Short Communication - Journal of Aging and Geriatric Psychiatry (2025) Volume 9, Issue 3

Neurodegeneration: Mechanisms, biomarkers, therapy

Martin Lauer^*

Department of Geriatric Psychiatry, University of Wurzburg

*Corresponding Author:

Martin Lauer
Department of Geriatric Psychiatry
University of Wurzburg.
E-mail: LaueM@ukw.de

Received : 10-Aug-2025, Manuscript No. aaagp-25-210; Editor assigned : 12-Aug-2025, PreQC No. aaagp-25-210(PQ); Reviewed : 01-Sep-2025, QC No aaagp-25-210; Revised : 10-Sep-2025, Manuscript No. aaagp-25-210(R); Published : 19-Sep-2025 , DOI : 10.35841/aaagp-9.3.210

Citation: Lauer M. Neurodegeneration: Mechanisms, biomarkers, therapie. J Age Geriat Psych. 2025;09(03):210.

Introduction

A significant body of research points to the critical role of neuroinflammation in the progression of Alzheimer's disease. Investigations into novel therapeutic strategies often focus on modulating inflammatory pathways, presenting promising avenues for intervention in this complex disorder [1].

Beyond inflammation, the cellular process of mitophagy, a specific form of autophagy, holds considerable importance for maintaining neuronal health. Its dysfunction is increasingly recognized in various neurodegenerative conditions, highlighting its potential as a crucial therapeutic target for these debilitating diseases [2].

Understanding Amyotrophic Lateral Sclerosis (ALS) requires a deep dive into its complex molecular mechanisms. Recent findings provide updated overviews focusing on genetic factors, protein aggregation, and mitochondrial dysfunction, all of which are considered essential for the development of effective treatments for ALS [3].

In the realm of genetic disorders, significant advancements are being made in gene therapy approaches for Huntington's disease. These include the development of antisense oligonucleotides and viral vector-mediated strategies, which offer considerable hope for targeted disease modification and improved patient outcomes [4].

Autophagy dysregulation, a broad cellular process, is a common thread in the pathogenesis of several major neurodegenerative disorders. This dysregulation underscores its potential as a universal therapeutic target aimed at restoring fundamental cellular homeostasis across different conditions [5].

Microglia, the resident immune cells of the brain, exhibit multifaceted roles in neurodegenerative diseases. Current research continues to update our understanding of their transition from protective to detrimental phenotypes, with significant therapeutic implications for modulating their activity to combat disease progression [6].

For Alzheimer's disease diagnosis, the landscape of fluid biomarkers is rapidly evolving. Reviews explore both current and emerging markers, emphasizing their potential for early detection and for monitoring disease progression, with particular attention to readily accessible blood-based markers [7].

Parkinson's disease pathogenesis is tightly intertwined with mitochondrial dysfunction and oxidative stress. Studies aim to elucidate this intricate link, discussing various therapeutic strategies designed to target these specific pathways and thereby mitigate neuronal damage associated with the disease [8].

The gut microbiota also presents a fascinating connection to neurodegenerative processes. Growing evidence links dysbiosis in the gut microbiota to Alzheimer's disease, exploring underlying mechanisms like neuroinflammation and amyloid pathology, and suggesting gut-targeting interventions as promising new therapeutic avenues [9].

Finally, lysosomal dysfunction represents another crucial factor implicated in various neurodegenerative disorders. Research in this area highlights strategies aimed at restoring lysosomal function, positioning this as a promising therapeutic approach to address cellular waste management issues inherent in these conditions [10].

Conclusion

Neuroinflammation plays a critical role in Alzheimer's disease progression, leading to exploration of therapeutic strategies to modulate inflammatory pathways. Mitophagy, a selective form of autophagy, is vital for neuronal health, and its dysfunction is a potential therapeutic target in neurodegenerative conditions. Understanding the complex molecular mechanisms of Amyotrophic Lateral Sclerosis (ALS), including genetic factors and mitochondrial dysfunction, is crucial for developing treatments. Gene therapy, particularly antisense oligonucleotides and viral vectors, shows promise for Huntington's disease by offering targeted disease modification. Autophagy dysregulation contributes significantly to the pathogenesis of major neurodegenerative disorders, suggesting it as a therapeutic target for cellular homeostasis. Microglia, pivotal in neurodegenerative diseases, transition from protective to detrimental phenotypes, making their modulation a therapeutic avenue. Fluid biomarkers are emerging for Alzheimer's disease diagnosis, offering potential for early detection and monitoring, including blood-based markers. Parkinson's disease pathogenesis is intricately linked to mitochondrial dysfunction and oxidative stress, with therapeutic strategies targeting these pathways aimed at mitigating neuronal damage. Growing evidence links gut microbiota dysbiosis to Alzheimer's disease through mechanisms like neuroinflammation and amyloid pathology, highlighting gut-targeting interventions as potential therapies. Lysosomal dysfunction is also a crucial factor in various neurodegenerative disorders, with restoring lysosomal function being a promising therapeutic approach.

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