Memory Loss Research Articles

The Effect of Apathy and Depressive Syndromes on Functional Outcomes in Alzheimer's Disease.

Alzheimer's disease (AD) is the most common cause of dementia. Its initially characterized by progressive short-term memory loss followed by cross-domain cognitive decline in later stages resulting in significant functional deficits and loss of activities of daily living (ADLs) independence. Apathy and depression are frequent neuropsychiatric sequelae in AD, but their contribution to functional deficits is poorly understood. We aimed to quantitatively investigate if apathy and depressive symptoms predict ADLs in AD. We also wanted to fractionate apathy dimensions by factor-analyzing the apathy evaluation scale (AES) and then investigate the dimensions' relation to ADLs. We recruited a sample of 115 patients with probable or possible AD and assessed them for depression, apathy, and ADLs alongside other measures. We hypothesized that apathy and depressive symptoms would predict ADLs and that AES items will load into cognitive, behavioral, and affective factors that would differentially relate to ADLs. Our results indicated that apathy symptoms predict ADLs deficits. The AES items resolved into a three-factor solution but the manner of clustering diverged from that proposed by AES authors. When these factors were regressed simultaneously, only behavioral apathy predicted global ADLs. Distinguishing basic from instrumental ADLs showed that behavioral and cognitive apathy symptoms associate with ADLs deficits while affective symptoms do not. Our results highlight the influence of apathy on ADLs in AD. This has important implications for patient care considering the high prevalence of apathy in AD and other dementing illnesses.

Light on Alzheimer's disease: from basic insights to preclinical studies.

Alzheimer's disease (AD), referring to a gradual deterioration in cognitive function, including memory loss and impaired thinking skills, has emerged as a substantial worldwide challenge with profound social and economic implications. As the prevalence of AD continues to rise and the population ages, there is an imperative demand for innovative imaging techniques to help improve our understanding of these complex conditions. Photoacoustic (PA) imaging forms a hybrid imaging modality by integrating the high-contrast of optical imaging and deep-penetration of ultrasound imaging. PA imaging enables the visualization and characterization of tissue structures and multifunctional information at high resolution and, has demonstrated promising preliminary results in the study and diagnosis of AD. This review endeavors to offer a thorough overview of the current applications and potential of PA imaging on AD diagnosis and treatment. Firstly, the structural, functional, molecular parameter changes associated with AD-related brain imaging captured by PA imaging will be summarized, shaping the diagnostic standpoint of this review. Then, the therapeutic methods aimed at AD is discussed further. Lastly, the potential solutions and clinical applications to expand the extent of PA imaging into deeper AD scenarios is proposed. While certain aspects might not be fully covered, this mini-review provides valuable insights into AD diagnosis and treatment through the utilization of innovative tissue photothermal effects. We hope that it will spark further exploration in this field, fostering improved and earlier theranostics for AD.

Memory loss induced by lisdexamfetamine in the rat: A behavioral, electrophysiological, and histopathological Study

Lisdexamfetamine (LDX) is one of the drugs commonly used to treat attention deficit hyperactivity disorder (ADHD). However, its neurological side effects, particularly on cognition, are not fully understood. The present study focused on memory in rats treated with four weeks of LDX injection. We compared LDX-treated rats with control ones, using several methods to evaluate the behavioral responses and electrophysiological, molecular, and histological properties in the hippocampus. Our findings demonstrated that subchronic administration of LDX impaired behavioral performance in all memory assessment tests (Y maze, Morris Water Maze, and Shuttle box). Although LDX did not alter population spike (PS) amplitude, it increased the field excitatory postsynaptic potential (fEPSP) slope of evoked potentials of LTP components. Also, in addition to an increase in expression of caspase-3 in the hippocampus, which indicates the susceptibility to apoptosis in LDX-treated rats, the number of microglia and astrocytes went up significantly in the LDX group. Moreover, Sholl's analysis showed an increase in the soma size and total process length in both hippocampal astrocytes and microglia. Overall, because of these destructive effects of LDX on the hippocampus, which is one of the critical memory-related areas of the brain, the findings of this investigation provide evidence to show the disruption of memory-related variables following the LDX. However, more research is needed to clarify it.

