neuroinflamation

Reducing neuroinflammation via therapeutic compounds and lifestyle to prevent or delay progression of Parkinson’s disease.Prevention of neuroinflammation in Parkinson’s disease

Diet and Exercise, Fasting, Parkinson's Disease, Therapies /

Parkinson’s disease (PD) is the second most common age-associated neurodegenerative disorder and is characterized by progressive loss of dopamine neurons in the substantia nigra. Peripheral immune cell infiltration and activation of microglia and astrocytes are observed in PD, a process called neuroinflammation. Neuroinflammation is a fundamental response to protect the brain but, when chronic, it […]

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Impact of Two Neuronal Sigma-1 Receptor Modulators, PRE084
and DMT, on Neurogenesis and Neuroinflammation in an
Aβ1-42-Injected, Wild-Type Mouse Model of AD

Ayahuasca, Parkinson's Disease /

Alzheimer’s disease (AD) is the most common form of dementia characterized by cognitivedysfunctions. Pharmacological interventions to slow the progression of AD are intensively studied. Apotential direction targets neuronal sigma-1 receptors (S1Rs). S1R ligands are recognized as promisingtherapeutic agents that may alleviate symptom severity of AD, possibly via preventing amyloid-β-(Aβ-) induced neurotoxicity on the endoplasmic reticulum

Impact of Two Neuronal Sigma-1 Receptor Modulators, PRE084
and DMT, on Neurogenesis and Neuroinflammation in an
Aβ1-42-Injected, Wild-Type Mouse Model of AD Read More »

The Complement System in the Central Nervous System:
From Neurodevelopment to Neurodegeneration

Uncategorized /

The functions of the complement system to both innate and adaptive immunity throughopsonization, cell lysis, and inflammatory activities are well known. In contrast, the role of complement in the central nervous system (CNS) which extends beyond immunity, is only beginning to berecognized as important to neurodevelopment and neurodegeneration. In addition to protecting thebrain against invasive

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From Neurodevelopment to Neurodegeneration Read More »

Neuroinflammation as a Common Mechanism Associated with the Modifiable Risk Factors for Alzheimer’s and Parkinson’s Diseases

Parkinson's Disease /

Alzheimer’s Disease (AD) and Parkinson’s Disease (PD) are among the most common causes of dementia, which increasingly contribute to morbidity and mortality worldwide. A common hallmark in the pathogenesis of these two diseases is neuroinflammation, which is initially triggered by the presence of pathological structures associated with these disorders. Chronic neuroinflammation is sustained by persistent

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Overview on Parkinson’s disease: pathophysiology, and experimental models

Parkinson's Disease /

Parkinson’s disease, a neurodegenerative disease, is caused by dopaminergic neurons death and accompanied byrigidity, and postural instability, as well as bradykinesia. The cause of these neurons’ death is still unclear. Since thedopaminergic neurons couldn’t regenerate, therefore Parkinson’s disease couldn’t be cured. Thus, over the pastdecades, significant effort has been made to explore the etiology of

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Bioactive lipids and their metabolism: new therapeutic opportunities for Parkinson’s disease

A-Synuclein, Dementia - Lewy Bodies, Non-Motor Symptoms, Parkinson's Disease, Pre-PD /

Parkinson’s disease (PD) is a neurological disorder characterized by motor dysfunction, which can also be associated with non-motor symptoms. Its pathogenesis is thought to stem from a loss of dopaminergic neurons in the substantia nigra pars compacta and the formation of Lewy bodies containing aggregated α-synuclein. Recent works suggested that lipids might play a pivotal

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Gram-negative bacteria and their lipopolysaccharides in Alzheimer’s disease: pathologic roles and therapeutic implications

Lipopolysaccharides (LPS) /

Alzheimer’s disease (AD) is the most serious age-related neurodegenerative disease and causes destructive and irreversible cognitive decline. Failures in the development of therapeutics targeting amyloid-β (Aβ) and tau, principal proteins inducing pathology in AD, suggest a paradigm shift towards the development of new therapeutic targets. The gram-negative bacteria and lipopolysaccharides (LPS) are attractive new targets

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Beta Amyloid, Tau Protein, and Neuroinflammation: An Attempt to Integrate Different Hypotheses of Alzheimer’s Disease Pathogenesis

Biomarkers /

Alzheimer’s disease (AD) is a neurodegenerative disease that inevitably results in dementia and death. Currently, there are no pathogenetically grounded methods for the prevention and treatment of AD, and all current treatment regimens are symptomatic and unable to significantly delay the development of dementia. The accumulation of β-amyloid peptide (Aβ), which is a spontaneous, aggregation-prone,

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Modulation of Neuroinflammation by the Gut Microbiota in Prion and Prion-Like Diseases

Gut Dysbiosis, Gut Microbiota, Mitochondria, Parkinson's Disease, Pre-PD /

One fundamental component of systemic homeostasis is the gut microbiota, which communicates withthe CNS via microbial metabolite production, the peripheral nervous system, and regulation oftryptophan metabolism. Over the past 10–15 years, research focused on the microbiota–gut–brainaxis has culminated in the discovery that dysbiosis, or an imbalance between commensal andpathogenic gut bacteria, can promote CNS pathologies.

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The role of oxidative stress and the underlying biological pathways in the pathogenesis of Parkinson’s Disease

Anti-oxidants, Mitochondria /

The mechanisms involved in pathogenesis and progression ofPD is not fully understood but there is overwhelming evidence thatmaintenance of redox potential is important for neuronal survival.Any disruption in the mitochondrial potential disrupts the cellularhomeostasis, which in turn causes more ROS production leadingto neuroinflammation and degeneration. The review attempts toconsolidate key signaling pathways, and proteins that

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