Boala Alzheimer și alte forme de demență.
73 de articoleThis study examined 92 amyloid-negative patients using the ATN biomarker classification framework to identify non-Alzheimer's pathologies causing cognitive decline. Results showed amyloid-negative profiles were associated with non-Alzheimer's dementia types and secondary neuropsychiatric conditions, though early-stage misclassification risks warrant further investigation.
This proteomics study analyzed cerebrospinal fluid from 490 amyloid-positive participants to identify 61 dysregulated proteins that distinguish those with Alzheimer's dementia from cognitively normal or mildly impaired individuals. The identified proteins were associated with cognitive progression and diagnostic conversion, with functional enrichment analyses revealing pathways relevant to neurodegeneration.
This research investigates alterations in gut microbiota composition and metabolic profiles in patients with Alzheimer's disease and type 2 diabetes using advanced molecular analysis techniques. The study aims to identify potential microbial and metabolic biomarkers associated with neurodegeneration and metabolic dysfunction.
This genome-wide association study investigates the distinct genetic factors underlying specific cognitive domains (memory, language, executive function) affected in Alzheimer's disease. The research identifies domain-specific genetic architecture, suggesting that different cognitive impairments in AD may have partially distinct genetic underpinnings.
This research examines how oral microbiome dysbiosis contributes to Alzheimer's disease through TLR/NLR immune signaling pathways that trigger systemic and neuroinflammation. The oral microbiome composition is proposed as a potential biomarker for early diagnosis and screening of cognitive decline, with discussion of targeted therapeutic approaches like TLR/NLR inhibitors.
This clinical study analyzed 184 Alzheimer's disease patients stratified by sex to examine relationships between sleep disturbances, neuropsychiatric symptoms, and cognitive progression. Patients with disturbed sleep showed worse cognitive performance and higher rates of depression, anxiety, and behavioral problems, with sex-specific patterns: women exhibited more disinhibition and depression while men showed greater cognitive decline and higher caregiver burden.
This 7-year retrospective study of 791 memory clinic patients examined cognitive decline patterns across three neurocognitive disorder etiologies: Alzheimer's disease, vascular encephalopathy, and mixed presentations. Alzheimer's disease showed steeper annual cognitive decline (~2.0 MMSE points/year) compared to vascular disease, while early diagnosis and higher baseline cognitive scores were associated with slower decline.
This case-control study of 240 participants examined how MTHFR gene variants (C677T and A1298C) influence Alzheimer's disease risk through disruptions in one-carbon metabolism and increased homocysteine levels. Researchers found these polymorphisms significantly associated with AD risk and correlated with metabolic alterations, reduced cognitive function, and white matter changes on MRI.
This work explores the vascular hypothesis as a mechanism underlying both Alzheimer's disease and vascular dementia, with particular attention to how cardiovascular risk factors contribute to dementia development. The research examines prevalence patterns and etiological factors specific to African populations, addressing potential disparities in dementia pathophysiology and risk profiles.
This retrospective study of 310 DLB patients examined whether sex-related clinical differences are explained by Alzheimer's disease cerebrospinal fluid biomarkers. While AD co-pathology accounts for some sex differences (REM sleep disorder, cognitive scores), other features like parkinsonism appear driven by additional mechanisms independent of AD biology.
This study examined the relationship between air pollution exposure and cognitive decline in older adults, finding that exposure to fine particulate matter (PM₁₀) increases Alzheimer's disease risk, with inflammatory marker C-reactive protein mediating approximately 43% of this effect. Using genetic and observational data from over 7,000 Chinese participants, the research provides evidence that air pollution may causally contribute to dementia through inflammation-related pathways.
This meta-analysis of 16 cohort studies found that high body weight fluctuation is associated with increased risk of all-cause dementia, Alzheimer's disease, and vascular dementia, with hazard ratios ranging from 1.33 to 1.40 compared to stable weight. No significant association was found between weight variability and general cognitive decline, and evidence certainty was assessed using rigorous GRADE methodology.
This article examines how anti-amyloid monoclonal antibodies used to treat Alzheimer's disease may interact with or influence depression, a common comorbidity in elderly patients. The review discusses the neurobiological connections between amyloid pathology and mood disorders, and implications for treatment outcomes.
This review examines aspirin's potential therapeutic role in Alzheimer's disease by targeting neuroinflammation and oxidative stress, two key pathological mechanisms in cognitive decline. The article discusses aspirin's multi-target pharmacological properties beyond its conventional anti-inflammatory COX inhibition, proposing it as a basis for developing disease-modifying treatments.
This review examines two disease-modifying monoclonal antibodies—lecanemab and donanemab—that target amyloid-beta pathology in early-stage Alzheimer's disease, showing modest cognitive decline reductions (27-29%) over 18-76 months in clinical trials. Key challenges addressed include variable efficacy across demographic groups, amyloid-related imaging abnormalities, cost barriers, and the need for more inclusive research and personalized treatment approaches.
This review examines death-associated protein kinase 1 (DAPK1) as a promising therapeutic target for Alzheimer's disease, exploring its involvement in key pathogenic mechanisms including amyloid-beta accumulation, tau phosphorylation, neuronal cell death, and mitochondrial dysfunction. The authors discuss potential treatment strategies using small molecules, microRNAs, and natural compounds that could modulate DAPK1 activity.
This longitudinal study of 75 Alzheimer's Disease Neuroimaging Initiative participants found that baseline brain structure measurements (particularly lateral ventricle size and hippocampal/thalamic volumes) were stronger predictors of cognitive decline and MCI conversion than rates of brain atrophy. The findings support the brain reserve concept, showing that structural capacity at baseline is more informative than dynamic changes for predicting cognitive trajectories across the disease continuum.
This study examined 465 participants across the Alzheimer's disease continuum to understand how amyloid-β pathology causes cognitive decline through hippocampal subfield atrophy. Progressive hippocampal degeneration at the mild cognitive impairment stage mediated amyloid-related cognitive decline in memory, global cognition, and attention, with the right subiculum identified as a key structural biomarker.