Utilizing Siamese 4D-AlzNet and Transfer Learning to Identify Stages of Alzheimer’s Disease

Alzheimer's disease (AD) is the general form of dementia, leading to a progressive neurological disorder characterized by memory loss due to brain cell damage. Artificial Intelligence (AI) assists in the early identification and prediction of AD patients, determining future risks and benefits for radiologists and doctors to save time and cost. Since deep learning (DL) approaches work well with massive datasets and have recently become helpful for AD detection, there remains an area for improvement in automating detection performance. Present approaches somehow addressed the challenges of limited annotated data samples for binary classification. This contrasts with prior state-of-the-art techniques, which were constrained by their incapacity to capture abstract-level information. In this paper, we proposed a Siamese 4D-AlzNet model comprised of four parallel convolutional neural network (CNN) streams (Five CNN layer blocks) and customized transfer learning models (Frozen VGG-19, Frozen VGG-16, and customized AlexNet). Siamese 4D-AlzNet was vertically and horizontally stored, and the spatial features were passed to the final layer for classification. For experiments, T1-weighted MRI images comprised of four distinct subject classes, normal control (NC), mild cognitive impairment (MCI), late mild cognitive impairment (LMCI), and AD, have been employed. Our proposed models achieved outstanding accuracy, with a remarkable 95.05% accuracy distinguishing between normal and AD subjects. The performance across remaining binary class pairs consistently exceeded 90%. We thoroughly compared our model with the latest methods using the same dataset as our reference. Our proposed model improved NC-AD and MCI-AD classification accuracy by 2% 7%.

Role of Probiotic Strain Lactobacillus acidophilus in the Reversal of Gut Dysbiosis Induced Brain Cognitive Decline

In the central nervous system, bidirectional communication between the brain and gut results in memory formation due to synaptic plasticity changes. During a healthy state, oral balanced microflora plays a pivotal role in memory formation by inhibiting the enterotoxin level produced by infectious pathogens. In disease conditions, beneficial microbial dysbiosis may result in excess enterotoxin production. Further, excess enterotoxin secretion prevents beneficial bacteria's proliferation and impairs neurotransmitter precursor compounds' transport to the brain. Blockade of neurotransmitter precursor compounds may result in the development of memory loss. The present study stated the role of Lactobacillus acidophilus in recovering memory loss. Reversal of cognitive impairment is shown with the help of a three-step behavioural analysis, which consists of one pre-infusive behavioural analysis and two post-infusive behavioural analyses (phase 1 and 2). The pre-infusive analysis showed no cognitive impairment in an assimilated environment without any infusions. After oral microbial infusions, phase 1 of post-infusive behavioural analysis showed the presence of cognitive impairment in the experimental groups who received oral infusions. Formed cognitive impairment is reverted with the help of L. acidophilus oral infusion in phase 2 of post-infusive analysis. Comparative three-step behavioural analysis proved that Pseudomonas aeuroginosa induced cognitive impairment may revert to normal conditions with the help of L. acidophilus. The outcome of the present study proves that cognitive impairment developed due to poor oral hygiene can be treated with the help of probiotic microorganisms.

Neurocognitive Effects of an Online Brain Health Program and Weekly Telehealth Support Group in Older Adults with Subjective Memory Loss: A Pilot Study.

