Degenerative Diseases Of Nervous System Research Articles

Lexical Retrieval Performance in Patients with Normal Pressure Hydrocephalus and Parkinson’s Disease

Objectives: This study aimed to investigate lexical retrieval performance in patients with similar patterns but different central nervous system degenerative diseases, specifically normal pressure hydrocephalus (NPH) and Parkinson’s disease (PD).Methods: A lexical retrieval task was performed on 14 patients with NPH, 14 patients with PD, and 14 healthy elderly subjects (HE) to compare their correct response scores, reaction times, and error types, and the Korean-Boston naming test (K-BNT) was additionally performed to determine the validity of the lexical retrieval task.Results: First, there was no significant difference in scores between the three groups on the K-BNT. Second, the scores of the NPH and PD groups were significantly lower than the HE group on the lexical retrieval task. Third, only the NPH group was significantly slower than the HE group in the reaction time on the lexical retrieval task. Fourth, the error type analysis showed that the NPH group made significantly more semantic and nonword errors and the PD group made significantly more semantic errors than the HE group. Fifth, the correlation analysis showed a significant static correlation between K-BNT and the lexical retrieval task scores with a correlation coefficient of .721.Conclusion: We suggest that the lexical retrieval task may be useful in the screening and differential diagnosis of patients with NPH and PD.

Age-related changes in meningeal lymphatic function are closely associated with vascular endothelial growth factor-C expression

Meningeal lymphatic vessels (MLVs) have crucial roles in removing metabolic waste and toxic proteins from the brain and transporting them to the periphery. Aged mice show impaired meningeal lymphatic function. Nevertheless, as the disease progresses, and significant pathological changes manifest in the brain, treating the condition becomes increasingly challenging. Therefore, investigating the alterations in the structure and function of MLVs in the early stages of aging is critical for preventing age-related central nervous system degenerative diseases. We detected the structure and function of MLVs in young, middle-aged, and aged mice. Middle-aged mice, compared with young and aged mice, showed enhanced meningeal lymphatic function along with MLV expansion and performed better in the Y maze test. Moreover, age-related changes in meningeal lymphatic function were closely associated with vascular endothelial growth factor-C (VEGF-C) expression in the brain cortex. Our data suggested that the cerebral cortex may serve as a target for VEGF-C supplementation to ameliorate meningeal lymphatic dysfunction, thus providing a new strategy for preventing age-related central nervous system diseases.

Use of opioids in geriatric palliative care

Introduction: Patients in Geriatric Palliative Care (GPC) complain of pain and opioids are the drugs used to manage it. This study aims to understand the sociodemographic, clinical and opioid use characteristics of GPC patients in a public hospital in the Federal District of Brazil.Methods: This is a cross-sectional approach based on analysis of prescriptions. The results are shown in tables after descriptive and bivariate analysis. Fisher’s exact test, Bonferroni’s post hoc for categorical variables and Kendall’s tau correlation coefficient for continuous variables were used.Results: Four hundred and forty-four prescriptions for 49 patients were analyzed. Data showed a mean age of 80.4 years, a prevalence of women (57.1 %), the main diagnoses being Alzheimer’s disease and neoplasia, and prevalent length of up to 7 days. Morphine was the most used medication (15.8 mg to 20.8 mg). The oral route was predominant at the beginning of hospitalization and the subcutaneous route at the end. There was a greater dose variation in degenerative disease of the nervous system and statistical significance between length of stay (1 to 7 days) and clinical diagnosis.Discussion: The sociodemographic and clinical characteristics are in line with the Brazilian epidemiological profile. The use of opioids was equivalent to that recommended and is more associated with dyspnea control. Dose variation in degenerative nervous system disease probably occurred due to the variability of diseases included in this group. The statistical significance between length of hospitalization and diagnosis can be justified by the clinical severity of the patients hospitalized.

