OBJECTIVE: To observe the effect of Butylphthalide soft capsules on improving cognitive function, activity of daily living, and dementia-related factors of elderly patients with Parkinson\'s disease dementia (PDD) during the coronavirus disease 2019 (COVID-19) pandemic.
METHODS: The clinical data of 126 elderly patients with PDD admitted to the Second Affiliated Hospital of Zhengzhou University during the COVID-19 pandemic were analyzed retrospectively. Patients were assigned to a control group (conventional clinical treatment, n=50) and a research group (conventional clinical treatment combined with Butylphthalide soft capsules, n=76). The clinical response, clinical symptoms, cognitive function, activity of daily living (ADL), cerebral blood flow velocity, serum inflammatory factors, oxidative stress indices, neurotrophic factors, dementia-related factors, and drug safety were analyzed and compared between the two groups.
RESULTS: The overall response rate was significantly higher in the research group than in the control group (97.37% vs. 84.00%, P=0.017). After treatment, the clinical symptom-based scores and levels of serum inflammatory factors, malondialdehyde, and Parkinson disease protein 7 were significantly lower in the research group than in the control group (all P<0.001); the cognitive function and ADL scores, cerebral blood flow velocities, and levels of catalase, glutathione peroxidase, superoxide dismutase, neurotrophic factors, and neurotrophin-3 were significantly higher in the research group (all P<0.001). The incidence of adverse reactions was comparable between the two groups (4.00% vs. 6.58%, P=0.825).
CONCLUSIONS: Butylphthalide soft capsules have a definite effect and good safety in elderly patients with PDD during the COVID-19 pandemic.

UNASSIGNED: Overwhelming evidence points to that genetic factors contributing to the development of Alzheimer\'s disease (AD) and Parkinson\'s disease (PD). Genome-Wide Association Study (GWAS) has come a long way in the last decade. So far, a large number of GWAS studies have been published on neurological diseases and many other diseases, providing us with a wealth of genetic information and unique biological insights.
UNASSIGNED: Genomic DNA was extracted from both patients\' and controls\' peripheral blood samples utilizing the Blood Genome Extraction Kit. Single nucleotide polymorphisms (SNPs) were genotyped employing the enhanced multiple ligase detection reaction (iMLDR) technology.
UNASSIGNED: A case-control study was conducted, involving 211 AD patients, 508 PD patients (including 117 with dementia), and 412 healthy individuals. Age and sex stratification analysis revealed that rs871269/TNIP1 was associated with LOAD (p = 0.035), and rs5011436/TMEM106B was associated with AD in males (p = 0.044) in the genotype model. In the allele model, rs871269/TNIP1 was found to be associated with PD in the Chinese Han population (p = 0.0035, OR 0.741, 95% CI 0.559-0.983), and rs708382/GRN was identified as a risk factor for Parkinson\'s disease dementia (PDD) in the Chinese Han population (p = 0.004, odds ratio (OR) 0.354, 95% confidence interval (CI) 0.171-0.733). However, no significant associations with AD or PD were observed for the remaining four loci (rs113020870/AGRN, rs6891966/HAVCR2, rs2452170/NTN5, rs1761461/LILRB2) in terms of allele or genotype frequencies.
UNASSIGNED: This study identifies rs871269/TNIP1 as a potential risk factor for both LOAD and PD, rs708382/GRN as a risk factor for PDD, and rs5011436/TMEM106B as associated with AD in males when stratified by age.

BACKGROUND: Functional near-infrared spectroscopy (fNIRS) is commonly used to study human brain function by measuring the hemodynamic signals originating from cortical activation and provides a new noninvasive detection method for identifying dementia.
OBJECTIVE: To investigate the fNIRS imaging technique and its clinical application in differential diagnosis of subtype dementias including frontotemporal lobe dementia, Lewy body dementia, Parkinson\'s disease dementia (PDD) and Alzheimer\'s disease (AD).
METHODS: Four patients with different types of dementia were examined with fNIRS during two tasks and a resting state. We adopted the verbal fluency task, working memory task and resting state task. Each patient was compared on the same task. We conducted and analyzed the fNIRS data using a general linear model and Pearson\'s correlation analysis.
RESULTS: Compared with other types of dementias, fNIRS showed the left frontotemporal and prefrontal lobes to be poorly activated during the verbal fluency task in frontotemporal dementia. In Lewy body dementia, severe asymmetry of prefrontal lobes appeared during both verbal fluency and working memory tasks, and the patient had low functional connectivity during a resting state. In PDD, the patient\'s prefrontal cortex showed lower excitability than the temporal lobe during the verbal fluency task, while the prefrontal cortex showed higher excitability during the working memory task. The patient with AD showed poor prefrontal and temporal activation during the working memory task, and more activation of frontopolar instead of the dorsolateral prefrontal cortex.
CONCLUSIONS: Different hemodynamic characteristics of four types of dementia (as seen by fNIRS imaging) provides evidence that fNIRS can serve as a potential tool for the diagnosis between dementia subtypes.