Adopting healthy lifestyle behaviors has the potential to slow cognitive decline in older adults by reducing risks associated with dementia. Curriculum-based group health coaching may aid in establishing behavior change centered for dementia risk factors. In this pilot clinical care patient group study (n = 6), we examined the effects of a six-month online Cognitive Health Program combined with a weekly telehealth support group led by the course creator, and personalized health optimization by a collaborating physician, in older adults with subjective cognitive decline. Cognition was assessed at baseline and post-intervention using a computerized battery. Cognitive changes were estimated with nonparametric tests and effect sizes (Cohen's d). Results showed significant improvements in global cognition (p < 0.03, d = 1.6), spatial planning (p < 0.01, d = 2.3), and visuospatial processing (p < 0.05, d = 1.1) compared to baseline. Participants reported high levels of satisfaction with the virtual group format and online curriculum. This small pilot study suggests that a virtual six-month personalized health coaching group with self-paced online health education is feasible and potentially efficacious for improving cognition in participants with subjective cognitive complaints. This format may facilitate behavior change to slow cognitive decline. Future studies should include a control group, a larger, more diverse sample as well as assessing mood and other subjective measures.

The Role of Mesenchymal Stem Cell Exosomes in the Onset and Progression of Alzheimer&amp;apos;s Disease

Alzheimer&amp;apos;s disease (AD) is a neurodegenerative disease with progressive loss of memory and cognitive function. Because its pathogenesis has not been fully elucidated, there is still a lack of understanding of its pathogenesis and effective treatment. Many studies have shown that Mesenchymal stem cells Exosomes (MSCs-Exo) can promote anti-inflammatory, regulate immune function, enhance amyloid (Aβ) degradation, and promote axon growth of nerve cells. Exosomes can effectively cross the blood-brain barrier, and have better biocompatibility and biosafety than nanomaterials, and more diverse ways to carry drugs. Adipose stem cell exosomes can not only treat AD by their own characteristics, but also regulate AD and other neurological diseases as A drug carrier that can efficiently and freely cross the blood-brain barrier: they can effectively reduce Aβ42 plaques and improve the neuronal microenvironment through microglia. In AD model mice, excessive activation of microglia demonstrated the formation of an inflammatory microenvironment in the brain. The inflammatory microenvironment erodes healthy neurons to a certain extent, forcing them to overactivate inflammatory signaling pathways so that they can&amp;apos;t function normally, Adipose stem cell exosomes can effectively clear the expression of inflammatory factors in hypoxia-induced AD neuronal model and promote synaptic repair through microRNA/ phosphatase and tensin homolog (miR-223/PTEN) and phosphatidylinositol kinase (PI3K/Akt) pathways. It can promote the polarization of microglia towards anti-inflammatory phenotype and promote neuronal repair. Adipose stem cell exosomes can also be used to improve memory and cognitive dysfunction by alleviating Tau phosphating or delaying hippocampus volume decay, targeting the core pathological mechanism of AD to achieve therapeutic effects. This article mainly introduces the role of MSC exosomes in the pathogenesis and development of AD.

In vivo Effects of Salicornia herbacea and Calystegia soldanella Extracts for Memory Improvement.

The global elderly population, aged 65 and over, reached approximately 10% in 2020, and this proportion is expected to continue rising. Therefore, the prevalence of neurodegenerative diseases such as Parkinson's disease (PD), which are characterized by declining memory capabilities, is anticipated to increase. In a previous study, we successfully restored the diminished memory capabilities in a fruit fly model of PD by administering an omija extract. To identify functional ingredients that can enhance memory akin to the effects of the omija extract, we conducted screenings by administering halophyte extracts to the PD model. Halophytes are plants that thrive in high-salt environments, and given Korea's geographic proximity to the sea on three sides, it serves as an optimal hub for the utilization of these plants. Upon examining the effects of the oral administration of 12 halophyte extracts, Salicornia herbacea and Calystegia soldanella emerged as potential candidates for ameliorating memory loss in PD patients. Moreover, our findings suggested that C. soldanella, but not S. herbacea, can mitigate oxidative stress in DJ-1β mutants.

MyD88-mediated signaling is critical for the generation of seizure responses and cognitive impairment in a model of anti-N-methyl-D-aspartate receptor encephalitis.

