Journal of Aging Science

The Impact of Aging on Neurodegenerative Diseases

Aaron Elliott^* Genes & Human Disease Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA
^*Correspondence: Aaron Elliott, Genes & Human Disease Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA, Email:

Received: 08-May-2024, Manuscript No. JASC-24-26123; Editor assigned: 10-May-2024, Pre QC No. JASC-24-26123 (PQ); Reviewed: 24-May-2024, QC No. JASC-24-26123; Revised: 03-Jun-2024, Manuscript No. JASC-24-26123 (R); Published: 11-Jun-2024, DOI: 10.35248/2329-8847.24.12.367

Description

Neurodegenerative diseases represent a group of disorders characterized by progressive degeneration of the structure and function of the nervous system. These diseases, which include Alzheimer's disease, Parkinson's disease, Huntington's disease, and Amyotrophic Lateral Sclerosis (ALS), pose significant challenges to global health due to their debilitating nature and lack of effective treatments. Aging is a primary risk factor for neurodegenerative diseases, influencing their onset, progression, and severity. Understanding how aging contributes to these conditions is important for developing strategies to mitigate their impact and improve patient outcomes.

Age-related changes in the brain

As individual’s age, the brain undergoes various structural and functional changes that contribute to increased vulnerability to neurodegenerative diseases:

Neuronal loss: Aging is associated with a gradual decline in the number and function of neurons. Neurons in regions important for cognitive and motor functions, such as the hippocampus and substantia nigra, are particularly vulnerable. This neuronal loss impairs brain networks involved in memory, movement, and coordination, predisposing individuals to neurodegenerative diseases.

Accumulation of protein aggregates: Many neurodegenerative diseases are characterized by the accumulation of abnormal protein aggregates within neurons and glial cells. For example, Alzheimer's disease is associated with the accumulation of beta- amyloid plaques and tau tangles, while Parkinson's disease involves alpha-synuclein aggregates (Lewy bodies). Aging disrupts protein homeostasis and clearance mechanisms, leading to the accumulation of these toxic proteins and promoting disease progression.

Oxidative stress and inflammation: Aging is accompanied by increased oxidative stress and chronic low-grade inflammation in the brain, known as neuroinflammation. These processes contribute to neuronal damage, glial activation, and the release of pro-inflammatory cytokines and Reactive Oxygen Species (ROS). Neuroinflammation exacerbates neuronal dysfunction and accelerates the progression of neurodegenerative diseases.

Genetic and molecular mechanisms

Genetic factors also play a significant role in the relationship between aging and neurodegenerative diseases:

Genetic susceptibility: Certain genetic mutations and variations influence an individual's susceptibility to neurodegenerative diseases. For example, mutations in the genes encoding Amyloid Precursor Protein (APP), Presenilin 1 (PSEN1), and Presenilin 2 (PSEN2) are associated with early-onset familial Alzheimer's disease. Aging interacts with these genetic factors to modulate disease onset and progression.

Mitochondrial dysfunction: Mitochondrial dysfunction, characterized by impaired energy production and increased ROS production, is implicated in aging and neurodegeneration. Aging-related mitochondrial dysfunction exacerbates neuronal vulnerability to oxidative stress and contributes to the pathogenesis of neurodegenerative diseases, such as Parkinson's disease and ALS.

Common neurodegenerative diseases

Each neurodegenerative disease has distinct pathological features and clinical manifestations, but they share common underlying mechanisms influenced by aging:

Alzheimer's disease: Alzheimer's disease is characterized by progressive cognitive decline, memory loss, and behavioral changes. Aging-related factors, such as tau hyperphosphorylation and amyloid-beta accumulation, disrupt neuronal communication and lead to synaptic dysfunction and neuronal death. The prevalence of Alzheimer's disease increases exponentially with age, highlighting the critical role of aging in its pathogenesis.

Parkinson's disease: Parkinson's disease primarily affects movement due to the degeneration of dopaminergic neurons in the substantia nigra. Aging-related mitochondrial dysfunction, oxidative stress, and protein aggregation contribute to the loss of dopaminergic neurons and the formation of Lewy bodies. Aging is the most significant risk factor for Parkinson's disease, with incidence rising sharply in older adults.

Huntington's disease: Huntington's disease is an inherited neurodegenerative disorder caused by a mutation in the huntingtin gene. The age of onset and progression of Huntington's disease are influenced by the length of the CAG repeat expansion in the huntingtin gene. Aging exacerbates the neurodegenerative process in Huntington's disease, leading to progressive motor dysfunction, cognitive decline, and psychiatric symptoms.

Therapeutic strategies and future directions

Developing effective treatments for neurodegenerative diseases requires addressing the complex interactions between aging, genetic factors, and disease-specific mechanisms:

Targeting protein aggregation: Therapies aimed at preventing or clearing protein aggregates hold potential for slowing disease progression. Strategies include immunotherapy targeting beta- amyloid and tau in Alzheimer's disease and enhancing autophagy to remove protein aggregates in Parkinson's disease.

Mitochondrial support: Interventions that improve mitochondrial function and reduce oxidative stress may mitigate neuronal damage in neurodegenerative diseases. Mitochondrial- targeted antioxidants and modulators of mitochondrial biogenesis are under investigation as potential therapies.

Neuroinflammation modulation: Anti-inflammatory drugs and immunomodulators may help reduce neuroinflammation and protect neurons from damage in neurodegenerative diseases. Clinical trials are evaluating the efficacy of anti-inflammatory agents in slowing disease progression and improving symptoms.

Conclusion

Aging significantly impacts the onset and progression of neurodegenerative diseases through complex genetic, molecular, and environmental mechanisms. By elucidating these mechanisms, researchers can develop targeted interventions to delay disease onset, slow progression, and improve the quality of life for individuals affected by these devastating disorders.