Extracellular proteases are key factors contributing to the virulence of pathogenic fungi from the genus . Their proteolytic activities are crucial for extracting nutrients from the external environment, degrading host defenses, and destabilizing the internal balance of the human organism. Currently, the enzymes most frequently described in this context are secreted aspartic proteases (Saps). This review comprehensively explores the multifaceted roles of Saps, highlighting their importance in biofilm formation, tissue invasion through the degradation of extracellular matrix proteins and components of the coagulation cascade, modulation of host immune responses via impairment of neutrophil and monocyte/macrophage functions, and their contribution to antifungal resistance. Additionally, the diagnostic challenges associated with infections and the potential of Saps as biomarkers were discussed. Furthermore, we examined the prospects of developing vaccines based on Saps and the use of protease inhibitors as adjunctive therapies for candidiasis. Given the complex biology of Saps and their central role in pathogenicity, a multidisciplinary approach may pave the way for innovative diagnostic strategies and open new opportunities for innovative clinical interventions against candidiasis.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11084781 | PMC |
http://dx.doi.org/10.3390/ijms25094775 | DOI Listing |
Alzheimers Dement
December 2024
Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada.
Background: N-acetyl-aspartate (NAA) and myo-inositol (mI) are neurometabolites reflecting neuronal viability and astrocyte activity, respectively. These can be quantified in vivo using proton magnetic resonance spectroscopy (1H-MRS). Previous studies have suggested that these metabolites could serve as biomarkers for Alzheimer's disease dementia (AD).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Science and Technology of China, Hefei, Anhui, China.
Background: The exact impacts of β-site APP cleaving enzyme (BACE1) on brain atrophy and cognitive decline in the Alzheimer's disease (AD) remain not fully understood. This study aimed to investigate the relationship between BACE1 in cerebrospinal fluid (CSF) and amyloid-β (Aβ) pathology, neurodegeneration and cognitive function.
Method: This study involved 359 participants from original individuals of the China Aging and Neurodegenerative Disorder Initiative (CANDI) cohort, who underwent measurements of AD biomarkers.
Alzheimers Dement
December 2024
Universidade Federal de Ciências da Saúde de Porto Alegre, Porto Alegre, RS, Brazil.
Background: The study of new blood biomarkers in addition to amyloid beta and hyperphosphorylated tau is fundamental to expanding the understanding of the pathophysiology of dementia, especially Alzheimer`s disease, in search of therapeutic approaches.
Method: In this study, we included individuals diagnosed with Alzheimer disease (AD), Mixed-type dementia (MD), Vascular dementia (VD) and a control group of cognitively healthy individuals. Demographics, clinical characteristics, neuroimages and plasma samples were collected.
Alzheimers Dement
December 2024
Laboratory of Neuroscience (LIM27), Departamento e Instituto de Psiquiatria, Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, São Paulo, Brazil.
Background: Due to the genetic characteristics of Down syndrome (DS), it is directly associated with a group of clinical manifestations resulting from premature aging and may present patterns of Alzheimer's disease (AD). Thus, this study aimed to investigate AD biological markers in peripheral blood samples from adults and elderly individuals with DS and compare them with individuals with normal karyotype.
Methods: The DS group was subclassified into 55 SD without evidence of cognitive decline (DSNC) and 27 DS with cognitive decline (SDAD).
Alzheimers Dement
December 2024
Laboratory of Neuroscience (LIM27), Departamento e Instituto de Psiquiatria, Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, São Paulo, Brazil.
Background: Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) was first identified as the rate limiting enzyme of amyloid-β-peptide (Aβ) production. The catalytic activity of BACE1 favors the generation of Aβ peptides and overproduction and accumulation of Aβ in the brain triggers downstream neurotoxic events that pertain to the amyloid cascade, leading to the formation of neuritic plaques. Furthermore BACE1 acts in the synapse through processing substrates such as APP-like proteins, Neuregulin-1 (Nrg 1), and β2 and β4 subunits of voltage-gated Na+ channels.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!