We previously demonstrated that interleukin-1 receptor-mediated immune activation contributes to seizure severity and memory loss in anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis. In the present study, we assessed the role of the myeloid differentiation primary response gene 88 (MyD88), an adaptor protein in Toll-like receptor signaling, in the key phenotypic characteristics of anti-NMDAR encephalitis. Monoclonal anti-NMDAR antibodies or control antibodies were infused into the lateral ventricle of MyD88 knockout mice (MyD88-/-) and control C56BL/6J mice (wild type [WT]) via osmotic minipumps for 2 weeks. Seizure responses were measured by electroencephalography. Upon completion of the infusion, the motor, anxiety, and memory functions of the mice were assessed. Astrocytic (glial fibrillary acidic protein [GFAP]) and microglial (ionized calcium-binding adaptor molecule 1 [Iba-1]) activation and transcriptional activation for the principal inflammatory mediators involved in seizures were determined using immunohistochemistry and quantitative real-time polymerase chain reaction, respectively. As shown before, 80% of WT mice infused with anti-NMDAR antibodies (n = 10) developed seizures (median = 11, interquartile range [IQR] = 3-25 in 2 weeks). In contrast, only three of 14 MyD88-/- mice (21.4%) had seizures (0, IQR = 0-.25, p = .01). The WT mice treated with antibodies also developed memory loss in the novel object recognition test, whereas such memory deficits were not apparent in MyD88-/- mice treated with anti-NMDAR antibodies (p = .03) or control antibodies (p = .04). Furthermore, in contrast to the WT mice exposed to anti-NMDAR antibodies, the MyD88-/- mice had a significantly lower induction of chemokine (C-C motif) ligand 2 (CCL2) in the hippocampus (p = .0001, Sidak tests). There were no significant changes in the expression of GFAP and Iba-1 in the MyD88-/- mice treated with anti-NMDAR or control antibodies. These findings suggest that MyD88-mediated signaling contributes to the seizure and memory phenotype in anti-NMDAR encephalitis and that CCL2 activation may participate in the expression of these features. The removal of MyD88 inflammation may be protective and therapeutically relevant.

Differentiation is accompanied by a progressive loss in transcriptional memory

BackgroundCell differentiation requires the integration of two opposite processes, a stabilizing cellular memory, especially at the transcriptional scale, and a burst of gene expression variability which follows the differentiation induction. Therefore, the actual capacity of a cell to undergo phenotypic change during a differentiation process relies upon a modification in this balance which favors change-inducing gene expression variability. However, there are no experimental data providing insight on how fast the transcriptomes of identical cells would diverge on the scale of the very first two cell divisions during the differentiation process.ResultsIn order to quantitatively address this question, we developed different experimental methods to recover the transcriptomes of related cells, after one and two divisions, while preserving the information about their lineage at the scale of a single cell division. We analyzed the transcriptomes of related cells from two differentiation biological systems (human CD34+ cells and T2EC chicken primary erythrocytic progenitors) using two different single-cell transcriptomics technologies (scRT-qPCR and scRNA-seq).ConclusionsWe identified that the gene transcription profiles of differentiating sister cells are more similar to each other than to those of non-related cells of the same type, sharing the same environment and undergoing similar biological processes. More importantly, we observed greater discrepancies between differentiating sister cells than between self-renewing sister cells. Furthermore, a progressive increase in this divergence from first generation to second generation was observed when comparing differentiating cousin cells to self renewing cousin cells. Our results are in favor of a gradual erasure of transcriptional memory during the differentiation process.

Oxidative Stress, Endoplasmic Reticulum Stress and Apoptosis in the Pathology of Alzheimer's Disease.