DEMENTIA DIAGNOSES PREDICT CAREGIVER EDUCATION DISCREPANCIES IN HOSPITAL SETTING

Abstract Many family caregivers report feeling unprepared to provide care for persons living with dementia (PLWD) after their hospital stay. Consequently, PLWD may experience poorer health outcomes and higher service utilization rates. Health systems can provide education to patients and their family caregivers, increasing preparedness, but these practices are less understood. This retrospective data analysis of electronic health records examines the role of diagnostic billing codes in predicting amount of education received by patients and their family caregivers. Our dataset includes 419 unique encounters of hospitalized older adult patients with a documented dementia diagnosis and a listed family caregiver between 1/1/2019 and 8/1/2022. Dementia-related ICD-10 billing codes determined unique patient diagnoses. Encounters were given designations of receiving more vs. less education if the amount of education received was above or below the sample median. Logistic regressions then determined the relationship between diagnostic billing codes and education received while controlling for demographic and contextual characteristics. We found that encounters with diagnostic codes “other degenerative disease of nervous system” and “Alzheimer’s disease” were 2.8 and 3.3 times as likely to receive more education, respectively (95% confidence interval = [1.051, 7.347], p = .0394; [1.175, 9.461], p = .0236). Conversely, encounters with the code “other frontotemporal dementia” were 3.3 times as likely to receive less education ([1.150, 9.684], p = .0266). Findings demonstrate certain dementia-related diagnoses predict differences in how likely caregivers are to receive education. Health systems should evaluate for these differences and incorporate new methods to increase caregiving preparedness.

Exploring the Connectivity of Neurodegenerative Diseases: Microglia as the Center.

Degenerative diseases affect people's life and health and cause a severe social burden. Relevant mechanisms of microglia have been studied, aiming to control and reduce degenerative disease occurrence effectively. This review discussed the specific mechanisms underlying microglia in neurodegenerative diseases, age-related hearing loss, Alzheimer's disease, Parkinson's disease, and peripheral nervous system (PNS) degenerative diseases. It also reviewed the studies of microglia inhibitors (PLX3397/PLX5622) and activators (lipopolysaccharide), and suggested that reducing microglia can effectively curb the genesis and progression of degenerative diseases. Finally, microglial cells' anti-inflammatory and pro-inflammatory dual role was considered the critical communication point in central and peripheral degenerative diseases. Although it is difficult to describe the complex morphological structure of microglia in a unified manner, this does not prevent them from being a target for future treatment of neurodegenerative diseases.

Pathophysiology of Cardiac Cell Injury in Post-COVID-19 Syndrome

Abstract: Recently, the scientific community has realized that COVID-19 effects are not limited to the acute period of infection but continue beyond that to cause more prolonged pathological changes. Post-COVID syndrome is a novel concept that describes the sequelae/persistent pathophysiological changes of post-COVID-19 infection. The current hypothesis suggests the involvement of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in cardiac arrhythmias, coronary artery aneurism, acute renal injury, central nervous system degenerative diseases, vascular endothelial cell dysfunction, and pulmonary dyspnea, as well as fibrotic lung damage. Therefore, COVID-19 has been identified as a poly-syndromic and poly-systemic inflammatory disease. Post-COVID extrapulmonary complications have been observed in approximately 85% of hospitalized COVID-19 survivors and 35% of COVID-19 outpatients. Furthermore, 25% of hospitalised COVID-19 survivors developed myocardiopathy.

Association between 23 drugs and Parkinson's disease: A two-sample Mendelian randomization study.

Parkinson's disease (PD) is a common degenerative nervous system disease. At present, there are certain limitations in various treatment options aimed at preventing or delaying the progression of PD. Therefore, the exploration of new drugs for PD is beneficial. Mendelian randomization (MR) analysis can be used to explore the association between drugs and diseases. In this study, MR analysis was adopted to investigate the causal relationship between 23 drugs and PD. These drugs have been approved for the treatment of different diseases, such as salicylic acid and derivatives (collectively called salicylates, e.g., aspirin, used for fever and pain relief), antithrombotic agents (e.g., warfarin, aspirin, used for preventing thrombotic events). The GWAS data for the 23 drugs were obtained from the UK Biobank (UKB) project, while the GWAS data for PD were sourced from FinnGen. Single-Nucleotide Polymorphisms (SNPs) were selected as instrumental variables (IVs). We first performed a series of quality control steps (including MR-PRESSO) to select the appropriate SNPs. Two-sample MR analysis was performed using five different methods, including inverse variance weighting (IVW) with random-effects model, weighted median, MR-Egger, simple model, and weighted model. At the same time, sensitivity analysis was carried out using the MR-Egger and Cochran's Q test to ensure the authenticity and reliability of the results. In MR-PRESSO, salicylates and antithrombotic agents showed statistically significant associations with PD, respectively. In the main MR analysis (IVW), there was a negative causal relationship between salicylates and PD (OR=0.73, 95% CI=0.54-0.98, p=.039). Similarly, there was a negative causal relationship between antithrombotic agents and PD (OR=0.70, 95%CI=0.52-0.96, p=.027). No statistically significant association was found between the remaining 21 drugs and PD. This MR study demonstrated that salicylates and antithrombotic agents can reduce the risk of PD, thus providing a novel avenue for future drug exploration in PD.

