Memory Loss Research Articles

Fibromyalgia progression and association with other diseases and inheritance with management practices in humans

Fibromyalgia is a widespread pain disorder characterized by chronic, diffuse pain, about 1 to 5% around world. While more prevalent in women and adults, it can also manifest in children and adolescents. The specific pathophysiology of fibromyalgia remains unclear, but it is associated with neuronal over sensitization, reduced conditioned pain modulation, cognitive dysfunction, memory loss, and impaired information processing. It has now been categorized as a somatic symptom disorder. This study aimed to investigate fibromyalgia, focusing on its potential hereditary connections and management practices. A key pathophysiological aspect of fibromyalgia is central sensitization, marked by increased functional connectivity with pre-receptive brain areas, decreased connectivity with antinociceptive areas, and alterations in central nervous system neurotransmitters, also in size and shape of specific brain areas. Fibromyalgia is not directly inherited from parents to offspring, it does exhibit a tendency to cluster within families. The serotonin transporter gene, characterized by single nucleotide polymorphism with "S" (short) allele, is more prevalent in individuals with fibromyalgia and psychological distress. In conclusion, fibromyalgia is a widespread pain disorder with a substantial impact on the central nervous system, resulting in significant disability and an elevated risk of chronic diseases. Early diagnosis and intervention can minimize the impact of fibromyalgia. Physical therapy and non-drug therapies should be customized for each patient. The FDA has approved three drugs including pregabalin, duloxetine, and milnacipran for fibromyalgia treatment.

Understanding Digital Dementia and Cognitive Impact in the Current Era of the Internet: A Review.

Dementia encompasses symptoms resulting from brain damage that impairs cognitive functions, surpassing natural aging effects. This condition affects emotional regulation, behavior, and motivation while preserving consciousness. Dr. Manfred Spitzer coined the term 'digital dementia,' highlighting the cognitive decline associated with excessive reliance on digital devices such as smartphones and Google, potentially exacerbating attention deficit hyperactivity disorder (ADHD) and memory loss. This condition mirrors terms like 'digital amnesia' and 'the Google Effect,' highlighting the brain's tendency to offload peripheral information, leading to panic and forgetfulness. Spitzer's book, Digital Dementia, focuses on gaming effects on children and has thus popularized the term. Teenagers are known to use electronic devices regularly, correlating with rising cognitive impairments. The advent of the internet's fifth generation (5G) has transformed technology use, impacting mental health treatments and clinical practices globally. Digital media's influence on the developing brain encompasses motor skills, language, and cognition. Excessive digital media use in young adults correlates with lower cognitive empathy, affecting interpersonal understanding and facial recognition. Studies link heavy reliance on web-based media to decreased white matter integrity, crucial for language skills. Adolescents may be more vulnerable to anxiety and unrealistic expectations due to digital media overuse. Digital media overuse impacts brain development, especially cognitive and inhibitory control, attention, memory, and reasoning, essential for adapting to dynamic environments. Early exposure to fast-paced media can impair motor skills, spatial awareness, problem-solving, and language learning. Neuroimaging studies reveal that environmental factors like screen usage affect brain networks controlling social-emotional behavior and executive functions. Overreliance on smartphones diminishes gray matter in key brain regions, affecting cognitive and emotional regulation. The internet generation, characterized by advancements such as Web 3.0, introduces artificial intelligence and semantic web technologies, reshaping digital content processing. The neurobiological basis of digital dementia involves changes in the brain structure and function, with excessive screen exposure linked to cognitive impairments. Neuroplasticity, or the brain's adaptability, plays a role in cognitive decline from digital media overuse. Early childhood and adolescent brain development stages exhibit significant plasticity, influencing cognitive trajectories. Addressing digital dementia requires strategies to reduce screen time, promote cognitive exercises, and enhance awareness. Parents should regulate children's screen usage, encourage digital detox periods, and substitute screen time with other activities. Cognitive training programs such as Cogmed (Neural Assembly Int AB, Stockholm, SWE) and CogniFit (San Francisco, CA, USA) can improve memory and attention in older adults. Promoting balanced technology use and educating on the risks of excessive digital media consumption is crucial for maintaining cognitive health in the digital age.

