There is little evidence in the literature about the possible relationship between sarcopenia and cognition in older adults. Our objective was to investigate the association between cognitive impairment and sarcopenia in older adults living in the community through a systematic review of published studies.

Alzheimer’s disease (AD) is associated with a progressive dementia, and there is good evidence that it is more pronounced in individuals that have fewer stimuli during their lives. Environmental stimulation promotes morphological and functional changes in the brain, leading to amplification of cognitive functions, and has been described in humans and animals. In this study, we evaluated the effects of enriched environment (EE) stimulation on spatial memory and senile plaque formation in transgenic mice PDGFB-APPSwInd (TG) that overexpress the human amyloid precursor protein, normally resulting in an increased density of senile plaques. We compared this group of EE stimulated transgenic mice (TG-EE) with an EE stimulated control group of age-matched C57Bl/6 wild type animals (WT-EE). Both groups were exposed to EE stimulation between the ages of 8 and 12 months. As controls of the experiment, there were a group of TG mice not exposed to EE (TG-Ctrl) and a group of WT mice not exposed to EE (WT-Ctrl). The TG-EE group presented improved spatial memory when compared to the TG-Ctrl animals. In addition, the TG-EE group showed a 69.2% reduction in the total density of senile plaques in the hippocampus when compared to the TG-Ctrl group. In this group, the concentration of senile plaques was greater in the dorsal part of the hippocampus, which is linked to spatial localization, and the reduction of this density after the submission to EE was as high as 85.1%. EE stimulation had no effect on the density of amyloid-β (Aβ) oligomers. However, amyloid scavenger receptor class B member 1 (SR-B1) density was significantly decreased in the TG-Ctrl mice, but not in the TG-EE mice, suggesting that cognitive stimulation had an effect on the formation of a cognitive reserve that could prevent the accumulation of senile plaques. It is suggested that the stimulation of old mice by EE for 4 months led to the formation of brain resilience that protected the brain from the deposition of senile plaques, one of the hallmarks of AD, leading to improvement in spatial memory.

Emerging studies indicate the persistence of symptoms beyond the acute phase of COVID-19. Cognitive impairment has been observed in certain individuals for months following infection. Currently, there is limited knowledge about the specific cognitive domains that undergo alterations during the post-acute COVID-19 syndrome and the potential impact of disease severity on cognition. The aim of this review is to examine studies that have reported cognitive impairment in post-acute COVID-19, categorizing them into subacute and chronic phases. The methodology proposed by JBI was followed in this study. The included studies were published between December 2019 and December 2022. The search was conducted in PubMed, PubMed PMC, BVS – BIREME, Embase, SCOPUS, Cochrane, Web of Science, Proquest, PsycInfo, and EBSCOHost. Data extraction included specific details about the population, concepts, context, and key findings or recommendations relevant to the review objectives. A total of 7,540 records were identified and examined, and 47 articles were included. The cognitive domains most frequently reported as altered 4 to 12 weeks after acute COVID-19 were language, episodic memory, and executive function, and after 12 weeks, the domains most affected were attention, episodic memory, and executive function. The results of this scoping review highlight that adults with post-acute COVID-19 syndrome may have impairment in specific cognitive domains.

Background: The link between sarcopenia and cognitive impairment has not yet been thoroughly evaluated, especially among older adults. Objective: To evaluate the relationship between probable sarcopenia and cognitive impairment among community-dwelling older adults in two Brazilian cities. Methods: Probable sarcopenia was assessed using the EWGSOP2 (2018) criteria. Thus, participants were classified as probably having sarcopenia if they had SARC-F (Strength, Assistance in walking, Rise from a chair, Climb stairs and Falls) ≥4 points and low grip strength. Cognitive function was evaluated through the Mini-Mental State Examination (MMSE), verbal fluency (VF) and clock drawing test (CDT). Results: In a sample of 529 older adults (mean age 80.8±4.9 years; mean education 4.2±3.67 years; 70.1% women), 27.3% of the participants had SARC-F≥4, 38.3% had low grip strength and 13.6% were classified as probable sarcopenia cases. After adjusting for possible confounders (age, sex, education, depression, diabetes, hypertension, leisure-time physical activity and obesity), probable sarcopenia was found to be associated with impairment in the MMSE (OR 2.52; 95%CI 1.42‒4.47; p=0.002) and in VF (OR 2.17; 95%CI 1.17‒4.01; p=0.014). Low grip strength was found to be associated with impairment in the MMSE (OR 1.83; 95%CI 1.18‒2.82; p=0.006) and in the CDT (OR 1.79; 95%CI 1.18‒2.73; p=0.006). SARC-F scores were found to be associated with impairment in the MMSE (OR 1.90; 95%CI 1.18‒3.06; p=0.008). Conclusion: The results suggested that probable sarcopenia and its components present a significant association with cognitive deficits among community-dwelling older adults. Future longitudinal studies will further explore the causal relationship.