Detection of Ferroptosis in Models of Brain Diseases.

Ferroptosis is a regulated form of non-apoptotic cell death driven by iron-dependent lipid peroxidation. In the past decade, ferroptosis has been reported to be involved in the pathological role in the central nervous system degenerative diseases (e.g., Alzheimer's disease, Huntington's disease, and Parkinson's disease), stroke, traumatic brain injury, and brain tumor. However, how to reliably detect and classify ferroptosis from other cell death in pathological conditions remains a great challenge, especially in primary brain cells and brain tissues. Here, we summarize the methods and protocols (such as real-time PCR, western blotting, immunofluorescence staining, lipid peroxidation assay kits and probe, immunofluorescence staining, GPX activity and glutathione depletion assay kits, iron detection, and TEM) used in the present study to detect and classify ferroptosis in the brain.

Multimorbidity and chronic co-prescription networks and potential interactions in adult patients with epilepsy: MorbiNet study.

We constructed epilepsy multimorbidity networks to study associations with chronic conditions, and co-prescriptions and drug-disease networks to assess potential interactions.We conducted a population-based study in Catalonia, Spain, with electronic files of 3,135,948 adult patients with multimorbidity, 32,625 of them with epilepsy (active diagnosis any time during 2006-2017). We constructed epilepsy comorbidity networks using logistic regression models from odds ratio estimates adjusted by age, sex, and comorbidities with R software and generated trajectories to study the progression of epilepsy. We constructed drug-disease and co-prescription networks using mixed models with repeated measures adjusting by age, sex, and period with chronic prescription invoiced data.Comorbidity more frequently preceding epilepsy included cerebrovascular accident (OR: 3.59), congenital anomalies (2.18), and multiple sclerosis (1.33); and following epilepsy: dementia (1.91), personality disorder (1.59), alcohol abuse (1.22), and Parkinson (1.21). Mental retardation (13.08), neurological cancer (8.49), benign neoplasm (4.69), infections (3.14), and psychosis (1.58) might precede or not epilepsy. A common progression was to schizophrenia, dementia, and other neurological diseases (mainly cerebral palsy and other degenerative diseases of nervous system).Co-prescription associations with major-moderate potential interactions were 54% for carbamazepine, 61% phenytoin, 53% phenobarbital, and 32% valproate. Major potential interactions were with antipsychotic, anxiolytic, opioid, cardiovascular, and other anti-seizure medications (ASMs).The most frequent comorbidities of epilepsy were congenital, cerebrovascular, and neurological and psychiatric conditions. High comorbidity and co-prescription with potential interactions can increase the complexity of care of patients with epilepsy.

Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer's Disease Mouse Models: A Potential Role for Aβ.

Emerging data have highlighted the coexistence of multiple sclerosis (MS) and Alzheimer’s disease (AD), both of which are common central nervous system degenerative diseases with a heavy burden on patients, their families, and society. However, it is unclear how MS progresses under an AD pathological background. We aimed to address the question of how MS progresses under an AD pathological background. We induced the experimental autoimmune encephalomyelitis (EAE) model of MS in two types of AD mouse models, Tg6799 and APP/PS1 mice. We found that, compared with wild-type mice, the clinical symptoms of EAE were significantly ameliorated in APP/PS1 mice but not in Tg6799 mice. Moreover, a much lower level of serum Aβ was observed in Tg6799 mice. EAE clinical symptoms in Tg6799 and C57BL/6J mice were ameliorated by intraperitoneal injection of Aβ42. Peripheral administration of Aβ42 peptides was able to inhibit Th17 development in vivo, which is likely to occur through the inhibition of IL-6 production in dendritic cells. Our findings revealed that AD and EAE could coexist in the same mouse, and Aβ residing in peripheral circulation likely plays an anti-inflammatory role in preventing EAE progression. These findings reveal the potential benefit of Aβ, one of the supervillains of AD, at least in certain contexts.

Fibroblast growth factors and their effect on cognitive functions and the course of central nervous system degenerative diseases

Fibroblast growth factors and their effect on cognitive functions and the course of central nervous system degenerative diseases

Programmed Cell Death Protein 1 Blockade Reduces Glycogen Synthase Kinase 3β Activity and Tau Hyperphosphorylation in Alzheimer's Disease Mouse Models.

