Jasbir Bisht
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Jasbir Bisht has a total of 3 co-authors. Here are the top co-authors by number of shared publications:
- Andrew C. Shin
Neurobiology of Nutrition Laboratory, Department of Nutritional Sciences, College of Health & Human Sciences, Texas Tech University, Lubbock, TX, 79409
1 shared publication - Priyanka Rawat
Obesity and Metabolic Health Laboratory, Department of Nutritional Sciences, Texas Tech University, Lubbock, TX 79409, USA
1 shared publication - Vijay Hegde
Department of Nutritional Sciences, Texas Tech University, Lubbock, USA
1 shared publication
Latest Publications
- Open Access
Mitochondrial Dysfunction in Alzheimer’s Disease and Mitochondria-Targeted Therapeutics
Alzheimer’s disease (AD) is the most prevalent form of dementia and is characterized by progressive cognitive decline due to the loss of neurons. The accumulation of extracellular senile plaques (Aβ) and intracellular tau neurofibrillary tangles (NFTs) is a key pathological feature of AD. Mitochondrial dysfunction is implicated in all key AD pathologies, whether as a cause or a consequence of disease progression. Growing evidence indicates that mitochondrial impairment plays a central role in AD pathogenesis by disrupting cellular homeostasis, promoting oxidative stress, and contributing to progressive neuronal death. Therefore, targeting mitochondria may offer promising insights into the development of disease-modifying therapies. In this review, we summarize current evidence on the role of mitochondrial dysfunction in the pathophysiology of AD and on its therapeutic potential.
Open AccessMitochondrial Dysfunction in Alzheimer’s Disease and Mitochondria-Targeted Therapeutics
Alzheimer’s disease (AD) is the most prevalent form of dementia and is characterized by progressive cognitive decline due to the loss of neurons. The accumulation of extracellular senile plaques (Aβ) and intracellular tau neurofibrillary tangles (NFTs) is a key pathological feature of AD. Mitochondrial dysfunction is implicated in all key AD pathologies, whether as a cause or a consequence of disease progression. Growing evidence indicates that mitochondrial impairment plays a central role in AD pathogenesis by disrupting cellular homeostasis, promoting oxidative stress, and contributing to progressive neuronal death. Therefore, targeting mitochondria may offer promising insights into the development of disease-modifying therapies. In this review, we summarize current evidence on the role of mitochondrial dysfunction in the pathophysiology of AD and on its therapeutic potential.