A meta-analysis of the effects of transcranial direct current stimulation combined with cognitive training on working memory in healthy older adults.

Working memory (WM) loss, which can lead to a loss of independence, and declines in the quality of life of older adults, is becoming an increasingly prominent issue affecting the ageing population. Transcranial direct current stimulation (tDCS), a non-invasive brain stimulation technique, is emerging as a potential alternative to pharmacological treatments that shows promise for enhancing WM capacity and May enhance the effects of cognitive training (CT) interventions. The purpose of this meta-analysis was to explore how different tDCS protocols in combination with CT enhanced WM in healthy older adults. Randomized controlled trials (RCTs) exploring the effects of tDCS combined with CT on WM in healthy older adults were retrieved from the Web of Science, PubMed, Embase, Scopus and the Cochrane Library databases. The search time period ranged from database inception to January 15, 2024. Methodological quality of the trials was assessed using the risk-of-bias criteria for RCTs from the Cochrane Collaboration Network, and RevMan 5.3 (Cochrane, London, United Kingdom) was used for the meta-analysis of the final literature outcomes. Six RCTs with a total of 323 participants were ultimately included. The results of the meta-analysis show that tDCS combined with CT statistically significantly improves WM performance compared to the control sham stimulation group in healthy older adults [standard mean difference (SMD) = 0.35, 95% CI: 0.11-0.59, I 2 = 0%, Z = 2.86, p = 0.004]. The first subgroup analysis indicated that, when the stimulus intensity was 2 mA, a statistically significant improvement in WM performance in healthy older adults was achieved (SMD = 0.39, 95% CI: 0.08-0.70, I 2 = 6%, Z = 2.46, p = 0.01). The second subgroup analysis showed that long-term intervention (≥ 10 sessions) with tDCS combined with CT statistically significantly improved WM compared to the control group in healthy older adults (SMD = 0.72, 95% CI: 0.22-1.21, I 2 = 0%, Z = 2.85, p = 0.004). tDCS combined with CT statistically significantly improves WM in healthy older adults. For the stimulus parameters, long-term interventions (≥ 10 sessions) with a stimulation intensity of 2 mA are the most effective.

DMT1 knockout abolishes ferroptosis induced mitochondrial dysfunction in C. elegans amyloid β proteotoxicity

Iron is critical for neuronal activity and metabolism, and iron dysregulation alters these functions in age-related neurodegenerative disorders, such as Alzheimer's disease (AD). AD is a chronic neurodegenerative disease characterized by progressive neuronal dysfunction, memory loss and decreased cognitive function. AD patients exhibit elevated iron levels in the brain compared to age-matched non-AD individuals. However, the degree to which iron overload contributes to AD pathogenesis is unclear. Here, we evaluated the involvement of ferroptosis, an iron-dependent cell death process, in mediating AD-like pathologies in C. elegans. Results showed that iron accumulation occurred prior to the loss of neuronal function as worms age. In addition, energetic imbalance was an early event in iron-induced loss of neuronal function. Furthermore, the loss of neuronal function was, in part, due to increased mitochondrial reactive oxygen species mediated oxidative damage, ultimately resulting in ferroptotic cell death. The mitochondrial redox environment and ferroptosis were modulated by pharmacologic processes that exacerbate or abolish iron accumulation both in wild-type worms and worms with increased levels of neuronal amyloid beta (Aβ). However, neuronal Aβ worms were more sensitive to ferroptosis-mediated neuronal loss, and this increased toxicity was ameliorated by limiting the uptake of ferrous iron through knockout of divalent metal transporter 1 (DMT1). In addition, DMT1 knockout completely suppressed phenotypic measures of Aβ toxicity with age. Overall, our findings suggest that iron-induced ferroptosis alters the mitochondrial redox environment to drive oxidative damage when neuronal Aβ is overexpressed. DMT1 knockout abolishes neuronal Aβ−associated pathologies by reducing neuronal iron uptake.

