness of inflammatory molecules is also inhibited to alleviate intestinal inflammation and barrier destruction, to reduce systemic inflammation.

4. This reduction of systemic inflammation can restore blood brain barrier impairment and suppress neuroinflammation, to overall decrease the damage in dopaminergic neurons, thus attenuating neurodegeneration.

5. Certain bacteria phylum and genus are found to play individual roles. Eg. Akkermansia is found to increase the susceptibility of the gut to foreign pathogens and can aid in degrading the intestinal mucus barrier, that causes local inflammation. Other potential interplay of other bacteria in the intestine.

--> Collectively, this shows that researchers were able to show that the FMT treatment can alleviate gut dysbiosis and systemic inflammation in the gut and brain.

# data[].attributes.headline
Potential Improvements & Future Outlook 

# data[].attributes.subject
Potential Improvements & Future Outlook 

# data[].attributes.body
Our study by Zhao et al. (2021):

Reduction of systemic inflammation can restore blood brain barrier (BBB) impairment and suppress neuroinflammation in in the substantia nigra (SN).

Composition of microbiome is shown to contain certain type of bacteria that can be found in PD and AD. Each as different roles in the pathology of the disease.

Another study by Sun et al. (2019):

Modulates gut microbiota, relieves A-beta accumulations, relieves neuroinflammation.

Similar influences via the gut-brain axis.

Similar accumulations of phylum Verrucomicrobial, genus Akkermansia, etc. --> However, not consistent throughout all AD studies.

--> We can see comparable evidence of neuroprotective effects of FMT in its restoration of cognitive deficits and reduction in neuroinflammation.

--> While also observing the similar interplay of bacterial species in the gut microbiome. This comparison highlights the clinical significance of FMT in its protective effects.

# data[].attributes.body
“A Window of Opportunity”

This entails that while FMT is not a novel treatment regime, it is certainly a new avenue in its potentiality against PD.

An potential treatment for gut microbiota dysbiosis as there is not yet an FDA-approved treatment.

An Emerging Avenue of FMT for neurological disorders.

Studies of FMT for other neurological disorders can offer a deeper understanding of the microbiota-gut-brain axis.

Mechanisms and efficacy of FMT treatment against PD.

This can then further validate the mechanism and efficacy of FMT in the restoration of the microbiome.

Efficacy of FMT in the restoration of the microbiome.

The efficacy of FMT as a treatment form can overall offer an option in the pursuit to improve the quality of life for patients with PD.

# data[].attributes.body
For the novelty of this study:

There is still a need for more in depth studies to verify the study’s findings. It was only mentioned in the study, that current data only reveals the indirect mechanisms of the gut and brain interaction.

For the application:

While researchers were able to make conclusive remarks on the use of FMT, there may be other mechanisms or factors that may affect the overall efficacy of the treatment. For example, there are certain bacterial species that may cause unpredictable stress in the colon and so, more experimental investigations are needed to verify its therapeutic use.

More studies needed to explore the underline role of FMT and how it effects the TLR4/MyD88 /NF-kB signaling pathway.

Need to study other PD-Gut-related symptoms: abdominal pain, distention (Fan et al., 2022)

# data[].attributes.body
The use of FMT in Parkinson's disease in a randomized, repeat-dose, placebo-controlled clinical pilot study.

Interestingly, subjective motor functions and non-motor symptoms are shown to display temporary improvement compared to baseline.

With improvements in diversity of the intestinal microbiome which is associated with reduced bowel symptoms and improved gut function.

Some improvement in quality of life (QOL).

--> However, study is only a pilot and is yet to show bigger improvements in QOL and other PD-related symptoms.

--> This still shows the amazing progression of such treatment.

# data[].attributes.body
Why FMT is being used as a form of treatment?

Used for its simplicity, the existing data on its use and is shown to have less adverse effects!

But there is still a lack of animal studies to prove its use.

--> This highlights more of the impact of our study on how it contributes to the exploration of treatment for PD patients.

# data[].attributes.attachment_link.title
Fecal Transplants for Parkinson’s: Hope or Hype?

# data[].attributes.attachment_link.description
Scientists conclude that more research is needed before supporting the use of fecal transplants to treat constipation in Parkinson’s disease patients.