Knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of Alzheimer’s disease DOI Creative Commons

Deepak Prasad Gupta,

Young‐Sun Lee, Youngshik Choe

et al.

Molecular Brain, Journal Year: 2023, Volume and Issue: 16(1)

Published: Jan. 2, 2023

Abstract Knee osteoarthritis (OA) is characterized by knee cartilage degeneration and secondary bone hyperplasia, resulting in pain, stiffness, gait disturbance. The relationship between OA neurodegenerative diseases still unclear. This study used an Alzheimer’s disease (AD) mouse model to observe whether accelerates dementia progression analyzing brain histology neuroinflammation. was induced destabilizing the medial meniscus (DMM) control (WT) AD (5xFAD) mice before pathological symptoms. Mouse joints were scanned with a micro-CT scanner. A sham operation as control. Motor cognitive abilities tested after induction. Neurodegeneration, β-amyloid plaque formation, neuroinflammation analyzed immunostaining, Western blotting, RT-PCR tissues. Compared controls, increased inflammatory cytokine levels Furthermore, significantly deposition neuronal loss compared controls. In conclusion, accelerated amyloid neurodegeneration AD-OA mice, suggesting that risk factor for AD.

Language: Английский

The Potential Benefits of Nanotechnology in Treating Alzheimer’s Disease DOI Creative Commons
Tan Sook Ling,

Shanthini Chandrasegaran,

Zhi Xuan Low

et al.

BioMed Research International, Journal Year: 2021, Volume and Issue: 2021, P. 1 - 9

Published: July 4, 2021

Alzheimer’s disease is a neurodegenerative disorder that caused by the accumulation of beta-amyloid plaques in brain. Currently, there no definitive cure available to treat disease. The medication market has ability only slow down its progression. However, nanotechnology shown superiority can be applied for medical usage and it great potential therapy disease, specifically diagnosis providing an alternative approach This done increasing efficiency drug delivery penetrating overcoming blood-brain barrier. Having said that, are limitations need further investigated researched order minimize adverse effects toxicity improve bioavailability. recent advances treatment using include regeneration stem cells, nanomedicine, neuroprotection. In this review, we will discuss advancement which helps disorders such as well challenges.

Language: Английский

Citations

44

Mechanistic roles for altered O-GlcNAcylation in neurodegenerative disorders DOI
Aaron T. Balana, Matthew R. Pratt

Biochemical Journal, Journal Year: 2021, Volume and Issue: 478(14), P. 2733 - 2758

Published: July 23, 2021

Neurodegenerative diseases such as Alzheimer's and Parkinson's remain highly prevalent incurable disorders. A major challenge in fully understanding combating the progression of these is complexity network processes that lead to progressive neuronal dysfunction death. An ideal therapeutic avenue conceivably one could address many if not all multiple misregulated mechanisms. Over years, chemical intervention for up-regulation endogenous posttranslational modification (PTM) O-GlcNAc has been proposed a potential strategy slow down neurodegeneration. Through development application tools allow dissection mechanistic roles this PTM, there now growing body evidence influences variety important neurodegeneration-pertinent mechanisms, with an overall protective effect. As PTM appended onto numerous proteins participate protein quality control homeostasis, metabolism, bioenergetics, communication, inflammation, programmed death, demonstrated beneficence animal models neurodegenerative diseases, its being pursued clinical studies.

Language: Английский

Citations

42

Coconut oil as a therapeutic treatment for alzheimer's disease: a review DOI Creative Commons

Poorni Sandupama,

Dilusha Munasinghe,

Madhura Jayasinghe

et al.

Journal of Future Foods, Journal Year: 2022, Volume and Issue: 2(1), P. 41 - 52

Published: March 1, 2022

The coconut tree (Cocos nucifera) which is also known as the "Tree of life" has its own values in each part and oil more prestigious among them. At present, consumption booming all around world owing to tremendous health benefits. unique chemical composition enriched with medium chain fatty acids (MCFAs) led exploration these nutritional therapeutic influences. Unlike long (LCFAs), MCFAs generated from digestion triglycerides (MCTs) a specific pathway for metabolism, it bypasses lymphatic system enter liver directly through portal vein. Due such distinct attributes absorption MCTs are readily capable forming ketone bodies than other triglycerides. These competent energy source brains, especially those having cognitive impairments like Alzheimer's disease (AD). AD neurodegenerative characterized clinically by accelerating shortfalls memory behavioral changes. principal biochemical hallmarks behind pathogenesis development extracellular amyloid β plaques accumulation intracellular neurofibrillary tangles. Occurrence Cardiovascular diseases (CVD) elevated LDL levels, hypertension, Type 2 diabetes, obesity, insulin resistance some key risk factors that responsible increasing prevalence incidence AD. There sufficient evidence prove metabolized absorbed way retards severity physiological factors. Besides, endowed many polyphenolic compounds serving antioxidants combating oxidative stress inflammation, turn downregulates etiology But depending on different processing conditions applied extraction techniques oil, variations antioxidant capacity can take place. Even though there inadequacies peer-reviewed large cohort clinical data run, this article reviews constituents, metabolism have positive findings potentiality treat supplement.

Language: Английский

Citations

35

Methamphetamine induced neurotoxic diseases, molecular mechanism, and current treatment strategies DOI Open Access

Prabhat Shrestha,

Nikita Katila, Sooyeun Lee

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2022, Volume and Issue: 154, P. 113591 - 113591

Published: Aug. 22, 2022

Methamphetamine (MA) is a extremely addictive psychostimulant drug with significant abuse potential. Long-term MA exposure can induce neurotoxic effects through oxidative stress, mitochondrial functional impairment, endoplasmic reticulum the activation of astrocytes and microglial cells, axonal transport barriers, autophagy, apoptosis. However, molecular cellular mechanisms underlying MA-induced neurotoxicity remain unclear. increases chances developing conditions such as Parkinson's disease (PD), Alzheimer's (AD) other diseases. risk PD by increasing expression alpha-synuclein (ASYN). Furthermore, linked to high AD subsequent neurodegeneration due biological variations in brain region or genetic epigenetic variations. To date, there no Food Drug Administration (FDA)-approved therapy for neurotoxicity, although many studies are being conducted develop effective therapeutic strategies. Most current now focused on therapies diminish MA, based mechanism neurotoxicity. This review article highlights research several techniques targeting multiple pathways reduce brain, well putative

Language: Английский

Citations

34

Knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of Alzheimer’s disease DOI Creative Commons

Deepak Prasad Gupta,

Young‐Sun Lee, Youngshik Choe

et al.

Molecular Brain, Journal Year: 2023, Volume and Issue: 16(1)

Published: Jan. 2, 2023

Abstract Knee osteoarthritis (OA) is characterized by knee cartilage degeneration and secondary bone hyperplasia, resulting in pain, stiffness, gait disturbance. The relationship between OA neurodegenerative diseases still unclear. This study used an Alzheimer’s disease (AD) mouse model to observe whether accelerates dementia progression analyzing brain histology neuroinflammation. was induced destabilizing the medial meniscus (DMM) control (WT) AD (5xFAD) mice before pathological symptoms. Mouse joints were scanned with a micro-CT scanner. A sham operation as control. Motor cognitive abilities tested after induction. Neurodegeneration, β-amyloid plaque formation, neuroinflammation analyzed immunostaining, Western blotting, RT-PCR tissues. Compared controls, increased inflammatory cytokine levels Furthermore, significantly deposition neuronal loss compared controls. In conclusion, accelerated amyloid neurodegeneration AD-OA mice, suggesting that risk factor for AD.

Language: Английский

Citations

22