Background: Peripheral diagnostics for Alzheimer's disease (AD) continue to be developed. Diagnostics capable of detecting AD before the onset of symptoms are particularly desirable, and, given the fact that early detection is imperative for alleviating long-term symptoms of the disease, methods which enable detection in the earliest stages are urgently needed. Saliva testing is non-invasive, and saliva is easy to acquire. A simple, non-invasive saliva test can potentially be used as an adjunct to diagnose AD during its earliest stages.
Methods: Salivary levels of beta amyloid 42 (Aβ) were quantitated with enzyme-linked immunosorbent-type assays. Fifteen AD patients (7 men, mean age 77.8 ± 1.8 years, mean Mini-Mental State Examination [MMSE] score 19.0 ± 1.3) and 7 normal controls (2 men, mean age 60.4 ± 4.7 years, mean MMSE 29.0 ± 0.4) were enrolled.
Results: Salivary Aβ levels were significantly higher in AD patients than in controls (51.7 ± 1.6 pg/mL for AD and 21.1 ± 0.3 pg/mL for controls, p < 0.001). Based on these results, saliva testing appears to be a promising method for detecting AD during its critical early stages.
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http://dx.doi.org/10.1186/s12883-018-1160-y | DOI Listing |
ACS Appl Mater Interfaces
January 2025
College of Food and Pharmaceutical Engineering, Nanjing Normal University, Nanjing 210023, PR China.
The number of cases of Alzheimer's disease (AD) characterized by progressive amnestic syndrome is dramatically increased with population aging. It is urgent to detect and diagnose this disease early. The state of amyloid-beta protein 1-42 (Aβ) was commonly regarded as a hallmark for early diagnosis of AD.
View Article and Find Full Text PDFAnn Med
December 2025
Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Cerebral amyloid angiopathy (CAA), characterized by the deposition of amyloid-β (Aβ) peptides in the walls of medium and small vessels of the brain and leptomeninges, is a major cause of lobar hemorrhage in elderly individuals. Among the genetic risk factors for CAA that continue to be recognized, the apolipoprotein E (APOE) gene is the most significant and prevalent, as its variants have been implicated in more than half of all patients with CAA. While the presence of the APOE ε4 allele markedly increases the risk of CAA, the ε2 allele confers a protective effect relative to the common ε3 allele.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Growth, Development, and Mental Health of Children and Adolescence Center, Pediatric Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Posttranslational modification (PTM) of the amyloid precursor protein (APP) plays a critical role in Alzheimer's disease (AD). Recent evidence reveals that lactylation modification, as a novel PTM, is implicated in the occurrence and development of AD. However, whether and how APP lactylation contributes to both the pathogenesis and cognitive function in AD remains unknown.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Institute for Translational Research, University of North Texas Health Science Center, Fort Worth, Texas, USA.
Introduction: The relationship between Alzheimer's disease (AD) plasma biomarkers, and physical functioning (PF) across diverse races and ethnicities remains unclear. This study aims to explore this association in an ethno-racially diverse sample of cognitively unimpaired community-dwelling adults.
Methods: Data clinical examinations, neuropsychological tests, blood draws, and PF exams (Timed Up and Go [TUG] and Short Physical Performance Battery [SPPB]) were analyzed.
Theranostics
January 2025
Laboratory of Molecular Genetics, College of Pharmacy, Chungbuk National University, Cheongju, 28160, Republic of Korea.
Cathepsin D (Ctsd) has emerged as a promising therapeutic target for Alzheimer's disease (AD) due to its role in degrading intracellular amyloid beta (Aβ). Enhancing Ctsd activity could reduce Aβ42 accumulation and restore the Aβ42/40 ratio, offering a potential AD treatment strategy. This study explored Ctsd demethylation in AD mouse models using dCas9-Tet1-mediated epigenome editing.
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