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Objective: To observe the effects of modified Wuzi Yanzong Granule (WYG) on memory function and the activity of serum superoxide dismutase (SOD), malondialdehyde (MDA) levels, leukocyte mitochondrial DNA (mtDNA) deletion rate and beta-amyloid protein(1-28) (A beta(1-28)) in patients with mild cognitive impairment (MCI).
Methods: Thirty-six patients with MCI were selected based on the internationally recognized Petersen's criteria, and equally and randomly assigned to two groups. The treated group was treated with WYG and the control group was treated with placebo for 3 months. In addition, 20 healthy subjects were included in the study as the normal control group. Changes of memory function, SOD activity, MDA content, leukocyte mtDNA deletion rate and A beta(1-28) content were observed before and after treatment.
Results: Compared with the normal control group, the memory quotient and SOD activity in patients with MCI decreased significantly (P < 0.01), while MDA, A beta(1-28) levels and the leukocyte mtDNA deletion rate increased significantly (P < 0.01). After treatment, levels of memory quotient and serum SOD activity increased while the serum MDA level, leukocyte mtDNA deletion rate and A beta(1-28) level decreased in the treated group compared with those before treatment (P<0.01, P<0.05). Meanwhile, leukocyte mtDNA deletion rate and A beta(1-28) content in the treated group were all lower than those in the control group (P<0.05).
Conclusion: WYG could improve memory function in patients with MCI and the therapeutic mechanism is possibly related to the increased activity of anti-oxidase, the improved free radical metabolism and the alleviation of leukocyte mtDNA oxidation damage. WYG shows clinical significance in delaying the progression of MCI.
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http://dx.doi.org/10.1007/s11655-007-0258-7 | DOI Listing |
Immunity
August 2025
Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai 201210, China; State Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai 200032, China; Shanghai K
Neuroinflammation drives Alzheimer's disease (AD) pathogenesis. Z-DNA, a non-canonical left-handed DNA structure, activates innate immune signaling through Z-DNA-binding protein 1 (ZBP1). However, the functional significance of ZBP1-mediated Z-DNA detection in AD remains undefined.
View Article and Find Full Text PDFAnn Clin Transl Neurol
September 2025
Department of Neurology, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Objective: Cerebrospinal fluid (CSF) cell-free mitochondrial DNA (cf-mtDNA) is a potential biomarker for Parkinson's disease (PD), but its clinical relevance remains unclear. We investigated associations between CSF cf-mtDNA levels, body composition, nutritional status, and metabolic biomarkers in PD.
Methods: CSF cf-mtDNA levels, defined as the copy numbers of two regions of the mtDNA circular molecule (mt64-ND1 and mt96-ND5), were quantified in 44 PD patients and 43 controls using multiplex digital PCR.
Parasit Vectors
August 2025
Laboratório de Ultraestrutura Celular Hertha Meyer, Centro de Pesquisa em Medicina de Precisão (CPMP), Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro, Cidade Universitária, Rio de Janeiro, RJ, CEP 21941-590, Brazil.
Background: One of the most intriguing and unusual features of trypanosomatids is their mitochondrial DNA, known as kinetoplast DNA (kDNA), which is organized into a network of concatenated circles. The kDNA is contained within the mitochondrial matrix and can exhibit distinct arrangements across different species and during cell differentiation. In addition to kDNA, the kinetoplast contains multiple proteins, including those involved in mitochondrial DNA topology and metabolism, such as the kinetoplast-associated proteins (KAPs).
View Article and Find Full Text PDFAdv Exp Med Biol
August 2025
Department of Agricultural, Food, and Nutritional Science, University of Alberta, Edmonton, AB, Canada.
This chapter describes a molecular basis for age-induced muscle fiber loss involving the mammalian mitochondrial genome (mtDNA). Early studies of human mitochondrial myopathies, which display many phenotypes associated with muscle aging, led to the search for and subsequent discovery of similar genetic and histopathological changes in aging skeletal muscle. A diverse spectrum of mtDNA deletion mutations increase in abundance with age and clonally accumulate to high abundance within individual cells.
View Article and Find Full Text PDFInt J Biol Macromol
August 2025
Department of Genetics, Microbiology and Immunology, Biosciences Institute, UNESP, Botucatu, Sao Paulo, Brazil. Electronic address:
We studied the impacts of deleting the telomerase reverse transcriptase component of the Leishmania major (LmTERT) telomerase complex. The Leishmania genus comprises species that cause leishmaniasis, a neglected disease that lacks effective treatment and control options, highlighting the need for alternative therapeutics. Telomerase plays a crucial role in maintaining the integrity of eukaryotic genomes by synthesizing telomeres through its TERT and telomerase RNA components.
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