OBJECTIVE: To explore the association between uric acid (UA) levels and vascular dementia (VaD) and Parkinson\'s disease dementia (PDD), a meta-analysis was conducted.
METHODS: The relevant studies were identified by searching PubMed, Embase, Web of Science, and Cochrane Collaboration Database up to May 2022. Pooled analysis, sensitivity analysis, and publication bias examination were all conducted. All analyses were performed by using STATA 16.
RESULTS: Twelve studies with a total of 2097 subjects were included. The pooled analysis showed that UA levels were not associated with VaD (WMD =  - 10.99 μmol/L, 95% CI (- 48.05, 26.07), P = 0.561) but were associated with PDD (WMD =  - 25.22 μmol/L, 95% CI (- 43.47, - 6.97), P = 0.007). The statistical stability and reliability were evaluated using sensitivity analysis and publication bias outcomes.
CONCLUSIONS: UA levels are associated with PDD but not with VaD. This study will help to strengthen our knowledge of the pathophysiologies of VaD and PDD, and promote the development of prevention and treatment strategies.

OBJECTIVE: To observe the effect of electroacupuncture (EA) of \"Xiusanzhen\" ［bilateral \"Yingxiang\"(LI20)+\"Yintang\"(GV24+)］ on synaptophysin (SYN), postsynaptic density protein-95 (PSD-95), Iba-1+ CD68+ microglia and complement C related protein expression of hippocampus in Parkinson\'s disease dementia (PDD) mice, so as to explore its mechanism in improving memory impairment of PDD.
METHODS: Male C57BL/6 mice were randomly divided into control, sham operation, model and EA groups, with 10 mice in each group. The PDD model was established by injecting 6-OHDA into the medial forebrain tract. EA (2 Hz, 1 mA) was applied to unilateral LI20 and GV29 for 20 min once daily for consecutive 14 days. Morris water maze and new object recognition test were used to evaluate the learning and memory ability. Western blot was used to detect the expression of SYN and PSD-95 proteins in hippocampus. Immunofluorescence was used to label Iba-1+ CD68+ microglia and C1q positive cells in hippocampal CA1 region. The content of C3 protein in hippocampus was detected by ELISA.
RESULTS: Compared with the control group, there was no statistical significance in all the observed indexes in the sham operation group. Compared with the sham operation group, the average escape latency (AEL) prolonged significantly (P<0.01), the target platform crossing times (TPCT) and new object recognition index (NORI) decreased remarkably (P<0.01); the expressions of SYN and PSD-95 proteins in hippocampal CA1 region were significantly decreased (P<0.01); the rate of Iba-1+CD68+ microglia, the rate of C1q positive cells and the content of C3 protein were significantly increased (P<0.01) in the model group. In comparison with the model group, the AEL was shortened (P<0.01), the TPCT and NORI were increased (P<0.05) remarkably; the expressions of SYN and PSD-95 proteins in hippocampal CA1 region were increased (P<0.01, P<0.05); the rate of Iba-1+ CD68+ microglia, the rate of C1q positive cells and the content of C3 protein were significantly decreased (P<0.01) in the EA group.
CONCLUSIONS: \"Xiusanzhen\" can alleviate the learning and memory impairment of PDD model mice, and improve the synaptic plasticity of hippocampal CA1 area. The mechanism may be related to the reduction of C1q and C3 deposition in hippocampal CA1 region and the reduction of microglia phagocytosis.
目的：观察电针干预对帕金森病痴呆(PDD)模型小鼠海马CA1区突触素(SYN)、突触后密度蛋白95(PSD-95)、离子钙结合接头分子1(Iba-1)+CD68+小胶质细胞数及补体（C）相关蛋白表达的影响，探讨“嗅三针”改善PDD记忆障碍的部分作用机制。方法：雄性C57BL/6小鼠随机分为空白组、假手术组、模型组和电针组，每组10只。采用单侧内侧前脑束注射6-羟多巴胺建立PDD小鼠模型。电针组予“嗅三针”电针干预，每日1次，每次20 min，连续14 d。采用Morris水迷宫及新物体识别实验评估各组小鼠学习记忆能力；Western blot法检测海马CA1区SYN、PSD-95蛋白的表达量；免疫荧光法标记海马CA1区Iba-1+ CD68+小胶质细胞及C1q阳性细胞并计算阳性细胞率；ELISA法检测海马CA1区C3蛋白含量。结果：与空白组比较，假手术组各指标差异均无统计学意义（P>0.05）。与假手术组比较，模型组小鼠逃避潜伏期延长(P<0.01)，穿越原平台次数、新物体识别认知指数（NORI）降低(P<0.01)；与模型组比较，电针组小鼠逃避潜伏期缩短(P<0.01)，穿越原平台次数、NORI升高(P<0.05)。与假手术组比较，模型组小鼠海马CA1区SYN、PSD-95蛋白表达量显著降低(P<0.01)，Iba-1+ CD68+小胶质细胞率、C1q阳性细胞率及C3蛋白含量显著升高(P<0.01)；与模型组比较，电针组小鼠海马CA1区SYN、PSD-95蛋白表达量升高(P<0.01, P<0.05)，Iba-1+ CD68+小胶质细胞率、C1q阳性细胞率及C3蛋白含量显著降低(P<0.01)。结论：“嗅三针”可缓解PDD模型小鼠学习记忆障碍，改善海马CA1区突触可塑性，其机制可能与减少海马CA1区C1q、C3表达，降低小胶质细胞吞噬能力有关。.

