Exploring the Geroprotective Potential of Nutraceuticals.

Aging is the result of the accumulation of a wide variety of molecular and cellular damages over time, meaning that "the more damage we accumulate, the higher the possibility to develop age-related diseases". Therefore, to reduce the incidence of such diseases and improve human health, it becomes important to find ways to combat such damage. In this sense, geroprotectors have been suggested as molecules that could slow down or prevent age-related diseases.

Towards a Novel Frontier in the Use of Epigenetic Clocks in Epidemiology.

Health problems associated with aging are a major public health concern for the future. Aging is a complex process with wide intervariability among individuals. Therefore, there is a need for innovative public health strategies that target factors associated with aging and the development of tools to assess the effectiveness of these strategies accurately.

GrimAge is elevated in older adults with mild COVID-19 an exploratory analysis.

COVID-19 has been contained; however, the side effects associated with its infection continue to be a challenge for public health, particularly for older adults. On the other hand, epigenetic status contributes to the inter-individual health status and is associated with COVID-19 severity. Nevertheless, current studies focus only on severe COVID-19.

Serum Levels of Glial Fibrillary Acidic Protein Association with Cognitive Impairment and Type 2 Diabetes.

Background: Peripheral biomarkers associated with neurocognitive disorders (NCD) have been evaluated in an attempt to improve diagnosis and early detection and potentially even prevent them. Along with increasing age, type 2 diabetes (T2D) increases the risk of central nervous system disorders and cognitive impairment due to the loss of synaptic function. Central damage triggers an astroglial response, increasing the expression of glial fibrillary acidic protein (GFAP), which can be found peripherally when the blood-brain barrier is compromised.

Citrulline supplementation improves spatial memory in a murine model for Alzheimer's disease.

Objectives: Alzheimer's disease (AD) correlates with the dysfunction of metabolic pathways that translates into neurological symptoms. An arginine deficiency, a precursor of nitric oxide (NO), has been reported for patients with AD. We aimed to evaluate the effect of citrulline oral supplementation on cognitive decline in an AD murine model.

Telomere length and oxidative stress variations in a murine model of Alzheimer's disease progression.

Alzheimer's disease (AD) is the most common cause of dementia, and ageing is its major risk factor. Changes in telomere length have been associated with ageing and some degenerative diseases. Our aim was to explore some of the molecular changes caused by the progression of AD in a transgenic murine model (3xTg-AD; B6; 129-Psen1 Tg (APPSwe, tauP301L) 1Lfa).

BDNF and Tau as biomarkers of severity in multiple sclerosis.

Aim: Determine if serum levels of tau and BDNF can be used as severity biomarkers in multiple sclerosis (MS).

Patients & Methods: Subjects with MS, older than 18 and younger than 55 years old were included; 74 patients with a diagnosis of relapsing-remitting MS, 11 with secondary-progressive MS, and 88 controls were included. Total tau and BDNF were measured by Western blot.

Role of glutamate receptors of central and basolateral amygdala nuclei on retrieval and reconsolidation of taste aversive memory.

There are a number of experiments showing an important involvement of amygdala N-methyl-d-aspartate (NMDA) glutamate receptors on consolidation of conditioned taste aversion (CTA) memory. Interestingly, recent evidence has shown that α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptors are particularly involved in CTA retrieval. Memory reconsolidation has been proposed as a destabilization and re-stabilization process induced by memory reactivation.

Taste aversion memory reconsolidation is independent of its retrieval.

Reconsolidation refers to the destabilization/re-stabilization memory process upon its activation. However, the conditions needed to undergo reconsolidation, as well as its functional significance is quite unclear and a matter of intense investigation. Even so, memory retrieval is held as requisite to initiate reconsolidation.

Differential participation of temporal structures in the consolidation and reconsolidation of taste aversion extinction.

The extinction process has been described as the decline in the frequency or intensity of the conditioned response following the withdrawal of reinforcement. Hence, experimental extinction does not reflect loss of the original memory, but rather reflects new learning, which in turn requires consolidation in order to be maintained in the long term. During extinction of conditioned taste aversion (CTA), a taste previously associated with aversive consequences acquires a safe status through continuous presentations of the flavor with no aversive consequence.

Simultaneous but not independent anisomycin infusions in insular cortex and amygdala hinder stabilization of taste memory when updated.

Reconsolidation has been described as a process where a consolidated memory returns to a labile state when retrieved. Growing evidence suggests that reconsolidation is, in fact, a destabilization/stabilization process that incorporates updated information to a previously consolidated memory. We used the conditioned taste aversion (CTA) task in order to test this theory.

Intrahippocampal anisomycin infusions disrupt previously consolidated spatial memory only when memory is updated.

Reconsolidation has proven to be a common phenomenon relevant to memory processing. However, the functional significance of this process is still a matter of debate. Previous work has shown that reconsolidation is indeed a process by which updated information is integrated, through the synthesis of proteins, to a memory trace.