Alzheimer’s disease (AD) is a central nervous system degenerative disease, with no effective treatment to date. Administration of immune checkpoint inhibitors significantly reduces neuronal damage and tau hyperphosphorylation in AD, but the specific mechanism is unclear. Here, we found that programmed cell death-receptor 1 (PD1) and its ligand PDL1 were induced by an intracerebroventricular injection of amyloid-β; they were significantly upregulated in the brains of APP/PS1, 5×FAD mice and in SH-SY5Y-APP cell line compared with control. The PD1 and PDL1 levels positively correlated with the glycogen synthase kinase 3 beta (GSK3β) activity in various AD mouse models, and the PDL1-GSK3β immune complex was found in the brain. The application of PD1-blocking antibody reduced tau hyperphosphorylation and GSK3β activity and prevented memory impairments. Mechanistically, we identified PD1 as a critical regulator of GSK3β activity. These results suggest that the immune regulation of the PD1/PDL1 axis is closely involved in AD.

Mortality in FTD: An Australian perspective

AbstractTHEME: Clinical manifestationsTOPIC: Neuropsychiatry & beh neurologySUBTOPIC: NeuropsychiatryBackgroundSurvival duration in frontotemporal dementia (FTD) remains inconsistent, depending on the clinical phenotype with different risk factors identified. Risk factors to mortality include the FTD‐MND presentation, a genetic predisposition (Agarwal S et al. 2019), deficits in neuropsychological tests, imaging changes (Agarwal et al. 2019; Hodges et al. 2003) and non‐tau pathology (Roberson et al. 2005; Hodges et al. 2003). We aimed to identify survival duration and cause of death in this group.MethodAll inpatients admitted to Neuropsychiatry, based at the Royal Melbourne Hospital, in metropolitan Australia from 1992 – 2014, who were diagnosed with probably FTD of any subtype were included. Linkage data was obtained by the Australian Institute of Health and Welfare (AIHW). We reviewed their clinical information including demographics, age of symptom onset, type of presenting symptom, neuroimaging and diagnosis.ResultOf the 528 individual inpatients identified with a dementia, there were n=100 who had a diagnosis of probable FTD. There were n=76 who had a behavioural‐variant FTD (bv‐FTD), n=14 who had a language‐variant FTD (lang‐FTD) and n=10 who had FTD‐MND. 67% of the group had died. Overall median duration of survival was 10.5 years (95% CI 7.9, 12.2). There were no differences in age of death nor age onset between the three FTD‐subtypes (p=0.479, p=0.289, respectively). As expected, there were significant differences in the median survival duration of the three FTD subtypes, with FTD‐MND having the shortest duration (p=0.004). Causes of death based on ICD‐10 were predominantly dementia‐related (26.3% Other degenerative diseases of nervous system; 17.5% unspecified dementia) but also included acute myocardial infarction (7%) and alcohol‐related (7%). Standardised mortality ratios (SMRs) revealed that compared to population norms, people with FTD had 8x mortality rate.ConclusionNot unsurprisingly, FTD‐MND had the shortest duration compared to the other subtypes of FTD. The duration of survival was comparable to other studies. Causes of death revealed that a dementia was identified in almost half of cases. High SMRs suggest that FTD is a particularly “fatal” type of dementia in younger people. Investigation into risk factors to death is required.

Sustained release triple drug loaded colloidosomes for management of Parkinson's disease

Parkinson's disease(PD) is well-known as a progressive and degenerative disease of nervous system. The degeneration of dopaminergic neurons in substantia nigra, and reduction in amount of neurotransmitter dopamine available in striatum relate symptoms of this disease. It is hypothesized that a drug delivery system that provides controlled and sustained release of PD drugs would afford better management of PD. Hollow microcapsules composed of PMMA(polymethyl methacrylate) and poly(caprolactone)(PCL) are prepared through a modified double-emulsion technique. They are loaded with three PD drugs, i.e., levodopa(LD), carbidopa(CD), and entacapone(ENT), at a ratio of 4:1:8.

Long non-coding RNA SNHG1 mediates neuronal damage in Parkinson's disease model cells by regulating miR-216a-3p/Bcl-2-associated X protein.