BACKGROUND: Geriatric symptoms are common in dementia cases, while few studies have focused on these symptoms in Lewy body dementia (LBD). The purpose of this study is to investigate the distributions of Apolipoprotein E (APOE) ε4 and geriatric symptoms, and explore their associaitons in Dementia with Lewy bodies (DLB) and Parkinson\'s disease dementia (PDD).
METHODS: A retrospective study with 185 mild-moderate probable DLB (n = 93) and PDD (n = 92) patients was assigned. Demographic and clinical characteristics, neuropsychological assessments, and APOE genotypes were recorded. Description, correlation and logistic regression models were used to analyze the presence of geriatric symptom complaints and their associations with APOE ε4.
RESULTS: DLB patients displayed more frequency of fluctuating cognition, visual hallucination, rapid eye movement sleep behavior disorder, delusion, depression, anxiety, apathy, and loss of appetite, whereas the PDD cases had constipation, fear of falling, and insomnia more frequently. The APOE ε4 allele was more common in DLB than PDD (29.9% vs. 7.0%, p < 0.001), and the patients with DLB + APOE ε4 (+) were presented more delusions (p = 0.005) and apathy (p = 0.007) than patients with PDD + APOE ε4 (+). We also found that the APOE ε4 allele was significantly associated with hyperhidrosis (OR = 3.472, 95%CI: 1.082-11.144, p = 0.036) and depression (OR = 3.002, 95%CI: 1.079-8.353, p = 0.035) in DLB patients, while there were no significant associations between APOE ε4 allele and the age at visit, the age at onset, scores of MDS-UPDRS III, H&Y stage, ADL, MMSE, MOCA and NPI, as well as the presences of fluctuating cognition, VH, parkinsonism and RBD in both groups.
CONCLUSIONS: The presence and co-incidence of geriatric symptoms are common in patients with mild-moderate LBD. The presence of APOE ε4 allele is associated with hyperhidrosis and depression, but not global cognition, activitives of daily life, motor function and other neuropsychitric symptoms in DLB. These findings improve the awareness of geriatric symptoms, and contribute to the healthcare management of mild-moderate DLB and PDD.

The role of astrogliosis in the pathology of brain aging and neurodegenerative diseases has recently drawn great attention. Imidazoline-2 binding sites represent a possible target to map the distribution of reactive astrocytes. In this study, we use 11C-BU99008, an imidazoline-2 binding sites-specific PET radioligand, to image reactive astrocytes in vivo in healthy controls and patients with established Parkinson\'s disease dementia. Eighteen healthy controls (age: 45-78 years) and six patients with Parkinson\'s disease dementia (age: 64-77 years) had one 11C-BU99008 PET-CT scan with arterial input function. All subjects underwent one 3 T MRI brain scan to facilitate the analysis of the PET data and to capture individual cerebral atrophy. Regional 11C-BU99008 volumes of distribution were calculated for each subject by the two-tissue compartmental modelling. Positive correlations between 11C-BU99008 volumes of distribution values and age were found for all tested regions across the brain within healthy controls (P < 0.05); furthermore, multiple regression indicated that aging affects 11C-BU99008 volumes of distribution values in a region-specific manner. Independent samples t-test indicated that there was no significant group difference in 11C-BU99008 volumes of distribution values between Parkinson\'s disease dementia (n = 6; mean age = 71.97 ± 4.66 years) and older healthy controls (n = 9; mean age = 71.90 ± 5.51 years). Our data set shows that astrogliosis is common with aging in a region-specific manner. However, in this set-up, 11C-BU99008 PET cannot differentiate patients with Parkinson\'s disease dementia from healthy controls of similar age.

