Lecture notes in computer science, Год журнала: 2024, Номер unknown, С. 185 - 195
Опубликована: Окт. 17, 2024
Язык: Английский
Progress in Neuro-Psychopharmacology and Biological Psychiatry, Год журнала: 2025, Номер 137, С. 111258 - 111258
Опубликована: Янв. 19, 2025
Язык: Английский
Процитировано
6
Neuroscience & Biobehavioral Reviews, Год журнала: 2025, Номер unknown, С. 106029 - 106029
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
3
Brain Research, Год журнала: 2025, Номер 1851, С. 149500 - 149500
Опубликована: Фев. 7, 2025
Язык: Английский
Процитировано
1
Molecular Neurodegeneration, Год журнала: 2024, Номер 19(1)
Опубликована: Дек. 4, 2024
Abstract Multisensory decline is common as people age, and aging the primary risk of Alzheimer’s Disease (AD). Recent studies have begun to shed light on possibility that age-related sensory could accelerate AD pathogenesis, or be a prodromal indicator AD. Sensory impairments, specifically in taste smell, often emerge before cognitive symptoms AD, indicating their potential early biomarkers. Olfactory dysfunction has been frequently associated with may offer valuable insights into detection. Hearing impairment significantly but its causal impact progression remains unclear. The review also discusses visual tactile deficits including retinal thinning changes perception, highlighting links disease progression. Focusing molecular mechanisms, explores roles amyloid-β (Aβ) accumulation tau protein pathology bidirectional relationship In summary, evidence presented conclusively supports advocating for an integrated approach understanding decline, enhance detection, implementing preventive strategies, developing therapeutic interventions This underscores significance health addressing neurodegenerative diseases, particularly
Язык: Английский
Процитировано
5
Biomedical Signal Processing and Control, Год журнала: 2025, Номер 104, С. 107566 - 107566
Опубликована: Янв. 27, 2025
Язык: Английский
Процитировано
0
Frontiers in Aging Neuroscience, Год журнала: 2025, Номер 17
Опубликована: Фев. 20, 2025
Mild cognitive impairment (MCI) is associated with an increased risk of dementia in older adults. Olfactory may indicate prodromal dementia, yet its underlying mechanisms are not fully understood. This study aimed to investigate the alterations functional connectivity (FC) odor-induced olfactory neural circuits MCI patients. The included 39 patients and 42 normal controls (NCs). All subjects underwent assessments, behavior tests, odor-based magnetic resonance imaging (fMRI). Differences FC within were analyzed using generalized psychophysiological interaction (gPPI) method. showed significant deficits, including lower scores on Mini-Mental State Examination (MMSE) Montreal Cognitive Assessment (MoCA), alongside impairments episodic memory, visuospatial executive function, language, attention, threshold, total function. Compared NCs, exhibited reduced activation bilateral primary cortex (bPOC) during stimulation. Odor-induced bPOC correlated thresholds across cohort. During odor stimulation, from right anterior frontal lobe, particularly middle gyrus (MFG) superior (SFG). Conversely, lobe medial temporal cortex, fusiform parahippocampal gyri, was Increased SFG/MFG negatively while decreased fusiform/parahippocampal gyri positively language ability, identification. indicates that impaired (POC)-anterior cortex-medial circuit a sensitive neuroimaging marker for early dysfunction appears POC, suggesting this region provide novel diagnostic therapeutic avenues intervention.
Язык: Английский
Процитировано
0
The Journal of Prevention of Alzheimer s Disease, Год журнала: 2025, Номер unknown, С. 100129 - 100129
Опубликована: Март 1, 2025
Type 2 diabetes (T2D) is commonly co-morbid with Alzheimer's disease (AD). However, it remains unclear whether T2D itself or the antidiabetic drug metformin contributes to progression of AD. This study aimed investigate overall and independent effects use on risk Summary genome-wide association datasets were utilized for Mendelian randomization (MR) multivariable MR (MVMR) analyses, including ones (N = 455,017), 456,276), AD 453,733). Additionally, using proportional imbalance method, we analyzed AD-related adverse events in FDA Adverse Event Reporting System (FAERS) database (covering Q1 2004 Q2 2024). Our two-sample analysis indicated that not associated (OR: 1.03, CI: 0.99-1.08, P 0.128). while statistically significant, genetic signature exposure demonstrated a trend toward an increased 1.05, 1.00-1.09, 0.053). Interestingly, MVMR analysis, which evaluates T2D, found robust decrease 0.82, 0.68-0.98, 0.031), was higher 1.26, 1.06-1.50, 9.45E-3). In FAERS database, total 228,283 metformin-related event reports from 67,742 cases found. For as target event, signal reported 29 (ROR: 0.83, 95 % 0.58-1.19, 0.3126). reveals opposite causal These findings highlight importance assessing when prescribing patients T2D.
