Editorial - Journal of Aging and Geriatric Psychiatry (2025) Volume 9, Issue 2

Shared pathways in neurodegeneration: Therapeutic strategies

Dr. Julia Müller^*

Department of Medicine, University of Athens

*Corresponding Author:

Dr. Julia Müller
Department of Medicine
University of Athens.
E-mail: julimuller@charite.de

Received : 05-Dec-2025, Manuscript No. AAAGP-25-201; Editor assigned : 09-Dec-2025, PreQC No. AAAGP-25-201(PQ); Reviewed : 29-Dec-2025, QC No AAAGP-25-201; Revised : 07-Jan-2026, Manuscript No. AAAGP-25-201(R); Published : 16-Jan-2026 , DOI : 10.35841/aaagp-9.2.201

Citation: Müller DJ. Shared pathways in neurodegeneration: Therapeutic strategie. J Age Geriat Psych. 2026;09(02):201.

Introduction

This article delves into the shared and distinct molecular pathways contributing to neurodegeneration in Alzheimer's, Parkinson's, and Huntington's diseases. It highlights commonalities like protein misfolding, mitochondrial dysfunction, and oxidative stress, while also pointing out unique mechanisms relevant to each specific condition. Understanding these underlying processes is crucial for developing targeted therapeutic strategies[1].

This clinical review provides an expansive overview of Parkinson's disease, covering its complex pathophysiology, diagnostic challenges, and evolving treatment strategies. It emphasizes the importance of early and accurate diagnosis, alongside a multidisciplinary approach to managing both motor and non-motor symptoms. The article also touches upon emerging therapeutic targets, offering a comprehensive look at current and future directions in PD management[2].

This review article explores the intricate mechanisms underlying Amyotrophic Lateral Sclerosis (ALS), focusing on genetic factors, protein aggregation, excitotoxicity, and inflammation. It discusses current therapeutic approaches and highlights promising new strategies, including gene therapies and stem cell interventions, aiming to halt disease progression and improve patient outcomes. The complex interplay of various pathological pathways in ALS underscores the need for multi-targeted treatments[3].

This article provides a thorough review of the current and developing therapeutic strategies for Huntington's disease. It covers symptomatic treatments, but more importantly, it highlights disease-modifying approaches targeting the underlying genetic mutation, such as antisense oligonucleotides and gene-editing techniques. The review underscores the significant progress in clinical trials, offering hope for slowing or preventing disease progression[4].

This article dissects the complex genetic landscape of frontotemporal lobar degeneration (FTLD), a key cause of frontotemporal dementia. It highlights the major gene mutations (e.g., C9orf72, GRN, MAPT) and their varied pathological consequences, impacting protein aggregation and cellular function. Understanding this genetic architecture is pivotal for personalized diagnostic approaches and the development of gene-targeted therapies to combat this progressive neurodegenerative disorder[5].

This review provides a comprehensive update on prion diseases, focusing on their diverse clinical presentations, advanced diagnostic methods, and the challenging therapeutic landscape. It highlights the significance of novel biomarkers and imaging techniques for early detection, alongside the urgent need for effective treatments to combat these rapidly progressive and fatal neurodegenerative conditions. The article underscores the unique protein misfolding mechanisms driving these diseases[6].

This article elucidates the central role of alpha-synuclein pathology in Dementia with Lewy Bodies (DLB), a challenging neurodegenerative condition. It explores how the aggregation and spread of misfolded alpha-synuclein contribute to the characteristic cognitive, motor, and neuropsychiatric symptoms of DLB. The review also discusses current and emerging therapeutic strategies that specifically target alpha-synuclein, aiming to modulate its pathology and improve patient outcomes[7].

This article provides a comprehensive overview of Multiple System Atrophy (MSA), a rare and rapidly progressive neurodegenerative disorder. It discusses the evolving understanding of MSA's unique alpha-synucleopathy, its distinct clinical subtypes, and the ongoing challenges in diagnosis and symptomatic management. The review also highlights the urgent need for disease-modifying therapies and the potential of various experimental approaches currently under investigation[8].

