Notes

γ' Fibrinogen as a Predictor associated with Tactical in Amyotrophic Side to side Sclerosis.
99mTc-ECD SPECT subtraction imaging indicated lower cerebral blood flow in the posterior cingulate gyrus among the patients with CMB-positive DLB than among those with CMB-positive PD; additionally, the cerebral blood flow was lower in the bilateral basal ganglia and midbrain among patients with CMB-positive DLB compared to those with CMB-negative DLB.

A reduction in occipital glucose metabolism may be related to CMBs in the occipital lobe of patients with DLB.
A reduction in occipital glucose metabolism may be related to CMBs in the occipital lobe of patients with DLB.
There is intense interest in the development of blood-based biomarkers, not only that can differentiate Alzheimer's disease (AD) from controls, but that can also predict conversion from mild cognitive impairment (MCI) to AD. Serum biomarkers carry the potential advantage over imaging or spinal fluid markers both in terms of cost and invasiveness.

Our objective was to measure the potential for serum lipid markers to differentiate AD from age-matched healthy controls as well as to predict conversion from MCI to AD.

Using a publicly-available dataset, we examined the relationship between baseline serum levels of 349 known lipids from 16 classes of lipids to differentiate disease state as well as to predict the conversion from MCI to AD.

We observed that several classes of lipids (cholesteroyl ester, phosphatidylethanolamine, lysophosphatidylethanolamine, and acylcarnitine) differentiated AD from normal controls. read more Among these, only two classes, phosphatidylethanolamine (PE) and lysophosphatidylethanolamine (lyso-PE), predicted time to conversion from MCI to AD. Low levels of PE and high levels of lyso-PE result in two-fold faster median time to progression from MCI to AD, with hazard ratios 0.62 and 1.34, respectively.

These data suggest that serum PE and lyso-PE may be useful biomarkers for predicting MCI to AD conversion. In addition, since PE is converted to lyso-PE by phospholipase A2, an important inflammatory mediator that is dysregulated in AD, these data suggest that the disrupted serum lipid profile here may be related to an abnormal inflammatory response early in the AD pathologic cascade.
These data suggest that serum PE and lyso-PE may be useful biomarkers for predicting MCI to AD conversion. In addition, since PE is converted to lyso-PE by phospholipase A2, an important inflammatory mediator that is dysregulated in AD, these data suggest that the disrupted serum lipid profile here may be related to an abnormal inflammatory response early in the AD pathologic cascade.
Advanced stages of dementia are characterized by severe cognitive and physical impairment. It has not yet been investigated whether persons with young onset dementia (YOD) and late onset dementia (LOD) differ in advanced disease stages.

To compare quality of life (QoL) between persons with advanced YOD and LOD; to explore the determinants of QoL; to investigate whether YOD and LOD differ with regard to symptoms and care.

The study was performed in the context of EPYLOGE (IssuEs in Palliative care for persons in advanced and terminal stages of YOD and LOD in Germany). Persons with advanced dementia (PWAD) were assessed and caregivers were interviewed. QoL was measured with the proxy rating Quality of Life in Late Stage Dementia (QUALID) scale.

93 persons with YOD and 98 with LOD were included. No significant differences in QoL were detected. Determinants of QoL were similar in YOD and LOD. Behavioral and psychological symptoms of dementia (BPSD), suffering and other distressing symptoms were associated with a lower QoL. In YOD but not in LOD antipsychotic treatment was associated with low QoL. The group of persons who were younger than 65 years at the time of the study visit experienced significantly more distressing symptoms than older PWAD.

Overall, persons with advanced YOD do not appear to be disadvantaged compared to old and oldest PWAD. Special attention, however, must be paid to the group of the very young persons who seem to be particularly vulnerable.
Overall, persons with advanced YOD do not appear to be disadvantaged compared to old and oldest PWAD. Special attention, however, must be paid to the group of the very young persons who seem to be particularly vulnerable.
Mild cognitive impairment (MCI) describes a borderland between healthy cognition and dementia. Progression to and reversion from MCI is relatively common but more research is required to understand the factors affecting this fluidity and improve clinical care interventions.

We explore these transitions in MCI status and their predictive factors over a six-year period in a highly-phenotyped longitudinal study, the Lothian Birth Cohort 1936.

MCI status was derived in the LBC1936 at ages 76 (n = 567) and 82 years (n = 341) using NIA-AA diagnostic guidelines. Progressions and reversions between healthy cognition and MCI over the follow-up period were assessed. Multinomial logistic regression assessed the effect of various predictors on the likelihood of progressing, reverting, or maintaining cognitive status.

Of the 292 participants who completed both time points, 41 (14%) participants had MCI at T1 and 56 (19%) at T2. Over the follow-up period, 74%remained cognitively healthy, 12%transitioned to MCI, 7%rkelihood of reversion to, and maintenance of healthy cognition.
Identifying modifiable risk factors, such as obesity, to lower the prevalence of Alzheimer's disease (AD) has gained much interest. However, whether the association is causal remains to be evaluated.

The present study was designed 1) to make a quantitative assessment of the association between obesity and AD; 2) to validate whether there was a causal association between them; and 3) to provide genetic clues for the association through a network-based analysis.

Two-sample Mendelian randomization (2SMR) analysis, meta-analysis, and protein-protein interaction (PPI) network analysis, were employed.

Firstly, the meta-analysis based on 9 studies comprising 6,986,436 subjects indicated that midlife obesity had 33%higher AD odds than controls (OR = 1.33, 95%CI = [1.03, 1.62]), while late-life obesity were inversely associated with AD risk (OR = 0.57, 95%CI = [0.47, 0.68]). Secondly, 2SMR analysis indicated that there was no causal association between them. Thirdly, CARTPT was identified to be shared by the anti-obesity drug targets and AD susceptibility genes.
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