On the lasting impact of mild traumatic brain injury on working memory: Behavioural and electrophysiological evidence

Despite increasing recognition of the significance of mild traumatic brain injury (mTBI), the long-term cognitive consequences of the injury remain unclear. More sensitive measures that can detect subtle cognitive changes and consideration of individual variability are needed to properly characterise cognitive outcomes following mTBI. Here, we used complex behavioural tasks, individual differences approaches, and electrophysiology to investigate the long-term cognitive effects of a history of mTBI. In Experiment 1, participants with self-reported mTBI history (n=82) showed poorer verbal working memory performance on the operation span task compared to control participants (n=88), but there were no group differences in visual working memory, multitasking, cognitive flexibility, attentional control, visuospatial ability, or information processing speed. Individual differences analyses revealed that time since injury and presence of memory loss predicted visual working memory capacity and visuospatial ability, respectively, in those with mTBI history. In Experiment 2, participants with mTBI history (n=20) again demonstrated poorer verbal working memory on the operation span task compared to control participants (n=38), but no group differences were revealed on a visuospatial complex span task or simpler visual working memory measures. We also explored the electrophysiological indices of visual working memory using EEG during a change detection task. No differences were observed in early sensory event-related potentials (P1, N1) or the later negative slow wave associated with visual working memory capacity. Together, these findings suggest that mTBI history may be associated with a lasting, isolated disruption in the subsystem underlying verbal working memory storage. The results emphasise the importance of sensitive cognitive measures and accounting for individual variability in injury characteristics when assessing mTBI outcomes.

Memory problems in elderly people with traumatic brain injury

AbstractThe aim of this study is to assess the effectiveness of various therapy methods in elderly individuals with traumatic brain injury (TBI), taking into account the degree of memory loss and the severity of the injury. The study was conducted in 2022 in Moscow, Russia, and Sofia, Bulgaria, involving six clinics. A total of 200 elderly patients with TBI participated in the study, with a mean age of 72 years. Patients were categorized into groups based on the degree of memory loss and severity of the injury. Standardized tests, including the Mini‐Mental State Examination (MMSE), Clock Drawing Test, Digit Symbol Substitution Test, and Free, and Cued Selective Reminding Test, were used to assess cognitive functions. The Progressive Learning Test evaluated patients' ability to memorize and reproduce information over time. Groups receiving physical therapy and cognitive rehabilitation showed statistically significant improvement in cognitive functions compared to other therapy methods. Specifically, the mean score of the MMSE in these groups increased by 7 points (p < .001). Patients with more severe memory loss demonstrated more pronounced improvement in cognitive functions following the integrated therapy approach. The mean MMSE score increased by 10 points (p < .001), whereas in patients with milder memory loss, the growth was less significant (mean increase of 5 points, p < .05). Groups receiving physical therapy and cognitive rehabilitation consistently demonstrated significantly better results compared to speech therapy and psychological support throughout the study period.

Degeneración combinada subaguda de la médula y gastritis atrófica: revisión de la literatura

Introduction: Subacute combined degeneration of the spinal cord is a consequence of vitamin B12 deficiency. Its clinical presentation includes paresthesia, and proprioception and vibratory sensation loss, which can become disabling. Case presentation: we report the case of an elderly patient who experienced initial paresthesia which progressed to paraparesis, as well as some memory loss. Based on his physical examination a diagnostic impression of myelitis was made. Further investigation evidenced cyanocobalamin deficiency. Conclusion: patient was treated with vitamin B12 supplementation, obtaining an adequate response. There are numerous causes of vitamin B12 deficiency, however, its treatment is simple, and its early initiation can prevent severe neurological symptoms leading to disability.

