PSAPP mice expressing the 'Swedish' amyloid precursor protein and the M146L presenilin 1 mutations are a well-characterized model for spontaneous amyloid beta plaque formation. Centella asiatica has a long history of use in India as a memory enhancing drug in Ayurvedic literature. The study investigated whether Centella asiatica extract (CaE) can alter the amyloid pathology in PSAPP mice by administering CaE (2.5 or 5.0 g/kg/day) starting at 2 months of age prior to the onset of detectable amyloid deposition and continued for either 2 months or 8 months. A significant decrease in amyloid beta 1-40 and 1-42 was detectable by ELISA following an 8 month treatment with 2.5 mg/kg of CaE. A reduction in Congo Red stained fibrillar amyloid plaques was detected with the 5.0 mg/kg CaE dose and long-term treatment regimen. It was also confirmed that CaE functions as an antioxidant in vitro, scavenging free radicals, reducing lipid peroxidation and protecting against DNA damage. The data indicate that CaE can impact the amyloid cascade altering amyloid beta pathology in the brains of PSAPP mice and modulating components of the oxidative stress response that has been implicated in the neurodegenerative changes that occur with Alzheimer's disease.
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http://dx.doi.org/10.1002/ptr.2405 | DOI Listing |
Geroscience
January 2025
Psychology, School of Social Sciences, Nanyang Technological University, 48 Nanyang Avenue S639818, Singapore, Singapore.
In Alzheimer's disease (AD), the accumulation of neuropathological markers such as amyloid-β plaques, neurofibrillary tangles, and cortical neurodegeneration occurs over many years before overt manifestation of cognitive impairment. There is thus a need for neuropsychological markers that are indicative of pathological changes in the early stages of the disease. Intra-individual cognitive variability (IICV), defined as the variation of an individual's performance across cognitive domains, is a promising neuropsychological marker measuring heterogeneous changes in cognition that may reflect these early pathological changes.
View Article and Find Full Text PDFMol Divers
January 2025
Department of Biophysics, Panjab University, Chandigarh, 160014, India.
Alzheimer's disease (AD) is a degenerative neurological disorder defined by the formation of β-amyloid (Aβ) plaques and neurofibrillary tangles within the brain. Current pharmacological treatments for AD only provide symptomatic relief, and there is a lack of definitive disease-modifying therapies. Chemical chaperones, such as 4-Phenylbutyric acid (4PBA) and Tauroursodeoxycholic acid, have shown neuroprotective effects in animal and cell culture models.
View Article and Find Full Text PDFJ Alzheimers Dis
January 2025
Department of General Internal Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Background: Alzheimer's disease (AD) is an irreversible age-related neurodegenerative condition characterized by the deposition of amyloid-β (Aβ) peptides and neurofibrillary tangles. Di Huang Yi Zhi (DHYZ) formula, a traditional Chinese herbal compound comprising several prescriptions, demonstrates properties that improve cognitive abilities in clinical. Nonetheless, its molecular mechanisms on treating AD through improving neuron cells mitochondria function have not been deeply investigated.
View Article and Find Full Text PDFAnal Chem
January 2025
State Key Laboratory of Chemical Resource Engineering, College of Chemistry, Beijing University of Chemical Technology, Beijing 100029, China.
The spontaneous aggregation of amyloid-β (Aβ) leads to neuronal cell death in the brain and causes the development of Alzheimer's disease (AD). The efficient detection of the aggregation state of Aβ holds significant promise for the early diagnosis and subsequent treatment of this neurodegenerative disorder. Currently, most of the fluorescent probes used for the detection of Aβ fibrils share similar recognition moieties, such as the ,-dimethylamino group, ,-diethylamino group, and piperidyl group.
View Article and Find Full Text PDFCurr Top Med Chem
January 2025
Department of Histology and Embryology, School of Basic Medicine, Hengyang Medical School, University of South China, Hengyang, 421001, China.
In recent years, an increasing number of studies have shown that increased activation of aspartic endopeptidases (AEPs) is a common symptom in neurodegenerative diseases (NDDs). AEP cleaves amyloid precursor protein (APP), tau (microtubule-associated protein tau), α- synuclein (α-syn), SET (a 39-KDa phosphoprotein widely expressed in various tissues and localizes predominantly in the nucleus), and TAR DNA-binding protein 43 (TDP-43), and promotes their aggregation, contributing to Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), and frontotemporal dementia (FTD) pathogenesis. Abundant evidence supports the notion that CCAAT/enhancer-binding protein β (C/EBPβ)/AEP may play an important role in NDDs.
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