Thereafter, we focused on the four miRNAs that showed group differences and measured their content in neurally derived blood EVs isolated from 63 subjects: 16 patients with early stage dementia and a CSF Aβ42+ tau profile consistent with AD, 16 individuals with mild cognitive impairment (MCI) and an AD CSF profile, and 31 cognitively intact controls with normal CSF Aβ42+ tau levels.
Thereafter, we focused on the four miRNAs that showed group differences and measured their content in neurally derived blood EVs isolated from 63 subjects: 16 patients with early stage dementia and a CSF Aβ42+ tau profile consistent with AD, 16 individuals with mild cognitive impairment (MCI) and an AD CSF profile, and 31 cognitively intact controls with normal CSF Aβ42+ tau levels.
Previous clinical trials testing whether cholinesterase inhibitors can slow the rate of progression from MCI to AD dementia have yielded disappointing results.
A multivariate Cox regression model indicated that compared to low levels of physical activity, medium-to-high levels of physical activity were associated with a reduced risk of dementia (hazard ratio, 95% confidence interval = 0.62, 0.44-0.89) after adjusting for age, sex, years of education, apolipoprotein E ɛ4, and other confounders.
To highlight deregulated mechanisms occurring in ALS-FTD linked to the CHMP2B gene, we performed a whole transcriptomic study on lumbar spinal cord from CHMP2B<sup>intron5</sup> mice, a model that develops progressive motor alterations associated with dementia symptoms reminiscent of both ALS and FTD.
To highlight deregulated mechanisms occurring in ALS-FTD linked to the CHMP2B gene, we performed a whole transcriptomic study on lumbar spinal cord from CHMP2B<sup>intron5</sup> mice, a model that develops progressive motor alterations associated with dementia symptoms reminiscent of both ALS and FTD.
We included 493 patients and controls from the Gothenburg MCI study and used the dementia groups for marker selection (CSF total-tau (T-tau), phospho-tau (P-tau), and amyloid-β42 (Aβ42), 11 neuropsychological tests, and 92 regional brain volumes) and to obtain cut-off values which were then applied to the MCI groups.
Acetylcholinesterase inhibitors have a consistent benefit across all stages of dementia; their benefit in mild cognitive impairment and prodromal AD is unproven.
We included 768 patients (subjective cognitive decline (SCD, n = 194), mild cognitive impairment (MCI, n = 127), dementia (AD and non-AD, n = 447) with amyloid-β PET and CSF Aβ<sub>42</sub> measurement within 1 year.
We included 768 patients (subjective cognitive decline (SCD, n = 194), mild cognitive impairment (MCI, n = 127), dementia (AD and non-AD, n = 447) with amyloid-β PET and CSF Aβ<sub>42</sub> measurement within 1 year.
In the amyloid-adjusted logistic regression models, p-tau was a significant predictor for PET-amyloid in SCD (OR = 1.02 [1.01-1.04], p<sub>FDR</sub> = 0.03), MCI (OR = 1.05 [1.02-1.07], p<sub>FDR</sub> < 0.01), and dementia (OR = 1.04 [1.03-1.05], p<sub>FDR</sub> < 0.001), but not for CSF-amyloid.
In the amyloid-adjusted logistic regression models, p-tau was a significant predictor for PET-amyloid in SCD (OR = 1.02 [1.01-1.04], p<sub>FDR</sub> = 0.03), MCI (OR = 1.05 [1.02-1.07], p<sub>FDR</sub> < 0.01), and dementia (OR = 1.04 [1.03-1.05], p<sub>FDR</sub> < 0.001), but not for CSF-amyloid.
The analysis used a 3-wave, individual-level data set of 1004 people living with dementia in residential care that included self-completed EQ-5D-5L and formal-carer and informal-carer proxy-completed EQ-5D-5L and DEMQOL-Proxy-U utility values, in addition to other nonutility cognitive measures (Functional Assessment Staging [FAST], Clinical Dementia Rating [CDR], Cohen-Mansfield Agitation Inventory [CMAI]) and health-related quality of life (HRQOL) measures (nursing home version of the Quality of Life with Alzheimer's disease scale [QOL-AD-NH], Quality of Life in Late-Stage Dementia [QUALID] scale).
Potential predictors included CSF biomarkers, cognitive performance (verbal learning and memory), apolipoprotein E (APOE) ε4 genotype, medial temporal lobe atrophy, family history of dementia, depressive symptoms, and vascular factors, including the Cardiovascular Risk Factors, Aging and Dementia (CAIDE) risk score.
Potential predictors included CSF biomarkers, cognitive performance (verbal learning and memory), apolipoprotein E (APOE) ε4 genotype, medial temporal lobe atrophy, family history of dementia, depressive symptoms, and vascular factors, including the Cardiovascular Risk Factors, Aging and Dementia (CAIDE) risk score.
Potential predictors included CSF biomarkers, cognitive performance (verbal learning and memory), apolipoprotein E (APOE) ε4 genotype, medial temporal lobe atrophy, family history of dementia, depressive symptoms, and vascular factors, including the Cardiovascular Risk Factors, Aging and Dementia (CAIDE) risk score.
A diagnosis of dementia is currently made in terms of probability and is based on clinical evaluation (neuropsycological tests) as well as on the results of morphological imaging investigations (MRI) that can be supported by biohumoral (CSF analysis), and functional imaging only in the case of uncertain diagnosis of disease.
A diagnosis of dementia is currently made in terms of probability and is based on clinical evaluation (neuropsycological tests) as well as on the results of morphological imaging investigations (MRI) that can be supported by biohumoral (CSF analysis), and functional imaging only in the case of uncertain diagnosis of disease.