Exploring the Role of Reactive Oxygen Species in the Pathogenesis and Pathophysiology of Alzheimer's and Parkinson's Disease and the Efficacy of Antioxidant Treatment.

Alzheimer's (AD) and Parkinson's Disease (PD) are life-altering diseases that are characterised by progressive memory loss and motor dysfunction. The prevalence of AD and PD is predicted to continuously increase. Symptoms of AD and PD are primarily mediated by progressive neuron death and dysfunction in the hippocampus and substantia nigra. Central features that drive neurodegeneration are caspase activation, DNA fragmentation, lipid peroxidation, protein carbonylation, amyloid-β, and/or α-synuclein formation. Reactive oxygen species (ROS) increase these central features. Currently, there are limited therapeutic options targeting these mechanisms. Antioxidants reduce ROS levels by the induction of antioxidant proteins and direct neutralisation of ROS. This review aims to assess the effectiveness of antioxidants in reducing ROS and neurodegeneration. Antioxidants enhance major endogenous defences against ROS including superoxide dismutase, catalase, and glutathione. Direct neutralisation of ROS by antioxidants protects against ROS-induced cytotoxicity. The combination of Indirect and direct protective mechanisms prevents ROS-induced α-synuclein and/or amyloid-β formation. Antioxidants ameliorate ROS-mediated oxidative stress and subsequent deleterious downstream effects that promote apoptosis. As a result, downstream harmful events including neuron death, dysfunction, and protein aggregation are decreased. The protective effects of antioxidants in human models have yet to directly replicate the success seen in cell and animal models. However, the lack of diversity in antioxidants for clinical trials prevents a definitive answer if antioxidants are protective. Taken together, antioxidant treatment is a promising avenue in neurodegenerative disease therapy and subsequent clinical trials are needed to provide a definitive answer on the protective effects of antioxidants. No current treatment strategies have significant impact in treating advanced AD and PD, but new mimetics of endogenous mitochondrial antioxidant enzymes (Avasopasem Manganese, GC4419 AVA) may be a promising innovative option for decelerating neurodegenerative progress in the future at the mitochondrial level of OS.

Long COVID is not the same for everyone: a hierarchical cluster analysis of Long COVID symptoms 9 and 12 months after SARS-CoV-2 test

BackgroundIdentifying symptom clusters in Long COVID is necessary for developing effective therapies for this diverse condition and improving the quality of life of those affected by this heterogeneous condition. In this study, we aimed to identify and compare symptom clusters at 9 and 12 months after a SARS-CoV-2 positive test and describe each cluster regarding factors at infection.MethodsThis is a cross-sectional study with individuals randomly selected from the Portuguese National System of Epidemiological Surveillance (SINAVE) database. Individuals who had a positive SARS-CoV-2 test in August 2022 were contacted to participate in a telephonic interview approximately 9 and 12 months after the test. A hierarchical clustering analysis was performed, using Euclidean distance and Ward’s linkage. Clustering was performed in the 35 symptoms reported 9 and 12 months after the SARS-CoV-2 positive test and characterised considering age, sex, pre-existing health conditions and symptoms at time of SARS-CoV-2 infection.Results552 individuals were included at 9 months and 458 at 12 months. The median age was 52 years (IQR: 40–64 years) and 59% were female. Hypertension and high cholesterol were the most frequently reported pre-existing health conditions. Memory loss, fatigue or weakness and joint pain were the most frequent symptoms reported 9 and 12 months after the positive test. Four clusters were identified at both times: no or minor symptoms; multi-symptoms; joint pain; and neurocognitive-related symptoms. Clusters remained similar in both times, but, within the neurocognitive cluster, memory loss and concentration issues increased in frequency at 12 months. Multi-symptoms cluster had older people, more females and more pre-existing health conditions at 9 months. However, at 12 months, older people and those with more pre-existing health conditions were in joint pain cluster.ConclusionsOur results suggest that Long COVID is not the same for everyone. In our study, clusters remained similar at 9 and 12 months, except for a slight variation in the frequency of symptoms that composed each cluster. Understanding Long COVID clusters might help identify treatments for this condition. However, further validation of the observed clusters and analysis of its risk factors is needed.