Parkinson\'s disease dementia (PDD) is a common complication of Parkinson\'s disease that seriously affects patients\' health and quality of life. At present, the process and pathological mechanisms of PDD remain controversial, which hinders the development of treatments. An increasing number of clinical studies have shown that alpha-synuclein (α-syn), tau, beta-amyloid (Aβ), and iron are closely associated with PDD severity. Thus, we inferred the vicious cycle that causes oxidative stress (OS), due to the synergistic effects of α-syn, tau, Aβ, and, iron, and which plays a pivotal role in the mechanism underlying PDD. First, iron-mediated reactive oxygen species (ROS) production can lead to neuronal protein accumulation (e.g., α-syn andAβ) and cytotoxicity. In addition, regulation of post-translational modification of α-syn by iron affects the aggregation or oligomer formation of α-syn. Iron promotes tau aggregation and neurofibrillary tangles (NFTs) formation. High levels of iron, α-syn, Aβ, tau, and NFTs can cause severe OS and neuroinflammation, which lead to cell death. Then, the increasing formation of α-syn, Aβ, and NFTs further increase iron levels, which promotes the spread of α-syn and Aβ in the central and peripheral nervous systems. Finally, iron-induced neurotoxicity promotes the activation of glycogen synthase kinase 3β (GSK3β) related pathways in the synaptic terminals, which in turn play an important role in the pathological synergistic effects of α-syn, tau and Aβ. Thus, as the central factor regulating this vicious cycle, GSK3β is a potential target for the prevention and treatment of PDD; this is worthy of future study.

BACKGROUND: Lewy body dementia (LBD), consisting of dementia with Lewy bodies (DLB) and Parkinson\'s disease dementia (PDD), is the second most common type of neurodegenerative dementia in older people. The current study aimed to investigate the clinical characteristics of LBD in Chinese memory clinics.
METHODS: A total of 8405 dementia medical records were reviewed, revealing 455 patients with LBD. Demographic data, neuropsychological scores, and the scale for Medial Temporal lobe Atrophy (MTA) were then analyzed from nine memory clinics in the China Lewy Body Disease Collaborative Alliance.
RESULTS: The clinical proportion of LBD among the subjects and among all dementia types was 5.4% (4.9-5.9%) and 7.3% (6.7-8.0%), respectively, with a mean onset age of 68.6 ± 8.4 years. Patients with DLB comprised 5.6% (n = 348, age of onset 69.1 ± 8.3), while PDD comprised 1.7% (n = 107, age of onset 66.7 ± 8.8) of all dementia cases. There were slightly more males than females with DLB (n = 177, 50.9%) and PDD (n = 62, 57.9%). Patients with DLB had a poorer performance compared to those with PDD on the MMSE (16.8 ± 7.1 vs. 19.5 ± 5.7, p = 0.001), the MoCA (11.4 ± 6.6 vs. 14.0 ± 5.8, p<0.001), the CDR (1.8 ± 0.7 vs. 1.6 ± 0.7, p = 0.002), and the MTA (1.8 ± 0.7 vs. 1.2 ± 0.6, p = 0.002). Diagnostic differences for LBD exist among the centers; their reported proportions of those with DLB ranged from 0.7 to 11.4 and those with PDD ranged from 0.0 to 2.9%.
CONCLUSIONS: Variations of diagnoses exists in different regions and the clinical proportion of LBD is likely to be underestimated in China and other regions.

Exploring the impact of glucocerebrosidase gene (GBA) polymorphisms and mutations on the pathogenesis of Parkinson\'s disease dementia (PDD) plays an important role in the diagnosis and treatment of this disease. This meta-analysis aimed to investigate the effects of GBA polymorphisms and mutations on the risk of PDD and to identify the relationship between GBA genotype and PDD.
A computer-based search was performed to retrieve publications from PubMed, Cochrane library, Embase, Chinese Biomedical Literature Database, China National Knowledge Infrastructure, and Wanfang databases using the search terms \"glucocerebrosidase\", \"Parkinson\'s disease\", and \"dementia\". After rigorous screening, cohort studies were included for meta-analysis.
The risk of PDD in GBA variant carriers was 1.94 times that in non-carriers (hazard ratio [HR], 1.94; 95% confidence interval [CI], 1.53-2.46). The risk of PDD in GBA polymorphism carriers was 1.87 times that in non-carriers (HR, 1.87; 95% CI, 1.18-2.98). The risk of PDD in GBA mutation carriers was 3.64 times that in non-carriers (HR, 3.64; 95% CI, 2.74-4.83). The risk of PDD in p.L444P variant carriers (HR, 4.81; 95% CI, 3.37-6.86) was significantly higher than that in p.N370S variant carriers (HR, 1.95; 95% CI, 1.29-1.94).
GBA polymorphisms and mutations are potential risk factors for PDD.