Journal of Brain and Neurology

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (202) 780-3397

Perspective - Journal of Brain and Neurology (2025) Volume 8, Issue 3

Neurodegeneration: Understanding progressive neural decline.

Sonsoles Alonso*

Department of Integrative Neuroscience, Aarhus University, Denmark

*Corresponding Author:
Sonsoles Alonso
Department of Integrative Neuroscience
Aarhus University, Denmark
E-mail: Sonles.alonso@cfin.au.dk

Received: 02-Aug-2025, Manuscript No. AAJBN-25-171418; Editor assigned: 03-Aug-2025, Pre QC No. AAJBN-25-171418 (PQ); Reviewed: 16-Aug-2025, QC No. AAJBN-25-171418; Revised: 20-Aug-2025, Manuscript No. AAJBN-25-171418 (R); Published: 27-Aug-2025, DOI: 10.35841/aajbn-8.3.209

Citation: Alonso S. Neurodegeneration: Understanding progressive neural decline. J Brain Neurol. 2025;8(3):209

Visit for more related articles at Journal of Brain and Neurology

Introduction

Neurodegeneration refers to the progressive loss of structure or function of neurons, including their death, which is central to a variety of debilitating neurological disorders. These conditions, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis (ALS), predominantly affect older adults, although some can manifest earlier in life. The loss of neurons disrupts the intricate communication networks within the brain and spinal cord, leading to cognitive decline, motor dysfunction, and a spectrum of behavioral changes. Understanding the mechanisms behind neurodegeneration is critical to developing effective therapeutic interventions and improving the quality of life for affected individuals. [1].

At the cellular level, neurodegeneration is often associated with abnormal protein accumulation, oxidative stress, mitochondrial dysfunction, and impaired cellular repair mechanisms. Misfolded proteins, such as beta-amyloid in Alzheimer’s disease or alpha-synuclein in Parkinson’s disease, tend to aggregate and interfere with normal neuronal function. Additionally, neurons are highly susceptible to oxidative damage due to their high metabolic demand and limited regenerative capacity. Mitochondrial dysfunction further exacerbates this vulnerability by reducing energy availability and increasing the production of reactive oxygen species, which can damage essential cellular components. [2].

Genetic factors also play a significant role in neurodegenerative disorders. Mutations in specific genes can predispose individuals to early-onset forms of these diseases. For example, mutations in the APP, PSEN1, and PSEN2 genes are linked to familial Alzheimer’s disease, while mutations in the LRRK2 or PARK7 genes contribute to familial Parkinson’s disease. In addition to inherited mutations, epigenetic changes and environmental factors, such as exposure to toxins or head trauma, can influence disease onset and progression. The interplay between genetic predisposition and environmental triggers highlights the complexity of neurodegenerative disorders.[3].

Inflammatory processes within the nervous system also contribute to neuronal damage. Microglia, the brain’s resident immune cells, become activated in response to injury or protein aggregates, releasing pro-inflammatory cytokines and chemokines. While this inflammatory response aims to protect the brain, chronic or excessive activation can lead to a toxic environment, further damaging neurons and supporting the progression of neurodegeneration. This neuroinflammation is increasingly recognized as a key target for therapeutic strategies aimed at slowing disease progression. [4].

Current therapeutic approaches primarily focus on managing symptoms rather than halting the underlying disease process. Pharmacological treatments, such as cholinesterase inhibitors for Alzheimer’s disease or dopaminergic medications for Parkinson’s disease, can improve cognitive or motor function temporarily. Emerging therapies, including monoclonal antibodies targeting toxic proteins, gene therapy, and stem cell-based interventions, hold promise for altering disease progression. Early diagnosis through biomarkers, neuroimaging, and genetic testing is also crucial for timely intervention and maximizing the effectiveness of these treatments. [5].

Conclusion

Research into neurodegeneration continues to evolve, emphasizing the need for a multidisciplinary approach that integrates molecular biology, genetics, immunology, and clinical neuroscience. By uncovering the complex mechanisms underlying neuronal loss, scientists aim to develop interventions that not only alleviate symptoms but also protect or restore neural function.

References

  1. Bricolo A, Turazzi S, Faccioli F, et al. Clinical application of compressed spectral array in long-term EEG monitoring of comatose patients. Electroencephalogr Clin Neurophysiol. 1978;45(2):211-25.

    2. Indexed at, Google Scholar, Crossref

  2. Jennett B, Plum F. Persistent vegetative state after brain damage: a syndrome in search of a name. Lancet. 1972;299(7753):734-7.

    3. Indexed at, Google Scholar, Crossref

  3. Dieckmann G. Cortical synchronized and desynchronized responses evoked by stimulation of the putamen and pallidum in cats. Journal of the neurological sciences. 1968;7(2):385-91.

    4. Indexed at, Google Scholar, Crossref

  4. Giacino JT, Ashwal S, Childs N, et al. The minimally conscious state: definition and diagnostic criteria. Neurology. 2002 Feb;58(3):349-53.

    5. Indexed at, Google Scholar

  5. Fujii M, Sadamitsu D, Maekawa T, et al. Spinal cord stimulation therapy at an early stage for unresponsive patients with hypoxic encephalopathy. No Shinkei geka. Neurological Surgery. 1998 ;26(4):315-21.

    6. Indexed at, Google Scholar

Get the App