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Journal : MNJ (Malang Neurology Journal)

EXERCISE PREVENTS AGE-RELATED MEMORY DECLINE: THE ROLE OF NEUROTROPHIC FACTORS Rivarti, Arina Windri; Herawati, Lilik; Hidayati, Hanik Badriyah
MNJ (Malang Neurology Journal) Vol. 6 No. 2 (2020): July
Publisher : PERDOSSI (Perhimpunan Dokter Spesialis Saraf Indonesia Cabang Malang) - Indonesian Neurological Association Branch of Malang cooperated with Neurology Residency Program, Faculty of Medicine Brawijaya University, Malang, Indonesia

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Abstract

Increasing aging population causes an increased prevalence of neurodegenerative diseases such as dementia that is associated with memory decline. Developing strategies for the prevention and therapy of age-related dementia is important to reduce the burden of treatment costs. Physical exercise is known to prevent cognitive decline and improve cognitive abilities. Physical exercise with moderate intensity for at least 150 minutes/week or 30 minutes/day for 5 days can reduce the incidence of degenerative diseases in the elderly. Thus, physical exercise appears as a simple, inexpensive, and affordable non-pharmacological therapy for most people. The processes of neurogenesis and neuronal survival involve the role of neurotrophic factors including BDNF, IGF-1 and VEGF, which are the three main neurotrophic factors that are known to increase after exercise. Many publications discuss about these neurotrophic factors, but their mechanism of signals and changes related to aging and exercise have not been completely studied. The purpose of this review is to discuss the mechanism of signals and changes of neurotrophic factors (focuses on BDNF, IGF-1, and VEGF) related to aging and exercise.
THE THE POTENTIAL ROLE OF NRF2 AS A TARGET SITE FOR THERAPEUTIC INTERVENTIONS IN ALZHEIMER'S DISEASE Rivarti, Arina Windri; Harahap, Herpan Syafii; Saputri, Legis Ocktaviana; Suryani, Dini; Rianawati, Sri Budhi
MNJ (Malang Neurology Journal) Vol. 11 No. 2 (2025): July
Publisher : PERDOSSI (Perhimpunan Dokter Spesialis Saraf Indonesia Cabang Malang) - Indonesian Neurological Association Branch of Malang cooperated with Neurology Residency Program, Faculty of Medicine Brawijaya University, Malang, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.mnj.2025.011.02.10

Abstract

Alzheimer's Disease (AD) is the most common form of dementia, characterized by progressive neurodegeneration leading to cognitive decline and memory impairment, affecting various cognitive functions. AD pathology involves the accumulation of neurotoxic substances such as amyloid beta (Aβ) and tau proteins, mitochondrial dysfunction, oxidative stress, and chronic neuroinflammation, resulting in synaptic loss and neuronal apoptosis. The transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) has emerged as a pivotal regulator of cellular defense mechanisms, including antioxidant response, autophagy, and inflammation. NRF2 not only inhibits Aβ synthesis and enhances tau protein clearance via autophagy but also reduces neuroinflammation by modulating microglial activation and cytokine production. Additionally, NRF2 activation preserves mitochondrial function by attenuating reactive oxygen species (ROS) production and sustaining mitochondrial biogenesis. Recent studies highlight the therapeutic potential of NRF2 activators, such as sulforaphane and echinacoside, in preclinical AD models, demonstrating reductions in Aβ and tau pathologies and improved cognitive outcomes. These findings underscore the multifaceted role of NRF2 in mitigating AD progression and its promise as a target for developing novel therapeutic interventions. By integrating NRF2-based strategies, future treatments may offer more effective approaches to combat the complex pathophysiology of AD.