BackgroundParkinson’s disease (PD) is a common central nervous system degenerative disease in middle-aged and elderly people. Our study aimed to illuminate the relationship and mechanism of long-chain non-coding RNA SNHG1 and miRNA (miR)-216a-3p in PD.MethodsHuman neuroblastoma cell lines were treated with MPP+ to construct a PD model. Real-time fluorescent quantitative PCR was used to detect the cellular expression of SNHG1. Neuronal cell activity and apoptosis were compared before and after SNHG1 knock-down, as was neuronal miR-216a-3p expression. Further, a luciferase reporter gene experiment was performed to verify BAX as the target of miR-216a-3p. Anti-miR-216a-3p and BAX were co-transfected into PD model cells, and neuronal cellular activity and apoptosis were observed. Finally, the potential regulatory network of SNHG1/miR-216a-3p/BAX in PD was investigated.ResultsThe expression of miR-216a-3p was decreased in the PD model cells, and re-expression reversed the high apoptotic rate and cell vitality inhibition in PD model cells. SNHG1 interacted with miR-216a-3p and negatively regulated its upstream molecules, while miR-216a-3p attenuated the effect of SNHG1 knock-down on neurons. The overexpression of BAX in the PD cell model blocked the damage by miR-216a-3p to neurons. At the same time, SNHG1 acted as a coordinator, mediating the regulation of BAX via miR-216a-3p, thereby affecting the activity and apoptotic rate of neurons in the PD model.ConclusionsSNHG1 interacts with miR-216a-3p to regulate the expression of BAX. This SNHG1/miR-216a-3p/BAX molecular regulatory network is implicated in the pathogenesis of PD.

Protective effects of resveratrol liposomes on mitochondria in substantia nigra cells of parkinsonized rats

Parkinson's disease (PD) is a central nervous system degenerative disease. The progressive death of dopaminergic neurons is closely correlated to mitochondrial dysfunction. Resveratrol contains three hydroxyl groups, and has a strong neuroprotective effect. This study aimed to investigate the protective effect of resveratrol liposome on mitochondria of substantia nigra cells in Parkinsonized rats through experiment. The investigators used 6-hydroxydopamine to establish the Parkinsonized rat model, and used resveratrol liposome from Polygonum cuspidatum (20 mg·kg-1) for gavage, up to a total volume of 1 mL, once-daily, for two weeks. After treatment, the levels of mitochondrial membrane potential, mitochondrial complexes I-IV, mitochondrial cytochrome C, apoptosis-inducing factor (AIF), PTEN-induced putative kinase 1 (PINK1), tumor necrosis factor-receptor-associated protein 1 (TRAP1) and phosphorylated TRAP1 in rat mesencephalic cells were detected according to the operation instructions of the kits. After two weeks of treatment, resveratrol liposomes could significantly enhance the activity of mitochondrial electron transfer chain complex I in the substantia nigra cells of Parkinsonized model rats, promote the expression of complex I subcomponent MT-ND1-37kD, improve mitochondrial membrane potential, inhibit the release of mitochondrial cytochrome C and apoptotic inducible factor, enhance the expression of mitochondrial functional protein PINK1, increase the phosphorylated TRAP1 level, and elevate the phosphorylated TRAP1/TRAP1 ratio. Resveratrol liposome has positive effects on mitochondria in substantia nigra cells of Parkinsonized rats, and may be one of its pharmacological mechanisms.

Dendrobium nobile Lindl alkaloid attenuates 6-OHDA-induced dopamine neurotoxicity.

Parkinson's disease (PD) is one of the most common central nervous system (CNS) degenerative disease and is characterized by a progressive loss of midbrain substantia nigra dopamine (DA) neurons. Dendrobium nobileLindl alkaloid (DNLA) is an active component extracted from D. nobile Lindl, which is a traditional Chinese herb. The various pharmacological effects of D. nobile are beneficial for human health. Recently, DNLA-mediated neuroprotective effects have been reported. However, the neuroprotection of DNLA on 6-hydroxydopamine (6-OHDA)-induced DA neurotoxicity is still unknown. This study aimed to explore the neuroprotective effects of DNLA on DA neurotoxicity induced by 6-OHDA. In PD rat model, continuous intragastric administration of DNLA (20mg/kg) for 7 days significantly ameliorated 6-OHDA-induced DA neurons loss in the midbrain substantia nigra. In addition, primary rat midbrain neuron-glia cocultures were used to explore the mechanisms underlying DNLA-related DA neuroprotection. The studies on neuron-glia cocultures revealed that neuroprotective effects of DNLA (2.5ng/mL) were mediated by inhibiting the release of proinflammatory cytokines. Taken together, DNLA holds neuroprotective effect on 6-OHDA-induced neurons neurodegeneration by selectively inhibiting the production of proinflammatory factors and could be a potential compound for PD treatment.