Extracellular vesicle and CRISPR gene therapy: Current applications in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease.

Neurodegenerative diseases are characterized by progressive deterioration of the nervous system. Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD) are prominently life-threatening examples of neurodegenerative diseases. The complexity of the pathophysiology in neurodegenerative diseases causes difficulties in diagnosing. Although the drugs temporarily help to correct specific symptoms including memory loss and degeneration, a complete treatment has not been found yet. New therapeutic approaches have been developed to understand and treat the underlying pathogenesis of neurodegenerative diseases. With this purpose, clustered-regularly interspaced short palindromic repeats/CRISPR-associated protein (CRISPR/Cas) technology has recently suggested a new treatment option. Editing of the genome is carried out by insertion and deletion processes on DNA. Safe delivery of the CRISPR/Cas system to the targeted cells without affecting surrounding cells is frequently investigated. Extracellular vesicles (EVs), that is exosomes, have recently been used in CRISPR/Cas studies. In this review, CRISPR/Cas and EV approaches used for diagnosis and/or treatment in AD, PD, ALS, and HD are reviewed. CRISPR/Cas and EV technologies, which stand out as new therapeutic approaches, may offer a definitive treatment option in neurodegenerative diseases.

Evaluation of altered cell-cell communication between glia and neurons in the hippocampus of 3xTg-AD mice at two time points.

Alzheimer's disease (AD) is the most common form of dementia and is characterized by progressive memory loss and cognitive decline, affecting behavior, speech, and motor abilities. The neuropathology of AD includes the formation of extracellular amyloid-β plaque and intracellular neurofibrillary tangles of phosphorylated tau, along with neuronal loss. While neuronal loss is an AD hallmark, cell-cell communication between neuronal and non-neuronal cell populations maintains neuronal health and brain homeostasis. To study changes in cellcell communication during disease progression, we performed snRNA-sequencing of the hippocampus from female 3xTg-AD and wild-type littermates at 6 and 12 months. We inferred differential cell-cell communication between 3xTg-AD and wild-type mice across time points and between senders (astrocytes, microglia, oligodendrocytes, and OPCs) and receivers (excitatory and inhibitory neurons) of interest. We also assessed the downstream effects of altered glia-neuron communication using pseudobulk differential gene expression, functional enrichment, and gene regulatory analyses. We found that glia-neuron communication is increasingly dysregulated in 12-month 3xTg-AD mice. We also identified 23 AD-associated ligand-receptor pairs that are upregulated in the 12-month-old 3xTg-AD hippocampus. Our results suggest increased AD association of interactions originating from microglia. Signaling mediators were not significantly differentially expressed but showed altered gene regulation and TF activity. Our findings indicate that altered glia-neuron communication is increasingly dysregulated and affects the gene regulatory mechanisms in neurons of 12-month-old 3xTg-AD mice.

Morphological Factors and Forces Acting in Normal and Sickled Erythrocytes in Sickle Cell Anemia: A Mathematical Model

We carried out a theoretical study that considers the morphological factors and forces acting on a normal and a sickled blood cell. Sickle cell disease is associated with vaso-occlusion which creates blood flow crises as a result of loss in shape memory of the normal red blood cell. Certain forces and chemical compositions acting on the cell could retain the shape memory. The problem of a second order partial differential equation modeled was solved to get the forces and chemical composition required to restore the sickled red blood cells back to its original shape. The results gotten showed that, increase in chemical reaction increased the RBC growth by creating a stretching force that causes the sickle cell to regain elasticity with improved oxygen.

Is SARS-CoV-2 the only cause of long-COVID?