Alzheimer's disease (AD) accounts for a major statistic among the class of neurodegenerative diseases. A number of mechanisms have been identified in its pathogenesis and progression which include the amyloid beta (Aβ) aggregation, hyperphosphorylation of tau protein, oxidative stress, endoplasmic reticulum (ER) stress and apoptosis. These processes are interconnected and contribute significantly to the loss of neurons, brain mass and consequential memory loss and other cognitive difficulties. Oxidative stress in AD appears to be caused by excess of oxygen free radicals and extracellular Aβ deposits that cause local inflammatory processes and activate microglia, another possible source of reactive oxygen species (ROS). ER Stress describes the accumulation of misfolded and unfolded proteins as a result of physiological and pathological stimuli including high protein demand, toxins, inflammatory cytokines, and mutant protein expression that disturbs ER homeostasis. When compared to age-matched controls, postmortem brain tissues from AD patients showed elevated levels of ER stress markers, such as PERK, eIF2α, IRE1α, the chaperone Grp78, and the downstream mediator of cell death CHOP. Apoptosis is in charge of eliminating unnecessary and undesired cells to maintain good health. However, it has been demonstrated that a malfunctioning apoptotic pathway is a major factor in the development of certain neurological and immunological problems and diseases in people, including neurodegenerative diseases. This article highlights and discussed some of the experimentally established mechanisms through which these processes lead to the development as well as the exacerbation of AD.

Targeting vulnerable microcircuits in the ventral hippocampus of male transgenic mice to rescue Alzheimer-like social memory loss

BackgroundEpisodic memory loss is a prominent clinical manifestation of Alzheimer’s disease (AD), which is closely related to tau pathology and hippocampal impairment. Due to the heterogeneity of brain neurons, the specific roles of different brain neurons in terms of their sensitivity to tau accumulation and their contribution to AD-like social memory loss remain unclear. Therefore, further investigation is necessary.MethodsWe investigated the effects of AD-like tau pathology by Tandem mass tag proteomic and phosphoproteomic analysis, social behavioural tests, hippocampal electrophysiology, immunofluorescence staining and in vivo optical fibre recording of GCaMP6f and iGABASnFR. Additionally, we utilized optogenetics and administered ursolic acid (UA) via oral gavage to examine the effects of these agents on social memory in mice.ResultsThe results of proteomic and phosphoproteomic analyses revealed the characteristics of ventral hippocampal CA1 (vCA1) under both physiological conditions and AD-like tau pathology. As tau progressively accumulated, vCA1, especially its excitatory and parvalbumin (PV) neurons, were fully filled with mislocated and phosphorylated tau (p-Tau). This finding was not observed for dorsal hippocampal CA1 (dCA1). The overexpression of human tau (hTau) in excitatory and PV neurons mimicked AD-like tau accumulation, significantly inhibited neuronal excitability and suppressed distinct discrimination-associated firings of these neurons within vCA1. Photoactivating excitatory and PV neurons in vCA1 at specific rhythms and time windows efficiently ameliorated tau-impaired social memory. Notably, 1 month of UA administration efficiently decreased tau accumulation via autophagy in a transcription factor EB (TFEB)-dependent manner and restored the vCA1 microcircuit to ameliorate tau-impaired social memory.ConclusionThis study elucidated distinct protein and phosphoprotein networks between dCA1 and vCA1 and highlighted the susceptibility of the vCA1 microcircuit to AD-like tau accumulation. Notably, our novel findings regarding the efficacy of UA in reducing tau load and targeting the vCA1 microcircuit may provide a promising strategy for treating AD in the future.

Bouldering & chronic traumatic encephalopathy – That is repeated mild traumatic brain injury from climbing

