Symptoms In Alzheimer's Disease Patients Research Articles

Abnormally decreased functional connectivity of the right nucleus basalis of Meynert in Alzheimer’s disease patients with depression symptoms

Dysfunction of the basal forebrain is the main pathological feature in patients with Alzheimer's disease (AD). The aim of this study was to explore whether depressive symptoms cause changes in the functional network of the basal forebrain in AD patients. We collected MRI data from depressed AD patients (n = 24), nondepressed AD patients (n = 14) and healthy controls (n = 20). Resting-state functional magnetic resonance imaging data and functional connectivity analysis were used to study the characteristics of the basal forebrain functional network of the three groups of participants. The functional connectivity differences among the three groups were compared using ANCOVA and post hoc analyses. Compared to healthy controls, depressed AD patients showed reduced functional connectivity between the right nucleus basalis of Meynert and the left supramarginal gyrus and the supplementary motor area. These results increase our understanding of the neural mechanism of depressive symptoms in AD patients.

Efficacy and safety of repetitive Transcranial Magnetic Stimulation and transcranial Direct Current Stimulation in memory deficits in patients with Alzheimer's disease: Meta-analysis and systematic review

Repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) are two of the most used non-pharmacological interventions for Alzheimer's Disease (AD). However, most of the clinical trials have focused on evaluating the effects on global cognition and not on specific cognitive functions. Therefore, considering that memory loss is one of the hallmark symptoms of AD, we aim to assess the efficacy and safety of tDCS and rTMS in memory deficits. For that, multilevel random effect models were performed considering the standardized mean difference (SMD) between active and sham stimulation. A total of 19 studies with 411 participants demonstrated positive effects in memory after tDCS (SMD=0.20, p = 0.04) and rTMS (SMD=0.44, p = 0.001). Subgroup analysis revealed that tDCS had greater efficacy when administered in temporal regions (SMD=0.32, p = 0.04), whereas rTMS was superior when applied in frontal regions (SMD=0.61, p < 0.001). Therefore, depending on the brain region of stimulation, both interventions produced a positive effect on memory symptoms in AD patients. Finally, the safety of both techniques was observed in the AD population after the reporting of almost no serious events.

Neuropsychological, plasma marker, and functional connectivity changes in Alzheimer's disease patients infected with COVID-19.

Patients with COVID-19 may experience various neurological conditions, including cognitive impairment, encephalitis, and stroke. This is particularly significant in individuals who already have Alzheimer's disease (AD), as the cognitive impairments can be more pronounced in these cases. However, the extent and underlying mechanisms of cognitive impairments in COVID-19-infected AD patients have yet to be fully investigated through clinical and neurophysiological approaches. This study included a total of 77 AD patients. Cognitive functions were assessed using neuropsychiatric scales for all participants, and plasma biomarkers of amyloid protein and tau protein were measured in a subset of 25 participants. To investigate the changes in functional brain connectivity induced by COVID-19 infection, a cross-sectional neuroimaging design was conducted involving a subset of 37 AD patients, including a control group of 18 AD participants without COVID-19 infection and a COVID-19 group consisting of 19 AD participants. For the 77 AD patients between the stages of pre and post COVID-19 infection, there were significant differences in cognitive function and psychobehavioral symptoms on the Montreal Scale (MoCA), the neuropsychiatric inventory (NPI), the clinician's global impression of change (CIBIC-Plus), and the activity of daily living scale (ADL). The COVID-19 infection significantly decreased the plasma biomarker level of Aβ42 and increased the plasma p-tau181 level in AD patients. The COVID-19-infected AD patients show decreased local coherence (LCOR) in the anterior middle temporal gyrus and decreased global correlation (GCOR) in the precuneus and the medial prefrontal cortex. The findings suggest clinical, cognitive, and neural alterations following COVID-19 infection in AD patients and emphasize the need for close monitoring of symptoms in AD patients who have had COVID-19 and further exploration of the underlying mechanisms.

Ginkgolides and Huperzine A for complementary treatment of Alzheimer's disease.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by gradual deterioration of cognitive function, memory, and inability to perform daily, social, or occupational activities. Its etiology is associated with the accumulation of β-amyloid peptides, phosphorylated tau protein, and neuroinflammatory and oxidative processes in the brain. Currently, there is no successful pharmacological treatment for AD. The few approved drugs are mainly aimed at treating the symptoms; however, due to the increasing discovery of etiopathological factors, there are great efforts to find new multifunctional molecules to slow down the course of this neurodegenerative disease. The commercial Ginkgo biloba formulation EGb 761® and Huperzine A, an alkaloid present in the plant Huperzia serrata, have shown in clinical trials to possess cholinergic and neuroprotective activities, including improvement in cognition, activities of daily living, and neuropsychiatric symptoms in AD patients. The purpose of this review is to expose the positive results of intervention with EGb 761® and Huperzine in patients with mild to moderate AD in the last 10 years, highlighting the pharmacological functions that justify their use in AD therapy.