LncRNA NR_030777 Alleviates Paraquat-Induced Neurotoxicity by Regulating Zfp326 and Cpne5.

Paraquat (PQ) is herbicide widely used in agricultural production. It is identified as an environmental toxicant that could lead to neurodegeneration damage. Parkinson's disease (PD) is a central nervous system degenerative disease that occurs in the elderly. Main risk factors for PD include genetic and environmental variables, but its specific mechanism is still not well understood. Emerging evidence suggests that long noncoding RNAs (lncRNAs) play an important role in PD. LncRNA NR_030777 has a full length of 2208 bp and is highly conserved among species. RNA profiling showed a significant alteration in lncRNA NR_030777 expression upon PQ-induced neurotoxicity. However, little is known on the functional relevance of lncRNA NR_030777 in the development of PQ. In this study, we discovered a vital protective role of lncRNA NR_030777 in PQ-induced neurotoxicity. The expression of NR_030777 correlates with elevated level of reactive oxygen species induced by PQ. In addition, activated expression of NR_030777 alleviates neurotoxicity by regulating the expression of Zfp326 and Copine 5. We report that lncRNA NR_030777 has a vital protective role in neurotoxicity induced by environmental toxicants such as PQ. This study could serve as an exemplary case for lncRNAs to be considered as a potential target for the prevention and treatment of PQ-induced neurodegenerative disorders such as PD.

Ellagic acid protects dopamine neurons from rotenone-induced neurotoxicity via activation of Nrf2 signalling.

Parkinson's disease (PD) is the second most prevalent central nervous system (CNS) degenerative disease. Oxidative stress is one of key contributors to PD. Nuclear factor erythroid‐2‐related factor 2 (Nrf2) is considered to be a master regulator of many genes involved in anti‐oxidant stress to attenuate cell death. Therefore, activation of Nrf2 signalling provides an effective avenue to treat PD. Ellagic acid (EA), a natural polyphenolic contained in fruits and nuts, possesses amounts of pharmacological activities, such as anti‐oxidant stress and anti‐inflammation. Recent studies have confirmed EA could be used as a neuroprotective agent in neurodegenerative diseases. Here, mice subcutaneous injection of rotenone (ROT)‐induced DA neuronal damage was performed to investigate EA‐mediated neuroprotection. In addition, adult Nrf2 knockout mice and different cell cultures including MN9D‐enciched, MN9D‐BV‐2 and MN9D‐C6 cell co‐cultures were applied to explore the underlying mechanisms. Results demonstrated EA conferred neuroprotection against ROT‐induced DA neurotoxicity. Activation of Nrf2 signalling was involved in EA‐mediated DA neuroprotection, as evidenced by the following observations. First, EA activated Nrf2 signalling in ROT‐induced DA neuronal damage. Second, EA generated neuroprotection with the presence of astroglia and silence of Nrf2 in astroglia abolished EA‐mediated neuroprotection. Third, EA failed to produce DA neuroprotection in Nrf2 knockout mice. In conclusion, this study identified EA protected against DA neuronal loss via an Nrf2‐dependent manner.

Auxiliary diagnosis of heterogeneous data of Parkinson’s disease based on improved convolution neural network

Parkinson’s disease (PD) is a kind of nervous system degenerative disease frequently occurring in the elderly over sixty years old. With the development of imaging technology, medical imaging has played a certain role in the diagnosis of Parkinson’s disease. The aim of the paper is to the diagnosis of Parkinson’s disease through deep learning. This paper selects the T2-MRI(T2-Magnetic Resonance Imaging) image and clinical data to diagnose Parkinson’s disease and integrates the heterogeneous data into the improved convolution neural network. In this paper, convolution neural network is added to the Gabor filter to make the whole convolution neural network have better effect; the activation function is improved and adjusted, which means the traditional sigmoid function and the tanh function are discarded, and the Relu activation function is used to improve the neural network. It is proved by experiments that the heterogeneous data diagnosis of T2-MRI image and clinical data (the accuracy is 77.9%) is better than the simple image data diagnosis (the accuracy is71.2%). For the same data, the improved convolution neural network is superior to the traditional network (the accuracy is 64.5%).