Mild traumatic brain injury (mTBI) is one of the most common neurological conditions resulting from linear accelerations in the range of 60 gravity. Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative syndrome. Its etiopathology is attributed to repeated blows to the head and the transmission of acceleration and deceleration forces to the brain. There are several types of climbing, the most popular are lead climbing, speed climbing and bouldering. Athletes involved in the latter sub-discipline (bouldering) appear to be most at risk of mTBI. Bouldering takes place on artificial walls or natural rock and involves climbing without a rope on routes up to several metres in height. We hypothesised that climbers in the bouldering sub-discipline are at risk of frequent mTBI and, as a consequence, may suffer from chronic traumatic encephalopathy. In the paper we presented physical formula to support our thesis, a verification of this formula and a survey of boulder climbers. The physical model was verified in a practical test. Differences in the range of ≈ 2g were demonstrated (MAE = 1.86, RMSE = 2.51). There is evidence in the form of a physiological model that boulderers are able to achieve accelerations that cause mTBI. The study population had a 12 % incidence of repeated falls and reported symptoms associated with mTBI during bouldering training sessions. Given the diagnosis of CTE, which can only be made after death, future research should focus on diagnosing and treating symptoms of mTBI and CTE (including depression, progressive memory loss, suicidal behaviour, cognitive impairment) in boulder climbers.

Enhancement of spin to charge conversion efficiency at the topological surface state by inserting normal metal spacer layer in the topological insulator based heterostructure

In this study, we report efficient spin to charge conversion (SCC) in the topological insulator (TI) based heterostructure (BiSbTe1.5Se1.5/Cu/Ni80Fe20) by using spin-pumping technique, where BiSbTe1.5Se1.5 is the TI and Ni80Fe20 is the ferromagnetic (FM) layer. The SCC, characterized by inverse Edelstein effect length (λIEE) in the TI material, gets altered with an intervening Copper (Cu) layer, and it depends on the interlayer thickness. The introduction of Cu layer at the interface of TI and FM metal provides a new degree of freedom for tuning the SCC efficiency of the topological surface states. The significant enhancement of the measured spin-pumping voltage and the increased linewidth of ferromagnetic resonance absorption spectra due to the insertion of Cu layer at the interface indicate a reduction in spin memory loss at the interface that resulted from the presence of exchange coupling between the surface states of TI and the local moments of FM metal. The temperature dependence (from 8 to 300 K) of the evaluated λIEE data for all the trilayer systems, TI/Cu/FM with different Cu thicknesses, confirms the effect of exchange coupling between the TI and FM layer on the SCC efficiency of the topological surface state. This study offers promising ways for designing more efficient spin-charge conversion devices of the TI-based heterostructure by controlling the interface effects.

Recovery of memory decline during aging - role of epigenetics

Aging is a natural phenomenon associated with the accumulation of multiple alterations, including memory loss. Such deterioration of memory is based on the susceptibility of specific brain regions and the disorders that coincide with aging in those areas. Previous findings suggest that the optimal expression of synaptic plasticity-related genes is essential for memory formation and consolidation. Epigenetic modifications are one of the most crucial factors that cause memory deterioration by inducing the differential expression of synaptic plasticity-related genes. Understanding the fundamental cause of cognitive alterations that arise with aging is very essential for the development of therapeutic and/or preventive approaches. Several strategies have been employed to restore or reverse the memory decline caused by age-associated epigenetic alterations. The present article emphasizes the role of epigenetic alterations caused by histone modifications, DNA methylation, and non-coding ribonucleic acids (RNAs) on memory during aging. Also, we highlight the mechanistic switches of brain aging, including physical exercise, nutraceuticals, epigenetic modifiers, modulators of non-coding RNAs, and associated targets for therapeutic interventions. The emerging field of neuropharmacology and pharmacoepigenomics provides evidence that small drug molecules are currently employed to treat memory loss associated with aging, particularly by targeting epigenetic systems like DNA methylation, chromatin remodeling, histone modifications, and small non-coding RNAs. Therefore, targeting epigenetic modifications could be a potential therapeutic approach for the improvement of synaptic plasticity, neuronal activities, memory, and other brain functions during aging.

Neuropathological stage-dependent proteome mapping of the olfactory tract in Alzheimer's disease: From early olfactory-related omics signatures to computational repurposing of drug candidates.