Effects of exercise therapy on cognitive function in Alzheimer's disease and mechanisms of action

Alzheimer's disease (AD) is the most common form of dementia, with patients initially experiencing mild memory impairment and then progressive cognitive loss, causing significant stress to families and society. As the number of patients continues to increase, it is important to explore a variety of treatment options. In recent years, non-pharmacological treatments have played a significant role in the prevention and relief of AD. Among them, exercise therapy has become one of the ideal options for non-pharmacological interventions as it can improve cognition and reduce neuropsychiatric symptoms in AD patients. In this paper, the effects and mechanisms of exercise therapy on the cognitive function of AD patients are reviewed in the hope of providing clinical practitioners with some assistance in the treatment and rehabilitation of AD.

The mitochondria-targeted antioxidant MitoQ inhibits memory loss, neuropathology, and extends lifespan in aged 3xTg-AD mice

Oxidative stress, likely stemming from dysfunctional mitochondria, occurs before major cognitive deficits and neuropathologies become apparent in Alzheimer's disease (AD) patients and in mouse models of the disease. We previously reported that treating 2- to 7-month-old 3xTg-AD mice with the mitochondria-targeted antioxidant MitoQ (mitoquinone mesylate: [10-(4,5-Dimethoxy-2-methyl-3,6-dioxo-1,4-cyclohexadien-1-yl)decyl](triphenyl)phosphonium methanesulfonate), a period when AD-like pathologies first manifest in them, prevents AD-like symptoms from developing. To elucidate further a role for mitochondria-derived oxidative stress in AD progression, we examined the ability of MitoQ to inhibit AD-like pathologies in these mice at an age in which cognitive and neuropathological symptoms have fully developed. 3xTg-AD female mice received MitoQ in their drinking water for five months beginning at twelve months after birth. Untreated 18-month-old 3xTg-AD mice exhibited significant learning deficits and extensive AD-like neuropathologies. MitoQ-treated mice showed improved memory retention compared to untreated 3xTg-AD mice as well as reduced brain oxidative stress, synapse loss, astrogliosis, microglial cell proliferation, Aβ accumulation, caspase activation, and tau hyperphosphorylation. Additionally, MitoQ treatment significantly increased the abbreviated lifespan of the 3xTg-AD mice. These findings support a role for the involvement of mitochondria-derived oxidative stress in the etiology of AD and suggest that mitochondria-targeted antioxidants may lessen symptoms in AD patients.

The power of sample size through a multi-scanner approach in MR neuroimaging regression analysis: evidence from Alzheimer's disease with and without depression.

The inconsistency of volumetric results often seen in MR neuroimaging studies can be partially attributed to small sample sizes and variable data analysis approaches. Increased sample size through multi-scanner studies can tackle the former, but combining data across different scanner platforms and field-strengths may introduce a variability factor capable of masking subtle statistical differences. To investigate the sample size effect on regression analysis between depressive symptoms and grey matter volume (GMV) loss in Alzheimer's disease (AD), a retrospective multi-scanner investigation was conducted. A cohort of 172 AD patients, with or without comorbid depressive symptoms, was studied. Patients were scanned with different imaging protocols in four different MRI scanners operating at either 1.5T or 3.0T. Acquired data were uniformly analyzed using the computational anatomy toolbox (CAT12) of the statistical parametric mapping (SPM12) software. Single- and multi-scanner regression analyses were applied to identify the anatomical pattern of correlation between GM loss and depression severity. A common anatomical pattern of correlation between GMV loss and increased depression severity, mostly involving sensorimotor areas, was identified in all patient subgroups imaged in different scanners. Analysis of the pooled multi-scanner data confirmed the above finding employing a more conservative statistical criterion. In the retrospective multi-scanner setting, a significant correlation was also exhibited for temporal and frontal areas. Increasing the sample size by retrospectively pooling multi-scanner data, irrespective of the acquisition platform and parameters employed, can facilitate the identification of anatomical areas with a strong correlation between GMV changes and depression symptoms in AD patients.

