Introduction: Alzheimer's disease (AD) and Lewy body dementia (LBD) are two common forms of dementia. There are still controversies regarding whether LBD patients have a worse clinical course than AD patients.
Methods: We retrospectively reviewed all biomarkers that supported AD and LBD patients presenting to the Memory Clinic of Queen Mary Hospital, Hong Kong, between 1 January 2008 and 30 December 2016. Diagnoses of AD and LBD were supported by clinical diagnostic criteria and biomarkers. LBD patients included those with dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD). Baseline demographics, presenting clinical features, degree of cognitive impairment and specified clinical outcomes were compared.
Results: We recruited 31 AD and 25 LBD patients (18 DLB, 7 PDD). When measured from disease onset, LBD patients were noted to have shorter overall survival (p = 0.02) with earlier occurrence of falls (p < 0.001), dysphagia (p < 0.001), pneumonia (p = 0.01), pressure injuries (p = 0.003) and institutionalisation (p = 0.03) than AD patients. Cox regression analyses showed that LBD predicted falls (hazard ratio [HR] 5.86, 95% confidence interval [CI] 2.29-15.01, p < 0.001), dysphagia (HR 10.06, 95% CI 2.50-40.44, p = 0.001), pressure injuries (HR 17.39, 95% CI 1.51-200.10, p = 0.02), institutionalisation (HR 2.72, 95% CI 1.12-6.60, p = 0.03) and death (HR 2.96, 95% CI 1.18-7.42, p = 0.02).
Conclusion: LBD patients had shorter overall survival with earlier occurrence of pre-specified long-term events compared with AD patients. LBD also independently predicted pre-specified long-term events.
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http://dx.doi.org/10.11622/smedj.2019103 | DOI Listing |
J Am Board Fam Med
December 2024
From the Department of Population Health Sciences, Geisinger, Danville, PA (BLJ, LBD); Center for Obesity and Metabolic Health, Danville, PA (GCW, AC, CDS, LBD); Department of Health Services Research, Management and Policy, University of Florida, Health Sciences Center, Gainesville, FL (AGM); Geisinger Department of Genomic Health, Danville, PA 17822 (AKR); Division of Genomic Medicine, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD (AKR).
Background: The association between interpersonal continuity of care (CoC) and progression from the prediabetic state to Type 2 Diabetes (T2D) remains unknown.
Aim: To evaluate the association between interpersonal CoC and the progression to T2D among persons with prediabetes.
Design And Setting: A retrospective cohort study using electronic health record (EHR) data from 6620 patients at Geisinger, a large rural health care system in Danville, PA.
Eur J Neurol
January 2025
Padova Neuroscience Center (PNC), University of Padova, Padova, Italy.
Psychiatry Res
December 2024
Black Dog Institute, Sydney, Australia; Discipline of Psychiatry and Mental Health, School of Clinical Medicine, University of New South Wales, Australia; The George Institute for Global Health, Sydney, Australia.
Background: Ketamine and its derivates (e.g. esketamine) are increasingly used in clinical settings for treatment-resistant depression (TRD).
View Article and Find Full Text PDFACS Pharmacol Transl Sci
December 2024
State Key Laboratory of Chemical Oncogenomics, Institute of Biopharmaceutical and Health Engineering, Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, China.
Breast cancer with positive expression of estrogen receptor α (ERα+) accounts for 70% of breast cancer cases, whose predominant treatment is currently endocrine therapy. The main strategy of endocrine therapy for ERα+ breast cancer is to inhibit the ERα signaling pathway and downregulate ERα levels, which often results in mutations in the ligand-binding domain (LBD) of ERα, leading to significant resistance to subsequent treatment in patients. To combat drug resistance, we first proposed a novel aptamer PROTAC strategy through specifically targeted degradation of ERα via targeting the DNA-binding domain (DBD) of ERα.
View Article and Find Full Text PDFBrain
December 2024
Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, 40139, Italy.
Evidence from neuropathological cohorts indicates that a CSF α-synuclein (α-syn) seed amplification assay (SAA) may provide quantitative kinetic parameters correlating with α-syn pathology burden in patients with Lewy body disease (LBD). Studies are needed to assess their longitudinal trend during the pre-symptomatic and clinical disease phases and their correlation with measures of disease progression. We aimed to assess the baseline α-syn CSF SAA kinetic parameters, their longitudinal variations and associations with clinical outcomes in a cohort of longitudinally repeatedly sampled Lewy Body disease patients, including clinically unimpaired (asymptomatic LBD) and neurologically impaired individuals.
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