Background: Alzheimer's disease (AD) pathological hallmarks were found in retinas of AD patients. Several studies showed a significant reduction of neuro-retina thickness measured through optical coherence tomography (OCT) in AD patients, but possible correlations between retina morphology, cognition, and cerebrospinal fluid (CSF) AD biomarkers (Aβ42, t-tau, and p-tau) have been poorly investigated so far.
Objective: In the present cross-sectional study, we measured the thickness of neuro-retinal layers through OCT searching for possible correlations with patients' cognitive performances and CSF AD biomarkers.
Methods: 137 consecutive subjects [43 with AD, 37 with mild cognitive impairment (MCI), and 57 healthy controls (HC)], received an OCT scan acquisition to measure the peripapillary retinal nerve fiber layer (RNFL) thickness. In a subsample of 21 AD, 18 MCI, and 18 HC, the macular volume of ganglion cell layer (GCL), inner plexiform layer (IPL), and inner nuclear layer was computed. A comprehensive neuropsychological assessment and CSF AD biomarkers' concentrations were available in AD and MCI patients.
Results: Peripapillary RNFL, global, and in superior quadrant was significantly thinner in AD and MCI patients when compared to HC, while macular GCL volume was significantly reduced only in AD. RNFL thickness in nasal and inferior quadrants was correlated with single CSF AD biomarker concentrations, but no differences were found in retina morphology depending on the presence of a CSF profile typical for AD. Memory performances were positively associated with GCL and IPL volume.
Conclusion: Our findings might propose OCT as a reliable and easy to handle tool able to detect neuro-retinal atrophy in AD in relation with cognitive performances.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.3233/JAD-200043 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Alterations of amino acids in older adults with Alzheimer's Disease and Vascular Dementia.
Amino Acids
January 2025
Institute of Brain Science, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, P. R. China.
Metabolomics provide a promising tool for understanding dementia pathogenesis and identifying novel biomarkers. This study aimed to identify amino acid biomarkers for Alzheimer's Disease (AD) and Vascular Dementia (VD). By amino acid metabolomics, the concentrations of amino acids were determined in the serum of AD and VD patients as well as age-matched healthy controls.
View Article and Find Full Text PDFComparison of the amyloid plaque proteome in Down syndrome, early-onset Alzheimer's disease, and late-onset Alzheimer's disease.
Acta Neuropathol
January 2025
Department of Neurology, NYU Grossman School of Medicine, New York, NY, USA.
Down syndrome (DS) is strongly associated with Alzheimer's disease (AD) due to APP overexpression, exhibiting Amyloid-β (Aβ) and Tau pathology similar to early-onset (EOAD) and late-onset AD (LOAD). We evaluated the Aβ plaque proteome of DS, EOAD, and LOAD using unbiased localized proteomics on post-mortem paraffin-embedded tissues from four cohorts (n = 20/group): DS (59.8 ± 4.
View Article and Find Full Text PDFUnsaturated Fatty Acids Are Decreased in Aβ Plaques in Alzheimer's Disease.
J Neurochem
January 2025
Center for Protein Diagnostics (PRODI) Biospectroscopy, Ruhr University Bochum, Bochum, Germany.
Alzheimer's disease (AD) is characterized by the accumulation of amyloid-beta (Aβ) plaques in the brain, contributing to neurodegeneration. This study investigates lipid alterations within these plaques using a novel, label-free, multimodal approach. Combining infrared (IR) imaging, machine learning, laser microdissection (LMD), and flow injection analysis mass spectrometry (FIA-MS), we provide the first comprehensive lipidomic analysis of chemically unaltered Aβ plaques in post-mortem human AD brain tissue.
View Article and Find Full Text PDFBlood biomarker profiles in young-onset neurocognitive disorders: A cohort study.
Aust N Z J Psychiatry
January 2025
Neuropsychiatry Centre, The Royal Melbourne Hospital, Parkville, VIC, Australia.
Introduction: Young-onset neurocognitive symptoms result from a heterogeneous group of neurological and psychiatric disorders which present a diagnostic challenge. To identify such factors, we analysed the Biomarkers in Younger-Onset Neurocognitive Disorders cohort, a study of individuals <65 years old presenting with neurocognitive symptoms for a diagnosis and who have undergone cognitive and biomarker analyses.
Methods: Sixty-five participants (median age at assessment of 56 years, 45% female) were recruited during their index presentation to the Royal Melbourne Hospital Neuropsychiatry Centre, a tertiary specialist service in Melbourne, Australia, and categorized as either early-onset Alzheimer's disease ( = 18), non-Alzheimer's disease neurodegeneration ( = 23) or primary psychiatric disorders ( = 24).
Effectiveness and utilization of a cognitive screening program for primary geriatric care.
Alzheimers Res Ther
January 2025
Department of Neurosciences, University of California, San Diego, La Jolla, CA, 92093-0948, USA.
Background: Effective detection of cognitive impairment in the primary care setting is limited by lack of time and specialized expertise to conduct detailed objective cognitive testing and few well-validated cognitive screening instruments that can be administered and evaluated quickly without expert supervision. We therefore developed a model cognitive screening program to provide relatively brief, objective assessment of a geriatric patient's memory and other cognitive abilities in cases where the primary care physician suspects but is unsure of the presence of a deficit.
Methods: Referred patients were tested during a 40-min session by a psychometrist or trained nurse in the clinic on a brief battery of neuropsychological tests that assessed multiple cognitive domains.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!