Neuroprotective Mechanisms of Salidroside in Alzheimer’s Disease: A Systematic Review and Meta-analysis of Preclinical Studies DOI
Nan Zhang, Jianfei Nao, Xiaoyu Dong

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2023, Volume and Issue: 71(46), P. 17597 - 17614

Published: Nov. 7, 2023

Alzheimer's disease (AD) is a neurodegenerative of the central nervous system that occurs in old age and pre-aging, characterized by progressive cognitive dysfunction behavioral impairment. Salidroside (Sal) phenylpropanoid mainly isolated from Rhodiola species with various pharmacological effects. However, exact anti-AD mechanism Sal has not been clearly elucidated. This meta-analysis aims to investigate possible mechanisms which exerts its effects evaluating indicators biochemical characteristics. A total 20 studies were included, results showed treatment significantly improved behavior abnormalities AD animal models. With regard neurobiochemical indicators, could effectively increase antioxidant enzyme superoxide dismutase, decrease oxidative stress indicator malondialdehyde, inflammatory interleukin 1β, 6, tumor necrosis factor α. was effective reducing neuropathological such as amyloid-β levels number apoptotic cells. When relevant literature on rodent models combined Sal, therapeutic potential through multiple confirmed. further confirmation higher quality studies, larger sample sizes, more comprehensive outcome evaluations clinical trials needed future.

Language: Английский

From imbalance to impairment: the central role of reactive oxygen species in oxidative stress-induced disorders and therapeutic exploration DOI Creative Commons
Sheryar Afzal, Aimi Syamima Abdul Manap, Ali Attiq

et al.

Frontiers in Pharmacology, Journal Year: 2023, Volume and Issue: 14

Published: Oct. 18, 2023

Increased production and buildup of reactive oxygen species (ROS) can lead to various health issues, including metabolic problems, cancers, neurological conditions. Our bodies counteract ROS with biological antioxidants such as SOD, CAT, GPx, which help prevent cellular damage. However, if there is an imbalance between these antioxidants, it result in oxidative stress. This cause genetic epigenetic changes at the molecular level. review delves into how plays a role disorders caused by We also look animal models used for researching pathways. study offers insights mechanism, pathology, changes, assist drug development disease understanding.

Language: Английский

Citations

116
Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease DOI
Marzia Perluigi, Fabio Di Domenico, D. Allan Butterfield

et al.

Physiological Reviews, Journal Year: 2023, Volume and Issue: 104(1), P. 103 - 197

Published: Oct. 16, 2023

Alzheimer disease (AD) is associated with multiple etiologies and pathological mechanisms, among which oxidative stress (OS) appears as a major determinant. Intriguingly, OS arises in various pathways regulating brain functions, it seems to link different hypotheses mechanisms of AD neuropathology high fidelity. The particularly vulnerable damage, mainly because its unique lipid composition, resulting an amplified cascade redox reactions that target several cellular components/functions ultimately leading neurodegeneration. present review highlights the “OS hypothesis AD,” including amyloid beta-peptide-associated role protein oxidation unraveled by proteomics, antioxidant strategies have been investigated modulate progression AD. Collected studies from our groups others contributed unraveling close relationships between perturbation homeostasis elucidating redox-regulated events potentially involved both pathogenesis However, complexity requires in-depth understanding intracellular affecting relevant for functions. This crucial developing pharmacological targeting OS-mediated toxicity may contribute slow well improve quality life persons this severe dementing disorder.

Language: Английский

Citations

77
Oxidative stress, inflammation and hormesis: The role of dietary and lifestyle modifications on aging DOI
Vinita Sharma, Mohammad Murtaza Mehdi

Neurochemistry International, Journal Year: 2023, Volume and Issue: 164, P. 105490 - 105490

Published: Jan. 24, 2023

Language: Английский

Citations

59
Mitochondrial Dysfunction in Neurodegenerative Diseases: Mechanisms and Corresponding Therapeutic Strategies DOI Creative Commons
Kai Meng, Hongyun Jia,

Xiaoqing Hou

et al.

Biomedicines, Journal Year: 2025, Volume and Issue: 13(2), P. 327 - 327

Published: Jan. 31, 2025

Neurodegenerative disease (ND) refers to the progressive loss and morphological abnormalities of neurons in central nervous system (CNS) or peripheral (PNS). Examples neurodegenerative diseases include Alzheimer's (AD), Parkinson's (PD), amyotrophic lateral sclerosis (ALS). Recent studies have shown that mitochondria play a broad role cell signaling, immune response, metabolic regulation. For example, mitochondrial dysfunction is closely associated with onset progression variety diseases, including ND, cardiovascular diabetes, cancer. The energy metabolism, imbalance dynamics, abnormal mitophagy can lead homeostasis, which induce pathological reactions such as oxidative stress, apoptosis, inflammation, damage system, participate occurrence development degenerative AD, PD, ALS. In this paper, latest research progress subject detailed. mechanisms mitophagy-mediated ND are reviewed from perspectives β-amyloid (Aβ) accumulation, dopamine neuron damage, superoxide dismutase 1 (SOD1) mutation. Based on mechanism research, new ideas methods for treatment prevention proposed.

Language: Английский

Citations

2
8-Hydroxyquinolylnitrones as multifunctional ligands for the therapy of neurodegenerative diseases DOI Creative Commons
Damijan Knez, Daniel Diez‐Iriepa, Mourad Chioua

et al.

