Neurobiological Mechanisms of Cognitive Decline Correlated with Brain Aging.

Cognitive decline has emerged as one of the greatest health threats of old age. Meanwhile, aging is the primary risk factor for Alzheimer's disease (AD) and other prevalent neurodegenerative disorders. Developing therapeutic interventions for such conditions demands a greater understanding of the processes underlying normal and pathological brain aging.

Biomolecular Markers of Brain Aging.

Characterized by the gradual loss of physiological integrity, impaired function, and increased susceptibility to death, aging is considered the primary risk factor for major human diseases, such as cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. The time-dependent accumulation of cellular damage is widely considered the general cause of aging. While the mechanism of normal aging is still unresolved, researchers have identified different markers of aging, including genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication.

Scutellarin Modulates the Microbiota-Gut-Brain Axis and Improves Cognitive Impairment in APP/PS1 Mice.

Background: Scutellarin, a flavonoid purified from the Chinese herb Erigeron breviscapus, has been reported to prevent Alzheimer's disease (AD) by affecting Aβ assembly. Given the low brain uptake rate of scutellarin, we hypothesize that the microbiota-gut-brain axis may be a potential route by which scutellarin prevents AD.

Objective: This study aimed to explore the microbiota-gut-brain mechanism by which scutellarin prevented AD.

Dengzhanxixin Injection Ameliorates Cognitive Impairment Through a Neuroprotective Mechanism Based on Mitochondrial Preservation in Patients With Acute Ischemic Stroke.

Acute ischemic stroke (AIS) is a global health burden and cognitive impairment is one of its most serious complication. Adequate interventions for AIS may have the potential to improve cognitive outcomes. In the present study, we selected (Vaniot) Hand.

Shenqi Yizhi granules protect hippocampus of AD transgenic mice by modulating on multiple pathological processes.

Ethnopharmacological Relevance: Chinese herbal medicine (CHM) draws more attention to explore effective therapeutic strategy for Alzheimer's disease (AD). CHM usually uses combinations of herbs or herbal ingredients to treat diseases, with the components targeting different disease processes. CHM might improve cognition in AD and MCI patients by optimizing network activity, promoting neural plasticity and repairing damaged neurons.

Dengzhan Shengmai capsules and their active component scutellarin prevent cognitive decline in APP/PS1 mice by accelerating Aβ aggregation and reducing oligomers formation.

There is currently no effective treatment to prevent the progress of Alzheimer's disease (AD). The traditional Chinese herbs Dengzhan Shengmai (DZSM) capsules and their active component scutellarin possess multiple effects and are clinically used for the treatment of cerebrovascular diseases. Scutellarin has been reported to affect Aβ aggregation.

SQYZ granules, a traditional Chinese herbal, attenuate cognitive deficits in AD transgenic mice by modulating on multiple pathogenesis processes.

The pathogenesis of Alzheimer's disease (AD) involves multiple contributing factors, including amyloid β (Aβ) peptide aggregation, inflammation, oxidative stress, and others. Effective therapeutic drugs for treating AD are urgently needed. SQYZ granules (SQYZ), a Chinese herbal preparation, are mainly composed of the ginsenoside Rg1, astragaloside A and baicalin, and have been widely used to treat dementias for decades in China.

Gamma rhythm low field magnetic stimulation alleviates neuropathologic changes and rescues memory and cognitive impairments in a mouse model of Alzheimer's disease.

Introduction: The abnormal amyloid β (Aβ) accumulation and Aβ-related neural network dysfunction are considered central to the pathogenesis of Alzheimer's disease (AD) at the early stage. Deep-brain reachable low field magnetic stimulation (DMS), a novel noninvasive approach that was designed to intervene the network activity in brains, has been found to alleviate stress-related cognitive impairments.

Methods: Amyloid precursor protein/presenilin-1 transgenic mice (5XFAD) were treated with DMS, and cognitive behavior and AD-like pathologic changes in the neurochemical and electrophysiological properties in 5XFAD mice were assessed.

Deep Brain Magnetic Stimulation Promotes Neurogenesis and Restores Cholinergic Activity in a Transgenic Mouse Model of Alzheimer's Disease.

Alzheimer's disease (AD) is characterized by progressive decline of memory and cognitive functions. Deep magnetic stimulation (DMS), a noninvasive and nonpharmacological brain stimulation, has been reported to alleviate stress-related cognitive impairment in neuropsychiatric disorders. Our previous study also discovered the preventive effect of DMS on cognitive decline in an AD mouse model.

The E3 Ubiquitin Ligase c-Cbl Inhibits Microglia-Mediated CNS Inflammation by Regulating PI3K/Akt/NF-κB Pathway.

Background: Microglia-mediated inflammation may play an important role in the pathophysiology progression of neurodegenerative diseases, such as Parkinson's disease (PD), but the molecular mechanisms are poorly understood.

Aims: This study sought to determine whether E3 ubiquitin ligase c-Cbl plays a role in the brain inflammation and to explore the relevant molecular mechanism.

Methods: After BV2 microglial cells and c-Cbl-deficient mice were treated with lipopolysaccharide (LPS), neuroinflammation and microglial activation were evaluated by immunohistochemistry, ELISA and Western blot.

Triptolide treatment reduces Alzheimer's disease (AD)-like pathology through inhibition of BACE1 in a transgenic mouse model of AD.

The complex pathogenesis of Alzheimer's disease (AD) involves multiple contributing factors, including amyloid β (Aβ) peptide accumulation, inflammation and oxidative stress. Effective therapeutic strategies for AD are still urgently needed. Triptolide is the major active compound extracted from Tripterygium wilfordii Hook.

Therapeutic effects of fucoidan in 6-hydroxydopamine-lesioned rat model of Parkinson's disease: Role of NADPH oxidase-1.

Aims: To explore the effect of fucoidan treatment on oxidative stress-mediated dopaminergic neuronal damage and its potential mechanisms.

Methods: The effect of fucoidan was investigated in a 6-hydroxydopamine (6-OHDA) rat model of PD, an animal model considered appropriate for preclinical studies of PD therapy. The effects of fucoidan treatment on animal behavior and the survival ratio of dopaminergic neurons were investigated.