Alzheimer's disease (AD) is the most common form of dementia, characterized by an early olfactory dysfunction, progressive memory loss, and behavioral deterioration. Albeit substantial progress has been made in characterizing AD-associated molecular and cellular events, there is an unmet clinical need for new therapies. In this study, olfactory tract proteotyping performed in controls and AD subjects (n = 17/group) showed a Braak stage-dependent proteostatic impairment accompanied by the progressive modulation of amyloid precursor protein and tau functional interactomes. To implement a computational repurposing of drug candidates with the capacity to reverse early AD-related olfactory omics signatures (OMSs), we generated a consensual OMSs database compiling differential omics datasets obtained by mass-spectrometry or RNA-sequencing derived from initial AD across the olfactory axis. Using the Connectivity Map-based drug repurposing approach, PKC, EGFR, Aurora kinase, Glycogen synthase kinase, and CDK inhibitors were the top pharmacologic classes capable to restore multiple OMSs, whereas compounds with targeted activity to inhibit PI3K, Insulin-like growth factor 1 (IGF-1), microtubules, and Polo-like kinase (PLK) represented a family of drugs with detrimental potential to induce olfactory AD-associated gene expression changes. To validate the potential therapeutic effects of the proposed drugs, in vitro assays were performed. These validation experiments revealed that pretreatment of human neuron-like SH-SY5Y cells with the EGFR inhibitor AG-1478 showed a neuroprotective effect against hydrogen peroxide-induced damage while the pretreatment with the Aurora kinase inhibitor Reversine reduced amyloid-beta (Aβ)-induced neurotoxicity. Taken together, our data pointed out that OMSs may be useful as substrates for drug repurposing to propose novel neuroprotective treatments against AD.

Cannabinoids for Behavioral Symptoms in Dementia: An Overview.

Dementia, with loss of memory, cognitive abilities, and independent daily functioning, is increasing worldwide, related to an aging population. Currently, there is no curative treatment for dementia. Treatment of the frequently occurring behavioral and psychological symptoms of dementia (BPSD) is partially effective and associated with significant side effects. Cannabinoids are lipophilic molecules acting on the CB1 end CB2 receptors, essential for main biological processes such as sleep, appetite, memory, and pain. Cannabinoids might have a positive impact on amyloid formation in Alzheimer's disease, the main form of dementia, and on BPSD symptoms. Most knowledge currently concerns delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD). In the context of dementia and BPSD, THC might be beneficial for associated spasticity and possible pain or lack of appetite and CBD probably works better on sleep, agitation, and anxiety. This overview of prospective clinical studies and randomized clinical trials, published between 2005 and April 2023, using cannabinoids for BPSD suggests that older studies using low-dose oral synthetic THC showed no positive results. Still, more recent studies using THC/CBD-based oral medication at higher doses show promising results and are feasible and safe in this elderly polymedicated population. Several RCTs are ongoing and planned worldwide, and we hope other trials will follow to establish clinical efficiency and optimal dosing, as well as other outcomes such as deprescribing other medications and facilitation of care. We suggest that researchers also address the more sociological aspects of prescribing cannabinoids for dementia and BPSD in their specific context.

Using therapeutic lies - an ethical challenge for nurses when caring for people with dementia.

People living with dementia can become vulnerable when experiencing symptoms such as memory loss and disorientation, as well as stigma attached to the condition. The care of people with dementia is fraught with ethical dilemmas and challenges regarding how nurses should respond to situations that put patients at risk of distress. For example, if a person with dementia asks to see a deceased relative, a nurse may have to decide whether to tell the truth, or a 'white lie' to avoid distress. This article examines the debates around the use of such 'therapeutic lying' when caring for people with dementia and provides guidance on how nurses could use this technique while protecting the individual's best interests.

