Design and Verification of Integrated Circuitry for Real-Time Frailty Monitoring.

In this study, a new wireless electronic circuitry to analyze weight distribution was designed and incorporated into a chair to gather data related to common human postures (sitting and standing up). These common actions have a significant impact on various motor capabilities, including gait parameters, fall risk, and information on sarcopenia. The quality of these actions lacks an absolute measurement, and currently, there is no qualitative and objective metric for it.

A Real-Time Clinical Decision Support System, for Mild Cognitive Impairment Detection, Based on a Hybrid Neural Architecture.

Clinical procedure for mild cognitive impairment (MCI) is mainly based on clinical records and short cognitive tests. However, low suspicion and difficulties in understanding test cut-offs make diagnostic accuracy being low, particularly in primary care. Artificial neural networks (ANNs) are suitable to design computed aided diagnostic systems because of their features of generating relationships between variables and their learning capability.

Early diagnosis of frailty: Technological and non-intrusive devices for clinical detection.

This work analyses different concepts for frailty diagnosis based on affordable standard technology such as smartphones or wearable devices. The goal is to provide ideas that go beyond classical diagnostic tools such as magnetic resonance imaging or tomography, thus changing the paradigm; enabling the detection of frailty without expensive facilities, in an ecological way for both patients and medical staff and even with continuous monitoring. Fried's five-point phenotype model of frailty along with a model based on trials and several classical physical tests were used for device classification.

[Patterns of brain ageing].

Neuroplasticity lends the brain a strong ability to adapt to changes in the environment that occur during ageing. Animal models have shown alterations in neurotransmission and imbalances in the expression of neural growth factor. Changes at the morphometric level are not constant.

[Inflammation and oxidation: predictive and/or causative factors].

Brain ageing leads to a series of changes that reduce the processes of adaptation and response. These transformations can end in cognitive impairment and/or dementia. Although the cause of these changes is diverse, inflammation and oxidative stress explain some of the pathophysiological mechanisms of these anomalies of brain functioning.

[Longitudinal analysis of nutrition parameters in a cohort of elderly people with and without dementia].

Introduction: It is important to assess longitudinal nutritional parameters during the ageing process in order to determine body composition changes. This procedure is more relevant when dealing with institutionalised geriatric patients suffering from cognitive impairment. The aim of this study was to assess the interactions, if any, between mental status and several nutritional parameters in a cohort of elderly people.

[Genetics and Alzheimer's disease: a population at risk].

The high prevalence of Alzheimer's disease, along with the possibility of new approaches in diagnosis through the use of biomarkers of cerebrospinal fluid is shifting the focus to the elderly with dementia or at risk. In this sense it seems important to review the genetic aspects of the elderly with familial Alzheimer's disease as well as those at risk. The wide distribution of genetic studies associated with this condition may also be helpful.

[Stereology as a tool to estimate brain volume and cortical atrophy in elders with dementia].

Introduction: stereology is a body of methods that allow unbiased and efficient estimation of geometric quantities defined in arbitrary physical structures. In particular, stereology is a valuable tool to assist neuroimaging in the estimation of morphometric parameters in the brain. Therefore, stereology may confer objectivity in the complementary and diagnostic evaluation of dementia by adding disease by adding quantitative data to clinical evaluation.

14-3-3 zeta and tau genes interactively decrease Alzheimer's disease risk.

Abnormal tau hyperphosphorylation has been suggested as being one of the central events in the development of neurofibrillary tangles, which are one of the characteristic neuropathological lesions found in Alzheimer's disease (AD) brains. 14-3-3 zeta protein is associated with tau in brain and stimulates tau phosphorylation. In a case-control study in 293 AD patients and 396 healthy controls, we examined whether the combined gene effects between 14-3-3 zeta (intron 4, rs 983583) polymorphism and tau (intron 9, rs 2471738) polymorphism might be responsible for susceptibility to AD.

No association of genetic variants of liver X receptor-beta with Alzheimer's disease risk.