Changes in serum brain-derived neurotrophic factor levels in patients with Alzheimer's disease

Objective To investigate changes in serum brain-derived neurotrophic factor(BDNF)levels in patients with Alzheimer's disease(AD). Methods Venous blood samples were collected from 40 AD patients, 40 amnestic mild cognitive impairment(aMCI)patients and 40 normal controls.Serum BDNF levels were analyzed by enzyme-linked immunosorbent assay(ELISA). The relationships of serum BDNF levels with age, gender, educational level, mini-mental state examination(MMSE)score and Beck depression scale-Ⅱ(BDⅠ-Ⅱ)score in AD patients were analyzed. Results Serum BDNF levels were lower in AD patients than in patients with aMCI and normal controls(4.6±1.9 μg/L vs.9.3±4.7 μg/L, 10.2±1.8 μg/L, F=71.083, P 0.05). Pearson correlation analysis showed that serum BDNF levels had a positive correlation with MMSE score(r=0.428, P<0.05). Conclusions Advanced age is associated with decreased serum levels of BDNF in AD patients.Decreased serum levels of BDNF in AD patients are related to the severity of cognitive impairment.There is no correlation between serum BDNF levels and depressive symptoms in AD patients. Key words: Alzheimer disease; Cognition disorders; Brain-derived neurotrophic factor

Antidepressant effects of creatine on amyloid β1–40-treated mice: The role of GSK-3β/Nrf2 pathway

Alzheimer's disease (AD) is characterized by progressive synaptic dysfunction and neuronal lost in specific brain areas including hippocampus, resulting in memory/learning deficits and cognitive impairments. In addition, non-cognitive symptoms are reported in AD patients, such as anxiety, apathy and depressed mood. The current antidepressant drugs present reduced efficacy to improve depressive symptoms in AD patients. Here, we investigated the ability of creatine, a compound with neuroprotective and antidepressant properties, to counteract amyloid β1–40 peptide-induced depressive-like behavior in mice. Moreover, we addressed the participation of the intracellular signaling pathway mediated by glycogen synthase kinase-3β (GSK-3β)/nuclear factor erythroid-2-related factor 2 (Nrf2) in the creatine effects. Aß1–40 administration (400 pmol/mouse, i.c.v.) increased the immobility time in the tail suspension test and decreased the grooming time and increased latency to grooming in the splash test, indicative of depressive-like behavior. These impairments were attenuated by creatine (0.01 and 10 mg/kg, p.o.) and fluoxetine (10 mg/kg, p.o., positive control). No significant alterations on locomotor performance were observed in the open field. Aß1–40 administration did not alter hippocampal phospho-GSK-3β (Ser9)/total GSK-3β, total GSK-3β and heme oxygenase-1 (HO-1) immunocontents. However, Aß1–40-infused mice treated with creatine (0.01 mg/kg) presented increased phosphorylation of GSK-3β(Ser9) and HO-1 immunocontent in the hippocampus. Fluoxetine per se increased GSK-3β(Ser9) phosphorylation, but did not alter HO-1 levels. In addition, Aß1–40 administration increased hippocampal glutathione (GSH) levels as well as glutathione reductase (GR) and thioredoxin reductase (TrxR) activities, and these effects were abolished by creatine and fluoxetine. This study provides the first evidence of the antidepressive-like effects of creatine in Aß1–40-treated mice, which were accompanied by hippocampal inhibition of GSK-3β and modulation of antioxidant defenses. These findings indicate the potential of creatine for the treatment of depression associated with AD.

Vitamin B12 in Association with Antipsychotic Drugs Can Modulate the Expression of Pro-/Anti-Inflammatory Cytokines in Alzheimer Disease Patients

Introduction: Patients with Alzheimer disease (AD) suffer from psychotic symptoms including pain. The current antipsychotic drugs confer limited effectiveness, and hence new strategies are being designed to decrease pain in order to increase antipsychological effectiveness. Vitamin B₁₂ is a safe supplementary drug to decrease pain. Additionally, cytokines participate in the pathogenesis of immune-related diseases such as AD. Thus, the main aim of this clinical trial study was to determine the effects of treatment with risperidone and quetiapine, as antipsychotic drugs, with and without vitamin B₁₂ on the psychotic symptoms of AD patients and the expression of IL-6, IL-8, tumor growth factor (TGF)-β, tumor necrosis factor (TNF)-α, and endothelin (ET)-1). Material and Methods: Serum levels of IL-6, IL-8, TGF-β, TNF-α, and ET-1 were evaluated in the following groups: healthy controls, nonpsychotic AD patients, psychotic AD patients, psychotic AD patients under treatment with risperidone, psychotic AD patients under treatment with risperidone plus vitamin B₁₂, psychotic AD patients under treatment with quetiapine, and psychotic AD patients under treatment with quetiapine plus vitamin B₁₂. Results: Treatment with antipsychotic drugs plus vitamin B₁₂ led to a decreased expression of IL-8 and TNF-α and an increased expression of TGF-β. Vitamin B₁₂ in association with quetiapine reduced the pain in psychotic AD patients. Discussion: Proinflammatory cytokines play important roles in the pathogenesis of psychosis in AD patients. Antipsychotic drugs plus vitamin B₁₂ can reduce and induce the expression of proinflammatory and anti-inflammatory cytokines to improve psychotic symptoms in AD patients.