Around 10% of adults infected with SARS-CoV-2 that survive a first episode of COVID-19 appear to experience long-term clinical manifestations. The signs and symptoms of this post-acute COVID-19 syndrome (PACS) include fatigue, dyspnea, joint pain, myalgia, chest pain, cough, anosmia, dysgeusia, headache, depression, anxiety, memory loss, concentration difficulties, and insomnia. These sequelae remind the constellation of clinical manifestations previously recognized as myalgic encephalomyelitis (ME) or chronic fatigue syndrome (CFS). This condition has been described following distinct infectious events, mostly acute viral illnesses. In this way, the pathophysiology of PACS might overlap with mechanisms involved in other post-infectious fatigue syndromes. The risk of PACS is more frequent in women than men. Additional host genetic factors could be involved. There is a dysregulation of multiple body organs and systems, involving the immune system, the coagulation cascade, endocrine organs, autonomic nervous system, microbiota-gut-brain axis, hypothalamic-pituitary-adrenal axis, hypothalamic-pituitary-thyroid axis, etc. Hypothetically, an abnormal response to certain infectious agents could trigger the development of postinfectious fatigue syndromes.

Mechanism of selenium-enriched Bacillus subtilis alleviating perfluorohexanoic acid toxicity in Carassius auratus through the microbiota–gut–brain axis

The extensive production and use of perfluorohexanoic acid (PFHxA) have established it as an emerging environmental pollutant on a global scale. Selenium has been shown to exert substantial antagonistic effects on harmful substances. Concurrently, probiotics may confer advantageous effects on the host's brain function by orchestrating modulation within the microbiota–gut–brain axis. However, despite the promising properties of selenium-enriched Bacillus subtilis, uncertainties persist regarding its impact on PFHxA and underlying mechanisms. This study evaluated the potential alleviating effects of selenium-enriched B. subtilis on brain damage in Carassius auratus exposed to PFHxA from the perspective of the microbiota–gut–brain axis. Supplementation with selenium-enriched B. subtilis significantly mitigated brain damage and memory loss in C. auratus. Nissl staining of the brain revealed that selenium-enriched B. subtilis mitigated neuronal damage induced by PFHxA. TUNEL staining of the intestine showed that selenium-enriched B. subtilis mitigated PFHxA-induced apoptosis, thus mitigating intestinal injury. Moreover, our study uncovered additional layers of complexity in the microbiota–gut–brain axis, as enhancements were noted in the gut microbiota. Concurrently, alterations in the expression of neurotransmitters and biomarkers associated with emotions, such as 5-hydroxytryptamine, Dopamine, Corticotropin Releasing Factor, Substance p, and ghrelin, highlighted the profound impact of selenium-enriched B. subtilis on the intricate interplay between gut health and emotional well-being. Expanding our focus to the molecular level, we found that supplementation with selenium-enriched B. subtilis further inhibited cellular apoptosis through the brain-derived neurotrophic factor (BDNF) / Tyrosine Kinase receptor B (TrKB) / Protein Kinase B (AKT) / Glycogen synthase kinase3β (GSK-3β) pathway. In conclusion, supplementation with selenium-enriched B. subtilis is a promising strategy to mitigate PFHxA-induced brain damage in C. auratus, offering a multifaceted approach through the microbiota–gut–brain axis. In addition, our study introduces the potential of selenium-enriched B. subtilis as a valuable source of micronutrients for fish, opening new avenues for developmental considerations in aquaculture practices.