Apolipoprotein E (APOE) epsilon4 allele is the strongest hitherto known risk factor for sporadic Alzheimer's disease (AD). Liver X receptor-beta (LXRbeta) is a transcription factor that controls expression of genes involved in brain cholesterol metabolism, and one of the main LXRbeta targets is APOE. To evaluate the relationship between LXRbeta genetic variants and AD, independently or in concert with the APOE epsilon4 allele, we examined three LXRbeta polymorphisms located in introns 2 (rs 2695121), 5 (rs 1052533), and 7 (rs 1405655), in 414 Spanish AD patients and 447 controls.

Interaction between poly(ADP-ribose) polymerase 1 and interleukin 1A genes is associated with Alzheimer's disease risk.

Excessive release of proinflammatory cytokines by activated microglia surrounding senile plaques might contribute to the neurodegeneration associated with Alzheimer's disease (AD). Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear protein recently implicated in the initial inflammatory response by modulating expression of inflammation-related genes, like interleukin 1 (IL-1). As PARP-1 overactivity has been shown in the AD brain, we tested the hypothesis that the PARP-1 -410 and -1672 polymorphisms would predispose people to AD due to overexpression of the PARP-1 gene, independently or in concert with the proinflammatory IL-1A -889 polymorphism.

The neurosecretory system is hypertrophied in senescence-accelerated mice.

The hypothalamic supraoptic and paraventricular nuclei form the neurosecretory system and synthesize the neurohormones oxytocin and arginine-vasopressin. The senescence-accelerated mouse is a model of rapid aging that displays senile amyloidosis and memory problems. This paper presents the characterization of the neurosecretory system and describes the presence of a bilateral constant cluster of neurosecretory neurons in these mice.

CD14 receptor polymorphism and Alzheimer's disease risk.

Activation of microglial cells is involved in the inflammatory component of Alzheimer's disease (AD), and it may be triggered by infectious pathogens. CD14, a receptor upregulated in activated microglia, plays a central role in innate immunity through recognition of bacterial lipopolysaccharide and initiation of inflammatory response. A polymorphism in the promoter region (-260) of the CD14 receptor has been found to be related to increased risk of bacterial infections and inflammatory diseases such as atherosclerosis.

The chemokine receptor CCR5-Delta32 gene mutation is not protective against Alzheimer's disease.

Chronic local inflammatory reaction involving reactive microglia is one of the major pathological events in Alzheimer's disease (AD). There is growing evidence that the chemokine receptor CCR5 is up-regulated in AD brain and plays a role in the recruitment and accumulation of microglia in senile plaques. A 32-base pair deletion in the CCR5 gene (CCR5-Delta32 mutant allele) confers resistance to HIV-1 infection by preventing expression of the receptor on the cell surface.

Age-dependent association between the Q7R polymorphism in the Saitohin gene and sporadic Alzheimer's disease.

A vigorous controversy exists over whether tau tangles or amyloid-beta plaques are the primary cause of neurodegeneration in Alzheimer's disease (AD), and it is not well established whether genetic variation in tau is associated with AD. A recently identified novel protein, named Saitohin (STH), shares tissue expression pattern with tau, and preliminary evidence in a North American population indicates that a polymorphism at codon 7 (Q7R) of the STH gene is a predisposing factor for sporadic AD. A case-control study utilizing a clinically well-defined group of 315 sporadic AD patients and 307 control subjects was performed to test this association.

The myeloperoxidase gene in Alzheimer's disease: a case-control study and meta-analysis.

Myeloperoxidase (MPO) presence has been demonstrated in microglia associated with senile plaques, and contributes to Alzheimer's disease (AD) pathology through oxidation-induced damage. Recently, a functional biallelic (G/A) polymorphism in the promotor region (-463) of the MPO gene has been associated with susceptibility to AD, but the reports of this association have been inconsistent. A case-control study utilizing a clinically well-defined group of 315 sporadic AD patients and 327 control subjects was performed to test this association.