Early Development of Symptomatic Drugs in AD: A Systematic Review of the Use of Biomarkers

Pharmacological therapies currently marketed for Alzheimer's disease (AD) are only symptomatic and show limited effects in terms of clinical benefit. Thus, the development of new symptomatic drugs remains essential. However the dramatic increase in costs associated with drug development together with the poor number of emerging drugs highlights how crucial it is to accelerate the findings aiming to bringing new drugs to market. In this respect, optimization of the development process by integrating, at early stage, reliable biomarkers able to predict clinical benefit in phase III clinical trials may help. The improvement of certain techniques such as imaging and electrophysiological methods has led to a more accurate assessment of the brain's physiological impact of pharmacological treatments used to alleviate symptoms in AD patients. This review aims to gather the main findings from clinical studies where the effect of anti-dementia drugs were assessed in healthy volunteers and AD patients through one or several such biomarkers (electroencephalography (EEG), magnetic resonance imaging (MRI), positron emission tomography (PET), single-photon emission computed tomography (SPECT)). Overall, evidence presented in this review suggests that various biomarkers associated with key impairments observed in AD were sensitive to acetylcholinesterase inhibitors (AChE-I) medication and memantine with a good correlation with enhancement of cognitive performance. In most of the reviewed studies, only one kind of biomarker was used. Among these, deficits in quantitative EEG profile, P300 latency, and regional brain activity measured by either functional MRI (fMRI) during face encoding and working memory task or by PET/SPECT have been shown to be reversed by anti-dementia drugs. It is therefore suggested that a single biomarker approach would be limited and not be sufficiently predictive to extensively assess the potential of a new symptomatic drug. Hence, it appears that a combination approach with the use of a panel of biomarkers rather than a single biomarker may be more appropriate to establish a good correlation between the disease and therapeutic intervention.

Impaired Frontolimbic Connectivity and Depressive Symptoms in Patients with Alzheimer's Disease

Background/Aims: Depressive symptoms are commonly observed in Alzheimer's disease (AD). The underlying mechanisms of depressive symptoms in AD remain unclear; frontolimbic circuitry dysfunction may play a role. We aimed to investigate the microstructural integrity of frontolimbic connectivity of specific fiber tracts in AD patients with and without depressive symptoms using diffusion tensor imaging (DTI). Methods: Eleven AD patients with depressive symptoms (dep-AD), 18 AD patients without depressive symptoms (nondep-AD), and 18 normal control (NC) subjects were included. The cingulum bundle (CB), uncinate fasciculus (UF), and fornix, mainly frontolimbic connectivity, were measured by DTI tractography and the metrics of fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity, and radial diffusivity (RD) were calculated. Results: Compared with NC subjects, both dep-AD and nondep-AD patients showed significant differences for all indices in the fornix and significantly decreased FA and increased MD and RD in the bilateral CB and UF. When compared to nondep-AD patients, dep-AD patients showed significantly increased MD and RD in the bilateral CB and right UF. Conclusion: Depressive symptoms in AD patients may be involved in greater microstructural abnormalities of frontolimbic connectivity and myelin injury in the bilateral CB and right UF might contribute to the pathophysiology of depressive symptoms in AD.