B - 32 Neurological Problems in Boxers during the 20th Century: a Review and Synthesis

Abstract Objective There are no validated clinical diagnostic criteria for chronic traumatic encephalopathy or traumatic encephalopathy syndrome (TES). To understand the historical clinical condition, its applicability to modern day athletes, and the pathogenesis of clinical problems, we examined the literature in boxers from the 20th century, with specific attention to neurological findings and characteristics of clinical disease progression. Data Selection Data were extracted for 243 boxers included in 45 articles published between 1928 and 1999, including cases from articles originally published in German. The presence or absence of 22 neurological signs and features were extracted. Data Synthesis The most common neurological problems were slurring dysarthria (49%), gait disturbances (44%), and memory loss (36%), with several other problems that were less frequent, including hyperreflexia (25%), ataxia (22%), increased tone (19%), and extensor Babinski sign (16%). Frank dementia appeared in some cases (17%). There were significantly fewer neurological deficits reported in boxers who fought in the latter part of the 20th century compared to boxers who fought earlier in the century. For most cases, there were no comments about whether the neurological problems were progressive (145, 60%). A progressive condition was described in 71 cases (29%) and a stationary or improving condition was described in 27 cases (11%). Canonical neurodegenerative disease-like progression was described in 15 cases (6%). Conclusions Neurological problems associated with boxing-related neurotrauma during the 20th century are the foundation for present day TES. However, the clinical signs and features in the 20th century differ in most ways from the modern criteria for TES.

A - 31 The Interaction of Cognitive Reserve and Multi-Modal Cognitive Training on the Cognitive Functioning of Older Adults at Risk for Dementia

Abstract Objective Multi-modal cognitive training improves cognition among those at risk for dementia. Although the mechanism is likely via improved cognitive flexibility, conceptually central cognitive reserve, it remains unclear whether cognitive reserve moderates cognitive training effects. The objective of this study was to determine whether baseline cognitive reserve moderates cognitive improvement following cognitive training. Methods Forty-one older adults (M = 72.7+/−4.9 years, 65.1% female, 17% non-white) with self-reported memory loss and baseline TICS score of 24–37 participated in a 6-month cognitive training intervention consisting of weekly computer-administered piano lesson and 30 minutes of daily homework. Cognition was assessed pre and post-intervention using CNS-Vital Signs. Specific domains tested were cognitive flexibility, psychomotor speed, and executive functioning. Cognitive reserve was operationalized as years of education. Results Significant post-training improvements occurred in all three cognitive domains (cognitive flexibility t = −6.34, p < 0.001; psychomotor speed t = −2.62, p = 0.01; executive functioning t = −6.49, p < 0.001). Years of education significantly moderated improvements in executive functioning (b = −0.06, SE(b) = 0.03, t(37) = −2.07, p = 0.045), but neither cognitive flexibility nor psychomotor speed. Specifically, participants with lower education improved most in executive functioning (b = 1.60, t = 2.78, p = 0.008). Conclusions Findings suggest that participants with lower cognitive reserve may benefit more from far-transfer effects of cognitive training on executive functioning. This was not observed in domains closely related (cognitive flexibility) and relatively unrelated (psychomotor speed) to cognitive reserve.

A - 124 A Case of Lewy Body Dementia and Charles Bonnet Syndrome in a Patient with Bilateral Enucleation

Abstract Objective The patient presented with a history of blindness due to bilateral enucleation (age 10 and 23) and visual hallucinations for approximately 2 years. Approximately 30% of visually impaired individuals are affected by Charles Bonnet syndrome, characterized by complex visual hallucinations in visually challenged patients, possibly stemming from the brain’s attempt to fill the visual void. Additionally, she was diagnosed with Lewy Body dementia (LBD) 2 years prior by her neurologist, and she reported challenges with completing instrumental activities of daily living (IADLs). Method The patient was a left-handed 83-year-old woman, with a history of total blindness and bilateral enucleation, who presented with progressive memory loss 3–4 years prior, along with balance/gait disturbances for 1–1.5 years. The patient and her family sought neuropsychological testing to clarify her cognitive functioning in light of her physical and neurologic symptoms. Results Premorbid functioning was estimated in the low average range, with 11 years of education. Due to her total vision loss, neuropsychological evaluation was limited. Her cognitive profile was marked by impairments in immediate memory, delayed memory, recognition, executive functioning, and language. Conclusions In light of the patient’s marked cognitive deficits in memory, attention, and executive functioning, along with visual hallucinations (although also attributed to possible Charles Bonnet syndrome), balance/gait disturbances, fluctuating awareness, autonomic dysfunction (i.e., bladder/bowel control), and sleep changes (i.e., acting out dreams), her presentation is consistent with LBD, in the moderate stage of severity. Given the symptomatology, it raises the possibility the patient may be experiencing Charles Bonnet syndrome along with LBD.