This article explores the critical role of neuroinflammation as a common underlying factor in various neurodegenerative diseases. It details the complex interplay between activated glial cells, inflammatory mediators, and neuronal damage. The authors discuss how targeting specific inflammatory pathways offers promising therapeutic avenues, emphasizing immune modulation as a key strategy to slow or prevent neuronal demise and disease progression[9].

This article thoroughly examines the pivotal role of mitochondrial dysfunction across various neurodegenerative diseases. It elaborates on how impaired mitochondrial dynamics, bioenergetic deficits, and increased oxidative stress contribute significantly to neuronal vulnerability and cell death. The review highlights emerging therapeutic strategies focused on restoring mitochondrial health, including approaches targeting mitochondrial quality control, biogenesis, and energy metabolism, offering promising avenues for intervention[10].

Conclusion

Neurodegenerative diseases like Alzheimer's, Parkinson's, and Huntington's share molecular pathways such as protein misfolding, mitochondrial dysfunction, and oxidative stress [1]. Parkinson's disease, for example, demands multidisciplinary management focusing on early diagnosis and emerging therapeutic targets [2]. Amyotrophic Lateral Sclerosis (ALS) involves genetic factors, protein aggregation, and inflammation, requiring multi-targeted treatments [3]. Huntington's disease therapies are advancing with genetic mutation-targeting strategies showing promise in clinical trials [4]. Other conditions include Frontotemporal Lobar Degeneration (FTLD), driven by specific gene mutations impacting protein aggregation [5], and prion diseases, defined by unique protein misfolding and rapid progression [6]. Dementia with Lewy Bodies (DLB) and Multiple System Atrophy (MSA) are characterized by alpha-synuclein pathology, necessitating therapies to modulate its aggregation [7, 8]. Neuroinflammation [9] and mitochondrial dysfunction [10] are crucial common underlying factors, with immune modulation and restoring mitochondrial health offering key therapeutic avenues. Understanding these shared and unique mechanisms is essential for developing effective, targeted neurodegenerative therapies.

References

1. Xia H, Min-Wei W, Yi-Dan M. Molecular mechanisms of neurodegeneration in Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease: commonalities and differences. Acta Pharmacol Sin. 2021;42(8):1183-1200.

Indexed at, Google Scholar, Crossref

1. Werner P, Werner S, Caroline MT. Parkinson’s disease: a clinical review. Lancet Neurol. 2019;18(9):893-903.

Indexed at, Google Scholar, Crossref

1. Mohsen G, Arash G, Seyed MMG. Amyotrophic lateral sclerosis: mechanisms and therapeutics. J Transl Med. 2021;19(1):167.

Indexed at, Google Scholar, Crossref

1. Sarah F, Julie CS, Erin KF. Huntington's disease: current and emerging therapeutic approaches. CNS Drugs. 2020;34(6):585-602.

Indexed at, Google Scholar, Crossref

1. Raffaele F, Sara BG, Laura DHS. Genetic architecture of frontotemporal lobar degeneration. Neurogenetics. 2020;21(1):1-13.

Indexed at, Google Scholar, Crossref

1. Simone B, Anna P, Sabina C. Prion diseases: an update on clinical aspects, diagnostics, and therapeutics. Expert Rev Neurother. 2020;20(10):1007-1021.

Indexed at, Google Scholar, Crossref

1. Thomas P, Anna MK, Ioannis AK. Dementia with Lewy bodies: the role of α-synuclein and its impact on therapeutic strategies. Transl Neurodegener. 2022;11(1):56.

Indexed at, Google Scholar, Crossref

1. Alessandro F, Gregor KW, Wassilios GM. Multiple system atrophy: current perspective and future directions. Mov Disord. 2020;35(10):1693-1704.

Indexed at, Google Scholar, Crossref

1. Nicholas MD, Hannah ML, Megan BB. Neuroinflammation in neurodegenerative diseases: mechanisms and therapeutic strategies. Prog Neurobiol. 2023;228(NA):102496.

Indexed at, Google Scholar, Crossref

1. Jia S, Chao Z, Qiuxia H. Mitochondrial dysfunction in neurodegenerative diseases: Pathological mechanisms and therapeutic opportunities. Signal Transduct Target Ther. 2022;7(1):27.

Indexed at, Google Scholar, Crossref