The association between the common variants of thyroid hormone receptor interactor 4 gene and Alzheimer disease

Objective To explore the association between the common variations of thyroid hormone receptor interactor 4(TRIP4) gene rs4776494 and Alzheimer disease(AD) in Chinese people. Method A case-control study was performed, consisting of 77 patients with AD(AD group) and 80 controls(control group) who were matched at age and gender with the AD patients. PCR and sequencing were used to determine the distribution of allele and genotype frequency of TRIP4 rs4776494.Every case was subjected to mini-mental state examinations(MMSE), clinical dementia rating(CDR) and behavioral and psychological symptoms of dementia(BPSD). Results The TT, CT and CC gene frequencies were 57/77(74.02%), 18/77(23.38%) and 2/77(2.6%) in AD group, and 38/80(47.5%), 39/80(48.75%) and 3/80(3.75%) in control group, respectively. T allele in cases group was significantly higher than that in control group(P<0.01). Cases with T allele were more susceptible to BPSD than those without T allele(P<0.05). Conclusion T Allele of TRIP4 rs4776494 might be a genetic risk factor of AD in Chinese population.To some degree, TRIP4 gene may be associated with mental symptoms in AD patients. Key words: Alzheimer disease; TRIP4; Single nucleotide polymorphism

Molecular and biochemical trajectories from diabetes to Alzheimer's disease: A critical appraisal.

Diabetes mellitus (DM), a metabolic disorder is a major orchestra influencing brain and behavioral responses via direct or indirect mechanisms. Many lines of evidence suggest that diabetic patients apparently face severe brain complications, but the story is far from being fully understood. Type 2 diabetes, an ever increasing epidemic and its chronic brain complications are implicated in the development of Alzheimer's disease (AD). Evidences from clinical and experimental studies suggest that insulin draws a clear trajectory from the peripheral system to the central nervous system. This review is a spot light on striking pathological, biochemical, molecular and behavioral commonalities of AD and DM. Incidence of cognitive decline in diabetic patients and diabetic symptoms in AD patients has brought the concept of brain diabetes to attention. Brain diabetes reflects insulin resistant brain state with oxidative stress, cognitive impairment, activation of various inflammatory cascade and mitochondrial vulnerability as a shared footprint of AD and DM. It has become extremely important for the investigators to understand the patho-physiology of brain complications in diabetes and put intensive pursuits for therapeutic interventions. Although, decades of research have yielded a range of molecules with potential beneficial effects, but they are yet to meet the expectations.

Progress in mechanisms of acetylcholinesterase inhibitors and memantine for the treatment of Alzheimer's disease

Alzheimer's disease (AD) is the most common causes of dementia in the elderly. Currently, only two classes of drugs, acetylcholinesterase inhibitors (AChEIs) and memantine are approved. AChEIs ameliorate cognitive and psychiatric symptoms in AD patients through activation of acetylcholine (ACh) receptors by increased synaptic ACh levels and also have protective effects against glutamate neurotoxicity and inflammation, whereas memantine appears to mainly protect against excitotoxicity and neurodegeneration. Herein, we review the pharmacologic properties of the available AChEIs and memantine, and focus on recent progress in the mechanisms of AD in relation to acetylcholinergic and glutamatergic involvement.

Systemic inflammation, blood-brain barrier vulnerability and cognitive/non-cognitive symptoms in Alzheimer disease: relevance to pathogenesis and therapy.

The incidence of dementia is increasing at an alarming rate, and has become a major public health concern. Alzheimer disease (AD) is the most common form of dementia and is characterized by progressive cognitive impairment. In addition to classical neuropathological features such as amyloid plaques and neurofibrillary tangles (NFT), accumulation of activated immune cells has been documented in the AD brain, suggesting a contribution of neuroinflammation in the pathogenesis of AD. Besides cognitive deterioration, non-cognitive symptoms, such as agitation, aggression, depression and psychosis, are often observed in demented patients, including those with AD, and these neuropsychological symptoms place a heavy burden on caregivers. These symptoms often exhibit sudden onset and tend to fluctuate over time, and in many cases, they are triggered by an infection in peripheral organs, suggesting that inflammation plays an important role in the pathogenesis of these non-cognitive symptoms. However, there is no mechanistic explanation for the relationship between inflammation and neuropsychiatric symptoms. Observations from experimental mouse models indicate that alteration of brain blood vessels, especially blood-brain barrier (BBB) dysfunction, may contribute to the relationship. The current review summarizes the results from recent studies on the relationship between inflammation and AD, while focusing on cerebrovascular alterations, which might provide an insight into the pathogenesis of cognitive/non-cognitive symptoms in AD patients and suggest a basis for the development of new therapeutic treatments for these conditions.

