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Sleep and brain/cognitive/neural reserve significantly impact well-being and cognition throughout life. This review aims to explore the intricate relationship between such factors, with reference to their effects on human cognitive functions. The specific goal is to understand the bidirectional influence that sleep and reserve exert on each other. Up to 6 February 2024, a methodical search of the literature was conducted using the PubMed database with terms related to brain, cognitive or neural reserve, and healthy or disturbed sleep. Based on the inclusion criteria, 11 articles were selected and analyzed for this review. The articles focus almost exclusively on cognitive reserve, with no explicit connection between sleep and brain or neural reserve. The results evidence sleep's role as a builder of cognitive reserve and cognitive reserve's role as a moderator in the effects of physiological and pathological sleep on cognitive functions. In conclusion, the findings of the present review support the notion that both sleep and cognitive reserve are critical factors in cognitive functioning. Deepening comprehension of the interactions between them is essential for devising strategies to enhance brain health and resilience against age- and pathology-related conditions. [ABSTRACT FROM AUTHOR]

Evidence in the literature indicates that aerobic physical activity may have a protective role in aging pathologies. However, it has not been clarified whether different types of aerobic exercise produce different effects. In particular, these potential differences have not been explored in patients with Alzheimer's disease (AD). The present narrative review has the specific aim of evaluating whether land (walking/running) and water (swimming) aerobic activities exert different effects on cognitive functions and neural correlates in AD patients. In particular, the investigation is carried out by comparing the evidence provided from studies on AD animal models and on patients. On the whole, we ascertained that both human and animal studies documented beneficial effects of land and water aerobic exercise on cognition in AD. Also, the modulation of numerous biological processes is documented in association with structural modifications. Remarkably, we found that aerobic activity appears to improve cognition per se, independently from the specific kind of exercise performed. Aerobic exercise promotes brain functioning through the secretion of molecular factors from skeletal muscles and liver. These molecular factors stimulate neuroplasticity, reduce neuroinflammation, and inhibit neurodegenerative processes leading to amyloid-β accumulation. Additionally, aerobic exercise improves mitochondrial activity, reducing oxidative stress and enhancing ATP production. Aerobic activities protect against AD, but implementing exercise protocols for patients is challenging. We suggest that health policies and specialized institutions should direct increasing attention on aerobic activity as lifestyle modifiable factor for successful aging and age-related conditions. [ABSTRACT FROM AUTHOR]

Increasing evidence suggests that motor rehabilitation may delay Parkinson's disease (PD) progression. Moreover, parallel treatments in animals up-regulate brain-derived neurotrophic factor (BDNF). Thus, we investigated the effect of a motor rehabilitation protocol on PD symptoms and BDNF serum levels. Motor rehabilitation training consisted of a cycle of 20 days/ month of physiotherapy divided in 3 daily sessions. Clinical data were collected at the beginning, at the end, and at 90 days follow-up. BDNF serum levels were detected by ELISA at 0, 7, 14, 21, 30, and 90 days. The follow-up period had a duration of 60 days (T30-T90). The results showed that at the end of the treatment (day 30), an improvement in extrapyramidal signs (UPDRS III; UPDRS III - Gait and Balance items), motor (6 Minute Walking Test), and daily living activities (UPDRS II; PDQ-39) was observed. BDNF levels were increased at day 7 as compared with baseline. After that, no changes in BDNF were observed during the treatment and in the successive follow-up. This study demonstrates that motor rehabilitation training is able to ameliorate PD symptoms and to increase temporarily BDNF serum levels. The latter effect may potentially contribute to the therapeutic action. Key words: motor rehabilitation, physical exercise, BDNF, Parkinson's disease. De plus en plus de donnees suggerent que la reeducation motrice peut retarder la progression de la maladie de Parkinson (MP). De plus, des traitements paralleles chez l'animal regulent a la hausse l'expression du facteur de croissance neurotrophique derive du cerveau BDNF. Ainsi, les auteurs ont etudie l'effet d'un protocole de reeducation motrice sur les symptomes de la MP et sur les niveaux seriques de BDNF. La reeducation motrice consistait en un cycle de 20 jours/mois de physiotherapie repartie en 3 sessions quotidiennes. Les donnees cliniques ont ete recoltees au debut, a la fin et au jour 90 en post-observation. Les niveaux seriques de BDNF ont ete mesures par ELISA a 0, 7,14, 30 et 90 jours. La periode post- observation avait une duree de 60 jours, (J30 cl J90). Les resultats ont montre qu'a la fin du traitement (J30), une amelioration des signes extrapyramidaux (echelle UPDRS III ; les items demarche et equilibre de l'echelle UPDRS III), des activites motrices (marche de 6 minutes) et quotidiennes (echelle UPDRS II; questionnaire PDQ-39) etait observee. Les niveaux de BDNF augmentaient au jour 7 comparativement au niveau de base, apres quoi, aucun changement des niveaux de BDNF n'etait observe durant le traitement et lors de la periode post-observation subsequente. Cette etude demontre que la reeducation motrice peut ameliorer les symptomes de la MP et accroitre temporairement les niveaux seriques de BDNF. Ce dernier effet peut potentiellement contribuer a l'action therapeutique observee. [Traduit par la Redaction] Mots-cles: reeducation motrice, exercice physique, BDNF, maladie de Parkinson., Introduction Parkinson's disease (PD) is a chronic neurodegenerative disease leading to motor dysfunctions characterized by resting tremor, bradykinesia, rigidity, and postural instability (Gazewood et al. 2013). PD is caused by [...]