Язык: Английский
Процитировано
0
Journal of Geriatric Psychiatry and Neurology, Год журнала: 2025, Номер unknown
Опубликована: Апрель 16, 2025
Background Olfactory impairment might be already present at the subjective cognitive (SCD) individuals, and deepens with disease severity in Alzheimer’s (AD) spectrum. However, neuroanatomical correlates of olfactory SCD individuals are not fully elucidated. Methods A hundred twenty enrolled older adults without dementia (25 healthy controls (HCs), 45 50 mild (MCI) individuals) completed assessment structural magnetic resonance imaging (MRI) scanning. function was evaluated by 16-item Sniffin’ Sticks odor identification test (SSIT). Region interest (ROI) analysis conducted for gray matter volume (GMV) 8 olfactory-related brain regions. Results In ROI analysis, from HC, to MCI group, smaller GMV regions became increasingly severe. For HC only associated entorhinal cortex ( P < 0.05). reduced GMVs hippocampus were decreased piriform cortex, amygdala, orbitofrontal parahippocampus significantly Conclusions The atrophy gradually increased corresponding MCI. mainly hippocampus.
Язык: Английский
Процитировано
0
Molecular Pharmaceutics, Год журнала: 2025, Номер unknown
Опубликована: Апрель 15, 2025
Olfactory impairment is a preclinical symptom of Alzheimer's disease (AD); however, the mechanism olfactory dysfunction in AD not clear. This study aims to explore by analyzing correlation between olfaction and cognition using positron emission tomography (PET) quantification biomarkers, including amyloid β (Aβ) abnormal tau proteins intracranial olfactory-related regions model mice, compares PET with pathological detection reliability transformation into clinical research. A total 14 3xTg mice (12 months old, n = 7) wild-type (WT) 7), were enrolled study. Behavioral experiments (olfactory: buried food test, cognitive: Morris water maze) performed assess whether had cognitive functions. quantified Aβ regions. The expression distribution phosphorylated observed immunofluorescence. Compared WT impairments. Quantitative immunofluorescence showed that significantly more accumulation areas than did mice. deposition suggests potential link pathology progression. elevated uptake further highlights olfactory-targeted molecular imaging as noninvasive biomarker for detection.
Язык: Английский
Процитировано
0
Molecular Neurobiology, Год журнала: 2025, Номер unknown
Опубликована: Апрель 28, 2025
Abstract While several hypotheses have been proposed to explain the underlying mechanisms of Alzheimer's disease, none entirely satisfactory. Both genetic and non-genetic risk factors, such as infections, metabolic disorders psychological stress, contribute this debilitating disease. Multiple lines evidence indicate that ceramides may be central pathogenesis Alzheimer’s Tumor necrosis factor-α, saturated fatty acids cortisol elevate brain levels ceramides, while mutations in APP , presenilin TREM2 APOE ε4, also ceramide synthesis. Importantly, displace sphingomyelin cholesterol from lipid raft-like membrane patches connect endoplasmic reticulum mitochondria, disturbing mitochondrial oxidative phosphorylation energy production. As a consequence, flattening rafts alters function γ-secretase, leading increased production Aβ 42 . Moreover, inhibit insulin-signaling cascade via at least three mechanisms, resulting activation glycogen synthase kinase-3 β. Activation kinase has multiple consequences, it further deteriorates insulin resistance, promotes transcription BACE1 causes hyperphosphorylation tau inhibits factor Nrf2. Functional Nrf2 prevents apoptosis, mediates anti-inflammatory activity improves blood–brain barrier function. Thus, various seemingly unrelated disease factors converge on production, whereas elevated give rise well-known pathological features Understanding targeting these provide promising foundation for development novel preventive therapeutic strategies.
Язык: Английский
Процитировано
0