Regional Atrophy of the Insular Cortex Is Associated with Neuropsychiatric Symptoms in Alzheimer's Disease Patients

Background: Alzheimer's disease (AD) is a devastating illness that results in progressive cognitive decline and neuropsychiatric symptoms. The neuropsychiatric symptoms are associated with a rapid decline in cognition and activities of daily living and increased mortality, however the neuroanatomical localisation involved in the development of neuropsychiatric symptoms remains poorly understood. The aim of this study was to identify the association with the regional volume of the insular cortex and each neuropsychiatric symptom in patients with AD. Methods: Subjects diagnosed with AD (n = 40) were evaluated. Magnetic resonance images were obtained and the insular cortex was subdivided into four subregions through the central sulcus of the insula and bilaterally: right anterior insular cortex, right posterior insular cortex, left anterior insular cortex and left posterior insular cortex. The neuropsychiatric symptoms were assessed using the Neuropsychiatric Inventory. A partial correlation analysis was performed. Results: A significant negative correlation existed between apathy, the irritability subscale score and the volume ratio of the bilateral anterior insular cortex and right posterior insular cortex (r = -0.457, -0.433 and -0.572, respectively, p = 0.032, 0.044 and 0.005, respectively). Conclusion: The findings suggest that the regional atrophy of the insular cortex is associated with neuropsychiatric symptoms in AD patients.

Subjective depressive mood and regional cerebral blood flow in mild Alzheimer's disease

Depressive symptoms are common in patients with Alzheimer's disease (AD) and increase the caregiver burden, although the etiology and pathologic mechanism of depressive symptoms in AD patients remain unclear. In this study, we tried to clarify the cerebral blood flow (CBF) correlates of subjective depressive symptoms in AD. Seventy-six consecutive patients with AD were recruited from outpatient units of the Memory Clinic of Okayama University Hospital. Subjective depressive symptoms were evaluated using the short version of the Geriatric Depression Scale (GDS). All patients underwent brain SPECT with 99mTc-ethylcysteinate dimer, and the SPECT images were analyzed by the Statistical Parametric Mapping 8 program. No significant differences between groups with high and low GDS scores were found with respect to age, sex, years of education, and revised Addenbrooke's Cognitive Examination scores. Compared to patients with low scores on GDS, patients with high scores showed significant hypoperfusion in the left inferior frontal region. The left inferior frontal region may be significantly involved in the pathogenesis of subjective depressive symptoms in AD. Subjective and objective depressive symptoms may have somewhat different neural substrates in AD.

Structural brain changes associated with depressive symptoms in the elderly with Alzheimer’s disease

ObjectiveTo examine neuroanatomical changes associated with depressive symptoms in Alzheimer's disease (AD) and the relationship between brain structure and cerebrospinal fluid (CSF) AD biomarkers in depressed and non-depressed patients.MethodsTwo independent...

Sleep problems associated with behavioral and psychological symptoms as well as cognitive functions in Alzheimer's disease.

Background and PurposeIt has been shown that sleep problems in Alzheimer's disease (AD) are associated with cognitive impairment and behavioral problems. In fact, most of studies have founded that daytime sleepiness is significantly correlated with cognitive decline in AD. However, a few studies have also shown that nighttime sleep problems are associated with cognitive function and behavioral symptoms in AD. Accordingly, the aim of this study was to evaluate the effects of nighttime sleep on cognition and behavioral and psychological symptoms of dementia (BPSD) in AD.MethodsThe study population comprised 117 subjects: 63 AD patients and 54 age- and sex-matched non-demented elderly subjects. Detailed cognitive functions and behavioral symptoms were measured using the Seoul Neuropsychological Screening Battery (SNSB) and the Korean version of the Neuropsychiatric Inventory (NPI-K). Sleep characteristics were evaluated using the Korean version of the Pittsburgh Sleep Quality Index (PSQI-K). The correlations between PSQI-K and SNSB scores and between PSQI-K and NPI-K scores were analyzed.ResultsIn AD patients, sleep latency was found to be negatively correlated with praxis (p=0.041), Rey-Osterrieth Complex Figure Test (RCFT) immediate recall (p=0.041), and RCFT recognition (p=0.008) after controlling for age and education, while sleep duration and sleep efficiency were positively correlated with praxis (p=0.034 and p=0.025, respectively). Although no significant correlation was found between PSQI-K and NPI-K scores, sleep disturbance and total PSQI-K scores were found to be significantly associated with apathy/indifference in AD.ConclusionsSleep problems such as prolonged sleep duration, sleep latency, and poor sleep efficiency in AD patients were correlated with cognitive dysfunction, and especially frontal executive and visuospatial functions, and BPSD. These findings suggest that treatment of nighttime sleep problems might improve cognition and behavioral symptoms in AD patients.