Neurodegeneration is a term used to describe progressive deterioration of structure and/or function of neurons that affects different parts of the central nervous system and leads to eventual death. Neurodegenerative diseases include Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and Down's syndrome (DS), multiple sclerosis (MS), glaucoma, age-related macular degeneration (AMD), and diabetic encephalopathy (DE). Although the initial events that trigger these disorders may be different from each other, they share similar biochemical reactions that lead to neurodegeneration. Curcuminoids, polyphenol compounds from turmeric (Curcuma longa), possess diverse biological properties that modulate debilitating biochemical processes involved in AD that include attenuation of mitochondrial dysfunction-induced oxidative stress and inflammatory responses to inflammatory cytokines, COX-2, and iNOS. Curcuminoids also bind to β-amyloid (Aβ) plaques to inhibit amyloid accumulation and aggregation in the brain, in addition to inhibiting the toxic Aβ oligomer formation and oligomer-dependent Aβ toxicity. These properties can be further elaborated to DS, glaucoma and AMD. Curcuminoids also prevent α-synuclein aggregation in PD; attenuate ROS-induced COX-2 expression in ALS; ameliorate the symptoms of MS, DE and traumatic brain injury, in addition to neurodamages caused by heavy metal poisoning. These results demonstrate curcuminoids may be potentially effective therapeutic means to treat neurodegenerative diseases. A bulk of patents discloses methods to improve bioavailability of curcuminoids for therapeutic development. This review provides a comprehensive description on the current progress on curcuminoids against neurodegenerative diseases.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.2174/157488912803252032 | DOI Listing |
Curr Top Med Chem
January 2025
Graphic Era (Deemed to be University), Clement Town Dehradun, India.
Alzheimer's Disease (AD), a progressive neurodegenerative disorder, is characterized by the accumulation of neurofibrillary tangles and β-amyloid plaques, leading to a decline in cognitive function. AD is characterized by tau protein hyperphosphorylation and extracellular β-amyloid accumulation. Even after much research, there are still no proven cures for AD.
View Article and Find Full Text PDFCurr Treat Options Neurol
July 2024
Department of Neurology, Division of Behavioral Neurology, Stanford Neuroscience Health Center, 453 Quarry Road, Palo Alto, CA 94304, USA.
Purpose Of Review: The purpose of this review is to discuss the clinical, radiological, and neuropathological heterogeneity of corticobasal syndrome (CBS), which can complicate the determination of underlying etiology and lead to inaccurate treatment decisions. Though the most common diagnosis is corticobasal degeneration (CBD), the spectrum of underlying pathologies expands beyond CBD and can overlap with other neurodegenerative diseases and even the neuroimmunology field. We will review possible clinical presentations and cues that can point towards the etiology.
View Article and Find Full Text PDFAlzheimers Dement (Amst)
January 2025
Weill Institute for Neurosciences, Department of Neurology, Memory and Aging Center University of California, San Francisco San Francisco California USA.
Introduction: Plasma amyloid beta/amyloid beta (Aβ/Aβ) and phosphorylated tau217 (p-tau217) identify individuals with primary Alzheimer's disease (AD). They may detect AD co-pathology in the setting of other primary neurodegenerative diseases, but this has not been systematically studied.
Methods: We compared the clinical, neuroimaging, and neuropathological associations of plasma Aβ/Aβ (mass spectrometry), p-tau217 (electrochemiluminescence), and neurofilament light ([NfL], single molecule array [Simoa]), as markers of AD co-pathology, in a sporadic frontotemporal dementia (FTD) cohort ( = 620).
Alzheimers Dement (Amst)
January 2025
Introduction: Increasing evidence links amyloid beta (Aβ) aggregation with inflammation. This pilot study investigated the use of an immunoassay panel to map biomarker changes in patients with Alzheimer's disease (AD). Furthermore, we evaluated the stability of protein quantification after multiple freeze-thaw cycles (FTCs).
View Article and Find Full Text PDFExpert Opin Drug Discov
January 2025
Geriatric Neuropsychiatry Division, The Glenn Biggs Institute for Alzheimer's & Neurodegenerative Diseases, Lozano Long School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Introduction: A substantial number of patients exhibit treatment-resistant depression (TRD), posing significant challenges to clinicians. The discovery of novel molecules or mechanisms that may underlie TRD pathogenesis and antidepressant actions are highly needed.
Areas Covered: Using the PubMed database, the authors searched for emerging evidence of novel approaches for TRD based on experimental and human studies.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!