Notes

Transition metallic complexes displaying atropisomeric saturated NHC ligands.
All raters evaluated the same 50 parietal lobes on brain MRI of 25 cognitively normal individuals with even distribution across all atrophy degrees from none to prominent according to the neurologist's rating.

Intra-rater agreement was almost perfect with the kappa value of 0.90. Inter-rater agreement was moderate to substantial with kappa values ranging from 0.43-0.86.

The Parietal Atrophy Score is the reliable visual scale among raters of different professions for a quick evaluation of parietal lobes on brain MRI within 1-2 minutes. We believe it could be used as an adjunct measure in differential diagnosis of dementias, especially early-onset AD.
The Parietal Atrophy Score is the reliable visual scale among raters of different professions for a quick evaluation of parietal lobes on brain MRI within 1-2 minutes. click here We believe it could be used as an adjunct measure in differential diagnosis of dementias, especially early-onset AD.
Identifying and classifying individuals with Cognitive Impairment-No Dementia (CIND) has further challenged diagnostic methods, since varying the cutoffs for objective impairment as well as the neuropsychological tests considered can significantly affect diagnosis. Therefore, we investigated the applicability of an actuarial neuropsychological approach for clinical subdivision of CIND and quantified the variability in diagnostic outcomes that results from diverse neuropsychologically derived definition of objective cognitive impairment.

1459 non-demented, clinic-based individuals were recruited from a monocentric memory clinic from 1/1/2016/ to 1/1/2018 and classified as Cognitively Normal (NC), Slight Cognitive Symptom (SCS), SSubtle Cognitive Decline (SCD) or Mild Cognitive Impairment (MCI) via different diagnostic strategies, which varied the composition of objective cognitive assessments involved in the diagnostic process.

We compared two methods of criteria proposed by Jak/Bondi and Petersen/Winblae symptomatic definition for early intervention.Neurodegenerative Diseases (NDD) are the major contributors to age-related causes of mental disability on a global scale. Most NDDs, like Alzheimer's Disease (AD), are complex in nature - implying that they are multi-parametric both in terms of heterogeneous clinical outcomes and underlying molecular paradigms. Emerging evidence from high throughput genomic, transcriptomic and small RNA sequencing experiments hint at the roles of long non-coding RNAs (lncRNAs) in AD. X-inactive Specific Transcript (XIST), a component of the Xic, the X-chromosome inactivation centre, is an RNA gene on the X chromosome of the placental mammals indispensable for the X inactivation process. An extensive literature survey shows that aberrations in Xist expression and in some cases, a disruption of the Xchromosome inactivation as a whole play a significant role in AD. Considering the enormous potential of Xist as an endogenous silencing molecule, the idea of using Xist as a non-conventional chromosome silencer to treat diseases harboring chromosomal alterations is also being implemented. Comprehensive knowledge about how Xist could play such a role in AD is still elusive. In this review, we have collated the available knowledge on the possible Xist involvement and deregulation from the perspective of molecular mechanisms governing NDDs with a primary focus on Alzheimer's disease. Possibilities of XIST mediated therapeutic intervention and linkages between XIC and preferential predisposition of females to AD have also been discussed.
Unlike autobiographical memory (i.e., memory for personal information) in Alzheimer's Disease (AD), little is known about Self-Defining Memories (SDM) (i.e., memories of highly significant personal events) in AD.

The characteristics of self-defining memories in AD were evaluated by analyzing their specificity, emotional valence, and integration, as well as their centrality and contribution to self-continuity. Results demonstrated fewer specific SDM in AD participants than in controls.

No significant differences were observed between AD participants and controls regarding the production of positive or integrated SDM. Furthermore, no significant differences were observed between AD participants and controls regarding the rating of the centrality of SDM and their contribution to self-continuity. These results demonstrate that, although AD participants produce fewer specific SDM than controls, both populations have similar levels of emotional valence, integration, centrality, and selfcontinuity of these memories.

It is concluded that patients with AD, at least those in the mild stages of the disease, can build on significant personal events and experiences (i.e., SDM) to reflect on how these events have changed the way they see themselves.
It is concluded that patients with AD, at least those in the mild stages of the disease, can build on significant personal events and experiences (i.e., SDM) to reflect on how these events have changed the way they see themselves.
The accumulation and aggregation of Aβ as amyloid plaques, the hallmark pathology of the Alzheimer's disease, has been found in other neurological disorders, such as traumatic brain injury. The axonal injury may contribute to the formation of Aβ plaques. Studies to date have focused on the brain, with no investigations of spinal cord, although brain and cord share the same cellular components.

We utilized a spinal cord transection model to examine whether spinal cord injury acutely induced the onset or promote the progression of Aβ plaque 3 days after injury in TgCRND8 transgenic model of AD.

Spinal cord transection was performed in TgCRND8 mice and its littermate control wild type mice at the age of 3 and 20 months. Immunohistochemical reactions/ELISA assay were used to determine the extent of axonal damage and occurrence/alteration of Aβ plaques or levels of Aβ at different ages in the spinal cord of TgCRND8 mice.

After injury, widespread axonal pathology indicated by intra-axonal co-accumulations oence that Aβ plaque pathology may not play a role in secondary injury cascades following spinal cord injury.
The findings underscore the dependence of traumatic axonal injury in governing acute Aβ plaque formation and provide evidence that Aβ plaque pathology may not play a role in secondary injury cascades following spinal cord injury.
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