Brain metastases as the first clinical manifestation of prostate cancer: a case report

Background. Intracranial metastases, as the first clinical symptom of prostate cancer (PC), are extremely rare, with only anecdotal case reports in the literature.&#x0D; Aim. To present a case of multiple brain metastases (MCI) as the first clinical manifestation of PC with isolated facial nerve injury (FNI).&#x0D; Materials and methods. A 66-year-old patient with PC and multiple brain and bone metastases was observed.&#x0D; Results. The patient considered himself sick for 4 months when weakness in the left arm, headache, dizziness, facial asymmetry, staggering when walking, and memory loss appeared. He received non-surgical treatment prescribed by a neurologist. A clinical examination revealed a neurological deficit in the form of FN central palsy of grade 3 according to the House-Brackmann score. Magnetic resonance imaging of the brain showed masses in the right insular, left temporal lobes, and left cerebellar hemisphere of 3.7×3.3×2.9, 1.1×0.8 and 0.5×0.6 cm, respectively, with marked perifocal edema. According to the magnetic resonance imaging of the pelvis in the right half of the prostate gland, a tumor of 2.2×1.0×2.7 cm and PI-RADS 5 score was detected, and a metastatic lesion of the left ilium was found. Bone scintigraphy showed metastases in the thoracic and lumbar spine. A core biopsy of the prostate was performed. Histological and immunohistochemical studies revealed acinar adenocarcinoma with a Gleason score of 6 (3+3) points. The level of total prostate-specific antigen was 8.6 ng/mL. A final diagnosis was made: stage IV prostate cancer, T2aN0M1c, with brain and bone metastases. Given the neurological symptoms, radiation therapy was performed on the brain with a total radiation dose of 30 Gy, followed by androgen deprivation and monochemotherapy with docetaxel and bisphosphonates.&#x0D; Conclusion. Multiple brain lesions as the first clinical manifestation of PC are extremely rare. An isolated lesion of FN with neurological deficit in the form of central palsy indicates an advanced metastatic process. The primary method of treatment is palliative radiation therapy with a total radiation dose of 30 Gy, followed by androgen deprivation and chemotherapy.

THE CORRELATION OF THE APOE GENE IN PATIENTS WITH PROGRESSIVE MEMORY LOSS AFTER COVID-19 CONTAMINATION

Progressive memory loss is one of the neurological sequelae reported in patients who have recovered from COVID-19. The APOE gene, which encodes apolipoprotein E, has been associated with neurodegenerative disorders and may play a role in the vulnerability of certain individuals to brain damage caused by coronavirus infection. Understanding this correlation can provide important insights for the treatment and follow-up of post-COVID-19 patients. The objectives of this study are to investigate the association between the APOE gene and progressive memory loss in post-COVID-19 patients, to assess whether the presence of certain APOE gene variants is related to a higher risk of developing progressive memory loss after infection, and to identify possible mechanisms by which the APOE gene may influence vulnerability to memory loss in patients with a history of COVID-19. The methodology in question is a bibliographic review, with a narrative and exploratory method, using the PubMed, Scopus, Web of Science and Google Scholar databases, using the health sciences descriptors “ApoE Gene and Covid-19”, “Covid-19 and Genetics”, “Covid-19 and Alzheimer’s Disease” and “Covid-19 and Memory Loss”, generating a total of 78 articles, 11 of which were selected for this study. In addition, guiding questions were outlined, as well as the use of inclusion and exclusion criteria for better performance. Studies have suggested that carriers of the APOE4 genetic variant have a higher risk of developing neurodegenerative diseases, such as Alzheimer’s disease. This variant may also be associated with an increased risk of brain damage in COVID-19 patients. The presence of the APOE4 gene may influence the inflammatory response and neuronal regeneration after infection, contributing to progressive memory loss. In addition, the severity of the COVID-19 infection and the presence of neurological complications during the disease may affect the risk of developing progressive memory loss in post-COVID-19 patients. Factors such as age, comorbidities and immune response may also play a role in this correlation. The correlation between the APOE gene and progressive memory loss in post-COVID-19 patients highlights the importance of genetic and clinical studies to identify individuals at greater risk of developing neurological sequelae after infection. Understanding the mechanisms underlying this correlation could lead to the development of more effective prevention and treatment strategies for these patients.