Acta Pharmaceutica Sinica B, Journal Year: 2023, Volume and Issue: 13(5), P. 2152 - 2175

Published: Jan. 19, 2023

We describe the development of quinolylnitrones (QNs) as multifunctional ligands inhibiting cholinesterases (ChEs: acetylcholinesterase and butyrylcholinesterase-hBChE) monoamine oxidases (hMAO-A/B) for therapy neurodegenerative diseases. identified QN 19, a simple, low molecular weight nitrone, that is readily synthesized from commercially available 8-hydroxyquinoline-2-carbaldehyde. Quinolylnitrone 19 has no typical pharmacophoric element to suggest ChE or MAO inhibition, yet unexpectedly showed potent inhibition hBChE (IC50 = 1.06 ± 0.31 nmol/L) hMAO-B 4.46 0.18 μmol/L). The crystal structures with provided structural basis binding, which was further studied by enzyme kinetics. Compound acted free radical scavenger biometal chelator, crossed blood-brain barrier, not cytotoxic, neuroprotective properties in 6-hydroxydopamine cell model Parkinson's disease. In addition, vivo studies anti-amnesic effect scopolamine-induced mouse AD without adverse effects on motoric function coordination. Importantly, chronic treatment double transgenic APPswe-PS1δE9 mice reduced amyloid plaque load hippocampus cortex female mice, underscoring disease-modifying 19.

Language: Английский

Citations

26
Immune Modulation in Alzheimer’s Disease: From Pathogenesis to Immunotherapy DOI Creative Commons
Sahar Balkhi,

Antimo Di Spirito,

Alessandro Poggi

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(4), P. 264 - 264

Published: Feb. 12, 2025

Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia, affecting significant proportion elderly population. AD characterized by cognitive decline functional impairments due to pathological hallmarks like amyloid β-peptide (Aβ) plaques neurofibrillary tangles (NFTs) composed hyperphosphorylated tau. Microglial activation, chronic neuroinflammation, disruptions in neuronal communication further exacerbate disease. Emerging research suggests that immune modulation could play key role treatment given involvement neuroinflammatory processes. This review focuses on recent advancements immunotherapy strategies aimed at modulating responses AD, with specific emphasis microglial behavior, clearance, tau pathology. By exploring these immunotherapeutic approaches, we aim provide insights into their potential alter progression improve patient outcomes, contributing evolving landscape treatment.

Language: Английский

Citations

1
Hormesis and Oxidative Distress: Pathophysiology of Reactive Oxygen Species and the Open Question of Antioxidant Modulation and Supplementation DOI Creative Commons
Mariapaola Nitti, Barbara Marengo, Anna Lisa Furfaro

et al.

Antioxidants, Journal Year: 2022, Volume and Issue: 11(8), P. 1613 - 1613

Published: Aug. 19, 2022

Alterations of redox homeostasis leads to a condition resilience known as hormesis that is due the activation redox-sensitive pathways stimulating cell proliferation, growth, differentiation, and angiogenesis. Instead, supraphysiological production reactive oxygen species (ROS) exceeds antioxidant defence oxidative distress. This induces damage biomolecules responsible or co-responsible for onset several chronic pathologies. Thus, dietary supplementation has been proposed in order prevent aging, cardiovascular degenerative diseases well carcinogenesis. However, this approach failed demonstrate efficacy, often leading harmful side effects, particular patients affected by cancer. In latter case, an based on endogenous depletion, ROS overproduction, shown interesting potential enhancing susceptibility anticancer therapies. Therefore, deep investigation molecular involved balance crucial identify new targets useful development more effective therapeutic approaches. The review herein provides overview pathophysiological role focuses attention positive negative aspects modulation with intent find insights successful clinical application.

Language: Английский

Citations

31
Oxidative Stress in Brain in Amnestic Mild Cognitive Impairment DOI Creative Commons
D. Allan Butterfield

Antioxidants, Journal Year: 2023, Volume and Issue: 12(2), P. 462 - 462

Published: Feb. 11, 2023

Amnestic mild cognitive impairment (MCI), arguably the earliest clinical stage of Alzheimer disease (AD), is characterized by normal activities daily living but with memory issues no dementia. Oxidative stress, consequent damaged key proteins and lipids, are prominent even in this early state AD. This review article outlines oxidative stress MCI how can account for neuronal loss potential therapeutic strategies to slow progression

Language: Английский

Citations

17
Non-invasive Biomarkers for Early Detection of Alzheimer’s Disease: a New-Age Perspective DOI
Niyamat M. A. Chimthanawala, Akash Haria, Sadhana Sathaye

et al.

Molecular Neurobiology, Journal Year: 2023, Volume and Issue: 61(1), P. 212 - 223

Published: Aug. 19, 2023

Language: Английский

Citations

17
Dementia and depression: Biological connections with amyloid β protein DOI Open Access
Helamã Moraes dos Santos, Amanda Gollo Bertollo, Maiqueli Eduarda Dama Mingoti

et al.

Basic & Clinical Pharmacology & Toxicology, Journal Year: 2024, Volume and Issue: 134(5), P. 563 - 573

Published: March 8, 2024

Dementia is an umbrella term for a broad group of age-associated neurodegenerative diseases. It estimated that dementia affects 50 million people worldwide and Alzheimer's disease (AD) responsible up to 75% cases. Small extracellular senile plaques composed filamentous aggregates amyloid β (Aβ) protein tend bind neuronal receptors, affecting cholinergic, serotonergic, dopaminergic noradrenergic neurotransmission, leading neuroinflammation, among other pathophysiologic processes subsequent death, followed by dementia. The cascade hypothesis points pathological process in the cleavage precursor (APP), resulting Aβ. There close relationship between pathologies lead depression. depression prevalent 90% individuals diagnosed with Parkinson's disease, varying severity, 20 30% cases disease. hypothalamic pituitary adrenal (HPA) axis great intermediary pathophysiological mechanisms diseases This review discusses role Aβ depression, considering HPA axis, oxidative stress, signalling pathways neurotransmission.

Language: Английский

Citations

7