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All Journal Jurnal Kesehatan Amanah Termometer: Jurnal Ilmiah Ilmu Kesehatan Dan Kedokteran
Sari Mariyati Dewi Nataprawira
Universitas Tarumanagara
Dentistry Health Professions Nursing Public Health

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Penyakit Parkinson : Tinjauan Terpadu Biomedis dan Kemajuan Terapi Terkini Sari Mariyati Dewi Nataprawira; Triyana Sari; Erick Sidarta
Jurnal Kesehatan Amanah Vol. 9 No. 2 (2025): Jurnal Kesehatan Amanah
Publisher : Universitas Muhammadiyah Manado

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.57214/jka.v9i2.914

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta, which plays a crucial role in regulating movement. The hallmark pathology of PD is the formation of Lewy bodies, abnormal protein aggregates composed primarily of α-synuclein. The pathophysiological mechanisms of this disease are multifactorial, involving a complex interaction between genetic and environmental factors. Molecularly, several key mechanisms involved include mitochondrial dysfunction, oxidative stress, chronic neuroinflammation, and genetic mutations in the LRRK2, DJ-1, PINK1, and SNCA genes, which have been shown to influence susceptibility to PD. In addition to genetic factors, the risk of developing PD is also influenced by environmental exposures, including pesticides, heavy metals, and exposure to certain toxins that can accelerate neuronal damage. The clinical manifestations of PD are characterized by classic motor symptoms, namely resting tremor, bradykinesia, rigidity, and gait disturbances, which are often accompanied by non-motor symptoms such as sleep disturbances, depression, autonomic dysfunction, and cognitive decline. Diagnosis generally follows the UK Brain Bank clinical criteria, supported by neuroimaging techniques such as DaTSCAN and MRI, and the development of biomarkers based on α-synuclein detection to improve the accuracy of early diagnosis. The main treatment option currently is pharmacological therapy, particularly levodopa, often combined with dopamine agonists or MAO-B inhibitors to optimize symptom control. In advanced cases, surgery in the form of deep brain stimulation can provide significant improvement. Innovative therapies such as gene therapy, stem cell therapy, and the integration of wearable devices and artificial intelligence are being developed to improve symptom monitoring and personalize treatment. Current research focuses on the development of more sensitive diagnostic methods and neuroprotective therapies that can slow disease progression.  
Demensia : Patofisiologi, Faktor Resiko dan Peran Inflamasi dalam Perkembangan Penyakit Erick Sidarta; Triyana Sari; Sari Mariyati Dewi Nataprawira
Termometer: Jurnal Ilmiah Ilmu Kesehatan dan Kedokteran Vol. 3 No. 1 (2025): Januari : Termometer: Jurnal Ilmiah Ilmu Kesehatan dan Kedokteran
Publisher : Lembaga Pengembangan Kinerja Dosen

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.55606/termometer.v3i1.4801

Abstract

Dementia is a complex neurodegenerative syndrome characterized by cognitive decline, including memory impairment, difficulty in thinking, and social interaction, which can affect daily activities. This condition is often caused by other diseases, including Alzheimer’s disease, vascular dementia, Lewy body dementia, and frontotemporal dementia, each with unique pathological mechanisms. Alzheimer’s disease, the leading cause of dementia, involves the accumulation of beta-amyloid plaques and tau tangles that disrupt neuronal function and trigger chronic inflammation. Vascular dementia results from impaired blood flow to the brain, while Lewy body dementia is associated with the misfolding of alpha-synuclein protein. Meanwhile, frontotemporal dementia is linked to the accumulation of tau or TDP-43 proteins, causing degeneration of the frontal and temporal lobes. Aging is the primary risk factor for dementia through the process of inflammaging, a low-grade chronic inflammation caused by persistent activation of the immune system. Inflammaging accelerates neurodegeneration by increasing oxidative stress, mitochondrial dysfunction, and the accumulation of pathological proteins. Additionally, neuroinflammation plays a crucial role by over activating microglia, which exacerbates neuronal damage. The combination of inflammation as both a trigger and a consequence create a pathological cycle that accelerates the progression of dementia. Preventive strategies include managing modifiable risk factors such as hypertension, diabetes, obesity, and adopting a healthy lifestyle, alongside developing therapies targeting inflammaging and neuroinflammation. A deeper understanding of these pathophysiological and inflammatory mechanisms is essential to support the development of multidisciplinary interventions to reduce the global burden of dementia.
Co-Authors Sidarta, Erick Triyana Sari