Recent Advances of Mitochondrial Alterations in Alzheimer's Disease: A Perspective of Mitochondrial Basic Events.

Alzheimer's disease (AD) is one of the most common neurodegenerative disorders and is characterized by a decrease in learning capacity, memory loss and behavioral changes. In addition to the well-recognized amyloid-β cascade hypothesis and hyperphosphorylated Tau hypothesis, accumulating evidence has led to the proposal of the mitochondrial dysfunction hypothesis as the primary etiology of AD. However, the predominant molecular mechanisms underlying the development and progression of AD have not been fully elucidated. Mitochondrial dysfunction is not only considered an early event in AD pathogenesis but is also involved in the whole course of the disease, with numerous pathophysiological processes, including disordered energy metabolism, Ca2+ homeostasis dysfunction and hyperactive oxidative stress. In the current review, we have integrated emerging evidence to summarize the main mitochondrial alterations- bioenergetic metabolism, mitochondrial inheritance, mitobiogenesis, fission- fusion dynamics, mitochondrial degradation, and mitochondrial movement- underlying AD pathogenesis; precisely identified the mitochondrial regulators; discussed the potential mechanisms and primary processes; highlighted the leading players; and noted additional incidental signaling pathway changes. This review may help to stimulate research exploring mitochondrial metabolically-oriented neuroprotection strategies in AD therapies, leading to a better understanding of the link between the mitochondrial dysfunction hypothesis and AD pathogenesis.

Assessing the effect of anthocyanins through diet and supplementation on cognitive function in older adults at risk for dementia: protocol for a randomised controlled trial

IntroductionPromising evidence is emerging for the procognitive, anti-inflammatory and neuroprotective properties of dietary flavonoids, particularly anthocyanins that provide red, purple and blue plant pigments.Methods and analysisThe ‘Food for Thought’ study...

The Impact of Physical Activity on Memory Loss and Concentration in Adults Aged 18 or Older in the U.S. in 2020.

This cross-sectional study used secondary data from the USA 2020 National Health Interview Survey database. The goal of this study is to outline the impact physical activity has on cognition and mental ability. The reason we chose to pursue this research was a result of the exponentially growing weight of economic and emotional burden caused by cognitive impairments and diseases. The main outcome was whether individuals experienced dementia symptoms such as memory loss and difficulty concentrating. The main exposure was following physical activity guidelines (none, strength only, aerobic only, both). The confounders included age, sex, region, heart disease status, smoking status, drinking status, and depression status. The sample is composed of 30,119 USA adults aged 18 or older. Of those participants, 46% were male and 54% were female. By age, 96% were 18-84 years old, and approximately 4% were 85 and older. Logistic regression analysis was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). There was a statistically significant association between difficulty following physical activity guidelines and cognitive difficulties. Those who met aerobic only increased the odds of cognitive difficulty by 52% (OR 1.52; 95% CI: 1.34-1.74) compared with those who met both criteria. Those who met the strength criteria had 1.7 greater odds of cognitive difficulties (OR 1.70; 95% CI: 1.42-2.02) than those who met both criteria. Those who met neither of these guidelines had almost threefold greater odds of having cognitive difficulties (OR 2.64; 95% CI: 2.36-2.96) than those who met both guidelines. Researchers and healthcare providers should collaborate to encourage meeting these guidelines and addressing barriers preventing people from being physically active, such as physical limitations and access to safe recreational spaces. Future studies should address the health disparities regarding physical activity.