Alzheimer's disease (AD) is a disorder characterized by the accumulation of abnormally folded protein fragments in neurons, i.e., β-amyloid (Aβ) and tau protein, leading to cell death. Several neuropeptides present in the central nervous system (CNS) are believed to be involved in the pathophysiology of AD. Among them, neuropeptide Y (NPY), a small peptide widely distributed throughout the brain, has generated interest because of its role in neuroprotection against excitotoxicity in animal models of AD. In addition, it has been shown that NPY modulates neurogenesis. Interestingly, these latter effects are similar to those elicited by neurotrophins, which are critical molecules for the function and survival of neurons that degenerate during the course of AD. In this review we summarize the evidence for the involvement of NPY and neurotrophins in AD pathogenesis, and the similarity between them in CNS neurons. Finally, we recapitulate our recent in-vitro evidence for the involvement of neurotrophin nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in the neuroprotective effect elicited by NPY in AD neuron-like models (neuroblastoma cells or primary cultures exposed to toxic concentrations of Aβ's pathogenic fragment 25-35), and propose a putative mechanism based on NPY-induced inhibition of voltage-dependent [Ca.sup.2+] influx in preand post-synaptic neurons. Key words: neuropeptide Y, neurotrophins, nerve growth factor, brain-derived neurotrophic factor, neuroprotection, Alzheimer's disease, amyloid β, in vitro models. La maladie d'Alzheimer (MA) se caracterise par une accumulation dans les neurones de fragments proteiques anormalement replies, comme l'amyloide-β (Aβ) et tau, resultant en une mort cellulaire. Plusieurs neuropeptides presents dans le systeme nerveux central (SNC) seraient impliques dans la pathophysiologie de la MA. Parmi ceux-ci, le Neuropeptide Y (NPY), un petit peptide largement distribue dans tout le cerveau, a suscite un certain interet a cause de son role dans la neuroprotection contre l'excitotoxicite dans des modeles animaux de MA. De plus, il a ete demontre que le NPY pouvait moduler la neurogenese. Fait interessant, ces derniers effets sont similaires a ceux produits par les neurotrophines, des molecules importantes a la fonction et a la survie des neurones qui degenerent au cours de l'evolution de la MA. Dans cet article de revue, les auteurs resument les preuves de l'implication du NPY et des neurotrophines dans la pathogenese de la MA et leurs similitudes dans les neurones du SNC. Finalement, ils recapitulent les dernieres donnees obtenues in vitro, qui demontrent une implication de deux neurotrophines, le NFG (<< nerve growth factor >>) et le BNDF (<< brain-derived neurotropic growth factor >>), dans les effets neuroprotecteurs assures par le NPY dans des modeles neuronaux de la MA (cellules de neuroblastomes ou cultures primaires exposees a des concentrations toxiques du fragment pathogene 25-35 de l'Aβ), et ils proposentunmecanisme possible surlabase de l'inhibition induite par le NPY de l'influx de [Ca.sup.2+] dependant du voltage dans les neurones pre- et post-synaptiques. [Traduit par la Redaction] Mots-cles: neuropeptide Y, neurotrophines, facteur neuronal NGF, facteur BNDF, maladie d'Alzheimer, amyloide p, modeles in vitro., Alzheimer's disease Alzheimer's Disease (AD) is the most common type of dementia, and consists of an age-related, slowly progressive mental disorder (Holtzman et al. 2011). It is characterized by an [...]

Abstract Background Systemic inflammation might cause neuronal damage and sustain neurodegenerative diseases and behavior impairment, with the participation of pro-inflammatory cytokines, like tumor necrosis factor (TNF)-α and interleukin (IL)-18. However, the potential contribution of these cytokines to behavioral impairment in the long-term period has not been fully investigated. Methods Wistar rats were treated with a single intraperitoneal injection of LPS (5 mg/kg) or vehicle. After 7 days and 10 months, the animal behavior was evaluated by testing specific cognitive functions, as mnesic, discriminative, and attentional functions, as well as anxiety levels. Contextually, TNF-α and IL-18 protein levels were measured by ELISA in defined brain regions (that is, frontal cortex, hippocampus, striatum, cerebellum, and hypothalamus). Results Behavioral testing demonstrated a specific and persistent cognitive impairment characterized by marked deficits in reacting to environment modifications, possibly linked to reduced motivational or attentional deficits. Concomitantly, LPS induced a TNF-α increase in the hippocampus and frontal cortex (from 7 days onward) and cerebellum (only at 10 months). Interestingly, LPS treatment enhanced IL-18 expression in these same areas only at 10 months after injection. Conclusions Overall, these results indicate that the chronic neuroinflammatory network elicited by systemic inflammation involves a persistent participation of TNF-α accompanied by a differently regulated contribution of IL-18. This leads to speculation that, though with still unclear mechanisms, both cytokines might take part in long-lasting modifications of brain functions, including behavioral alteration.