» ГЛАВНАЯ > К содержанию номера
» Все публикации автора
Журнал научных публикаций
«Наука через призму времени»
Декабрь, 2025 / Международный научный журнал
«Наука через призму времени» №12 (105) 2025
Автор: Agayeva D., Teacher
Рубрика: Педагогические науки
Название статьи: The role of the gut microbiome in modulating neurodegenerative diseases
Дата публикации: 12.12.2025
скачать
УДК 61
THE ROLE OF
THE GUT MICROBIOME IN MODULATING NEURODEGENERATIVE DISEASES
Agayeva D.
Teacher,
Rozykulyyev B.
Student
The
International University of Industrialists and Entrepreneurs
Ashgabat,
Turkmenistan
Abstract. The intricate relationship between
the gut microbiome and the central nervous system—known as the gut-brain
axis—is gaining significant recognition in the pathogenesis of
neurodegenerative disorders (NDs). This study investigates the mechanisms by
which microbial communities in the gut influence the onset and progression of
diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and
Amyotrophic Lateral Sclerosis (ALS). Key pathways explored include the
production of microbial metabolites, particularly short-chain fatty acids
(SCFAs) like butyrate, which affect blood-brain barrier integrity,
neuroinflammation, and mitochondrial function.
Keywords: gut microbiome, neurodegenerative
diseases, gut-brain axis, Alzheimer's disease (AD), Parkinson's disease (PD),
short-chain fatty acids (SCFAs), neuroinflammation, dysbiosis, probiotics,
therapeutic targets, diagnostic biomarkers.
The field
of neuroscience has undergone a profound shift, moving beyond the central
nervous system (CNS) to acknowledge the critical influence of peripheral
systems, particularly the gastrointestinal tract. The gut microbiome, a vast
and complex community of microorganisms, is now recognized as a key regulator
of systemic health.
This
dynamic ecosystem is integral to immune regulation, metabolic processes,
and—most significantly—neurological function. Its ability to communicate with
the brain through the gut-brain axis positions it at the nexus of health and
neurological disease.
The
gut-brain axis represents a sophisticated, bidirectional communication highway
linking the gut and the CNS via neural (vagus nerve),
endocrine (hormonal), and immunological pathways. It is the primary mechanism
through which microbial activity influences cerebral function.
Disruptions
to the balanced microbial community, a state referred to as dysbiosis, are
increasingly implicated in the etiology and progression of chronic and
debilitating neurodegenerative diseases (NDs). These diseases include
Alzheimer's disease (AD) and Parkinson's disease (PD).
Alzheimer's
disease, the leading cause of dementia, is pathologically defined by the
accumulation of amyloid-beta plaques and hyperphosphorylated tau protein
tangles. Emerging evidence suggests microbial metabolites contribute to
systemic inflammation that exacerbates the neuroinflammatory response in the
brain.
Parkinson's
disease, characterized by the progressive loss of dopaminergic neurons,
frequently presents with gastrointestinal symptoms, such as chronic
constipation, often preceding motor symptoms by many years. This temporal
relationship strongly suggests a potential peripheral, gut-based origin for the
pathology.
The
molecular connection is mediated by a multitude of signaling molecules
synthesized by the gut microbiota. Among the most widely studied are short-chain
fatty acids (SCFAs), which include butyrate, propionate, and acetate.
SCFAs are
produced through the microbial fermentation of undigested dietary fibers and
serve as crucial signaling molecules that modulate both the host's immune
system and neurophysiological processes.
Butyrate,
in particular, exhibits strong neuroprotective qualities by enhancing the
integrity of the intestinal barrier and regulating the activity of microglia,
the brain's resident immune cells.
Furthermore,
the gut microbiome plays a role in the biosynthesis and regulation of key
neurotransmitters, including serotonin and GABA (gamma-aminobutyric acid).
Alterations in their synthesis can directly or indirectly impact cognitive
function and mood, contributing to ND progression.
A crucial
factor in ND pathogenesis is the link between gut dysbiosis and increased
systemic and neuroinflammation. Dysbiosis can compromise the integrity of the
intestinal mucosal barrier.
This
compromised barrier allows bacterial products, such as lipopolysaccharides
(LPS), to leak into the systemic circulation. This phenomenon, often called
"leaky gut," triggers a chronic low-grade inflammatory response
throughout the body.
Upon
reaching the brain, these pro-inflammatory signals can activate glial cells
(astrocytes and microglia), driving the sustained neuroinflammatory state that
is characteristic of both AD and PD.
The
current focus of research is shifting toward leveraging the microbiome for
therapeutic intervention. Strategies such as the administration of probiotics
and prebiotics aim to restore eubiosis and enhance
beneficial metabolite production.
More
radical approaches, such as Fecal Microbiota Transplantation (FMT), are being
explored to fundamentally restructure the host's microbial community in hopes
of slowing or reversing disease progression.
Identifying
specific microbial signatures or metabolic profiles that correlate strongly
with ND stages is essential for developing non-invasive diagnostic biomarkers.
A simple gut-based test could offer earlier and more accurate diagnosis than
current methods.
Targeting
the gut microbiome offers a promising avenue for novel therapeutic development,
shifting treatment paradigms from solely focusing on the brain to addressing
peripheral drivers of pathology. Modifying the bacterial composition or
augmenting the functionality of existing beneficial species could potentially
mitigate the neurotoxic environment associated with protein misfolding.
The
research also needs to address the variability in response to diet and
interventions, which is highly dependent on the individual's unique microbial
landscape. Personalized medicine approaches, informed by metagenomic
sequencing, will be crucial for tailoring prebiotic or probiotic regimens to
maximize their neuroprotective effects.
Beyond
inflammation and metabolites, the microbiome can influence NDs through the
regulation of mitochondrial function. Healthy bacteria contribute to
mitochondrial stability and energy production in host cells, while dysbiosis can
lead to oxidative stress and impaired neuronal energy metabolism—a hallmark of
aging and neurodegeneration.
Furthermore,
the influence of the gut microbiome extends to the clearance mechanisms of
misfolded proteins. Studies suggest that a healthy gut environment can
indirectly enhance the brain's ability to dispose of toxic aggregates, thereby
limiting the spread of pathology from the periphery to the CNS.
Ultimately,
integrating knowledge from microbiology, immunology, and neuroscience will be
essential to translate these fascinating correlational findings into definitive
causal relationships and, critically, into effective clinical treatments for
patients suffering from neurodegenerative diseases.
In
conclusion, understanding the intricate molecular and cellular crosstalk along
the gut-brain axis is paramount. The microbiome is not merely an associated
factor but a pivotal modulator of neurodegenerative risk and severity.
Reference::
- Cryan, J. F., O’Riordan, K. J., Cowan, C. S. M., Sandhu, V., Bastiaanssen, T. F. S., Codagnone, M. N., ... & Dinan, T. G. (2019). The microbiota–gut–brain axis. Physiological Reviews, 99(4), 1877–2013.
- Hao, F., & Lee, B. S. (2020). Gut Microbiota and Neurodegenerative Diseases: An Interplay with the Immune System. Biomedicines, 8(11), 470.
- Sampson, T. R., Debelius, S. K., Thron, T., Phillips, S., Garfinkel, J., Sonnenburg, J. L., ... & Hsiao, E. Y. (2016). Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkinson's disease. Cell, 167(6), 1492–1506.e12.
- Zhuang, X., Gong, W., Lu, J., Zhang, C., Xiong, F., Sun, X., ... & Hu, M. (2020). The role of the gut microbiota in the pathogenesis of Alzheimer’s disease. Frontiers in Neuroscience, 14, 1184.
Комментарии:
