Analysis Of Urinary Symptoms And Urodynamic Findings In Multiple Sclerosis Patients By Gender And Disease Subtype

Article Information

Article Type: Research Article

Citation: Cox L, Cameron AP, Wittman D, Papin JE, Mao-Draayer Y, et al. (2015) Analysis of Urinary Symptoms and Urodynamic Findings in Multiple Sclerosis Patients by Gender and Disease Subtype. J Neurol Neurobiol 1 (2): http://dx.doi.org/10.16966/2379-7150.105

Copyright:© 2015 Cox L, et al. This is an openaccess article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Publication history:

 Received date: 22 April, 2015

 Accepted date: 29 April, 2015

 Published date: 05 May, 2015


Authors :

Cox L,      Cameron AP,      Wittman D,      Papin JE,      Mao-Draayer Y,      He C,      Clemens JQ,      Wei JT,      Sarma AV,      Stoffel JT*

Department of Urology, University of Michigan, 1500 E. Medical Center Dr. SPC 5330 Ann Arbor, MI, USA

*Corresponding author: John Stoffel, MD, University of Michigan,Department of Urology 1500 E. Medical Center Dr. SPC 5330 Ann Arbor, MI, USA, Tel: 48109-5330; E-mail: jstoffel@med.umich.edu

Abstract

Background: Although urinary symptoms are prevalent in multiple sclerosis (MS), there is little information whether bladder function differs by gender or disease subtype.

Objective: Differences in MS bladder function within subgroups were investigated by comparing female to male and relapsing remitting (RRMS) to secondary progressive (SPMS) patients.

Methods: We reviewed 118 MS patients referred for urologic evaluation between 2007 and 2012 and extracted demographic, questionnaire (AUASI, M-ISI), and urodynamic data. Variables were analyzed by gender and MS subtype, and a multivariable regression model was generated to adjust for age and gender

Results: The cohort consisted of83/35 female/male and 57/61RRMS/SPMS subjects. Urinary questionnaire and urodynamic findings were similar between genders, with the exception of higher maximum voiding pressures in males (p=0.003). RRMS patients reported more bothersome urinary symptoms compared to SPMS (AUASI21 vs. 15, p=0.004) and RRMS was independently associated with higher symptom scores on multivariable analysis (OR 17.1, p=0.008). There were no differences in urodynamic findings between subtypes.

Conclusions: Male and female MS patients had similar urinary symptom scores and urodynamic findings, with the exception of higher voiding pressures in males. RRMS patients reported significantly more severe urinary symptoms on AUASI, compared to SPMS, despite having similar urodynamic findings

Keywords
Multiple sclerosis; Neurogenic bladder; Urodynamic testing; Gender

Table 1: Characteristics by of Multiple Sclerosis Cohort Grouped by Disease Subtype


Table 2: Characteristics by of Multiple Sclerosis Cohort Grouped by Gender


Table 3:Characteristics by of Multiple Sclerosis Cohort Grouped by Disease Subtype


Table 4:Multivariable Analysis for Association between MS Subtype and Urinary Symptoms and Voiding PressuresAdjusted for Age and Gender

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Somatomotor and Behavioral Changes Following Traumatic Brain Injury

Article Information

Article Type: Research Article

Citation: Citation: Adams S, Condrey JA, Wen Tsai H, Svetlov SI, Prima V, Davenport PW (2015) Somatomotor and Behavioral Changes Following Traumatic Brain Injury. Neurol Neurobiol, Volume1.1: http://dx.doi.org/10.16966/2379-7150.104

Copyright: © 2015 Adams S et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Publication history:

 Received date: 26 February, 2015.

 Accepted date: 12 March, 2015.

 Published date: 17 March, 2015.

Authors :

 Sherry Adams ¹       Jillian A. Condrey ¹       Hsiu-Wen Tsai ¹       Stanislav I. Svetlov ²       Victor Prima ²       Paul W. Davenport ^1*    
1Department of Physiological Sciences, University of Florida, Gainesville FL, USA
²2Department of Medicine and Psychiatry, 1600 SW Archer Road, Box 100274, University of Florida, Gainesville, FL, USA

*Corresponding author: Dr. Paul W. Davenport, Department of Physiological Sciences, University of Florida, Gainesville, FL 32603, USA, Tel: 352-294-4025; Fax: 352-392-5145; E-mail: pdavenpo@ufl.edu

Abstract

Overpressurization blast (OB) exposure used to induce traumatic brain injury (TBI) in the rodent model can result in somatomotor and behavioral changes. Increased anxiety is evidenced after OB TBI in Dorsal and Frontal blast-wave exposed injured animals. Sustained impaired somatosensory functions occur after multiple OB injuries in Dorsal animals. Somatomotor function is impaired acutely but partially recovers after OB injury in Frontal animals. The Dorsal Group had reduction in risk-taking behavior in Group 1 (low pressure OB) and in total exploration in Group 2 (high pressure OB). The critical time point for somatosensory and somatomotor function impairment occurs at 24 hours post-OB injury with Group 1 demonstrating somatosensory and Group 2 demonstrating somatomotor deficits. The results suggest orientation and pressure magnitude have a significant impact on behavioral outcome measures following OB injuries as well as cumulative effects of repeated OB.



Table 1: Somatomotor evaluation after OB injury in sprague-dawley rats

Table 2: EPM evaluation after OB injury in sprague-dawley rats

Data expressed as mean ± SD. One-way ANOVA test followed by post hoc analysis by Tukey HSD method. *Denotes statistically significant change of values within group. Intergroup comparison one-way ANOVA test followed by post hoc analysis by Tukey HSD method.

Table 3: EPM evaluation after dorsal OB injury in sprague-dawley rats

Data expressed as mean ± SD. One-way ANOVA test followed by post hoc analysis by Tukey HSD method. *Denotes statistically significant change of values within group. Intergroup comparison one-way ANOVA test followed by post hoc analysis by Tukey HSD method.

Table 4: Somatomotor tests for sham, dorsal and frontal groups

Data expressed as mean ± SD. One-way ANOVA test followed by post hoc analysis by Tukey HSD method. Intergroup comparison one-way ANOVA test followed by post hoc analysis by Tukey HSD method.

Table 5: Somatomotor tests for dorsal groups 1 and 2

Data expressed as mean ± SD. One-way ANOVA test followed by post hoc analysis by Tukey HSD method. *Denotes statistically significant change from time value within group. Intergroup comparison one-way ANOVA test followed by post hoc analysis by Tukey HSD method.

Table 6: Somatosensory tests for sham, dorsal and frontal groups

Data expressed as mean ± SD. One-way ANOVA test followed by post hoc analysis by Tukey HSD method. *Denotes statistically significant change of values within group. Intergroup comparison one-way ANOVA test followed by post hoc analysis by Tukey HSD method.

Table 7: Somatosensory tests for dorsal groups 1 and 2

Data expressed as mean ± SD. One-way ANOVA test followed by post hoc analysis by Tukey HSD method. *Denotes statistically significant change from time value within group. Intergroup comparison one-way ANOVA test followed by post hoc analysis by Tukey HSD method.


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Biophysical Mind-Brain Sleep Regulation in Health and Pathology

Article Information

Article Type: Review Article

Citation: Naisberg Y (2015) Biophysical Mind-Brain Sleep Regulation in Health and Pathology. J Neurol Neurobiol 1 (2): doi http://dx.doi.org/10.16966/2379-7150.107

Copyright: © 2015 Naisberg Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Publication history:

 Received date: 22 April 2015

 Accepted date: 29 May 2015

 Published date: 31 May, 2015

Authors :

Yakov Naisberg*

AMCHA- Branch Netanya, National Israeli Center for Psychosocial Support of Survivors of the Holocaust and the Second Generation, Netanya, Israel

*Corresponding author: Yakov Naisberg M.D., AMCHA- Branch Netanya, National Israeli Center for Psychosocial Support of Survivors of the Holocaust and the Second Generation, Netanya, Mendel Singer St. 13/2, Haifa, Israel, Tel: 04- 8341966; Fax: 04- 8341966; E-mail: naisberg@012.net.il

Abstract

Why people sleep? What kind of kinetics drive human to nighttime sleep phases? What kind of fundamentals night sleep performs? The medical macro biophysical physiological neuropsychiatric operational (MBPNPO) model provides key answers. Human circadian cycles with daytime excitable wakeful body operational ranges (BOR) based on non-automatic velocity-increasing kinetics and nighttime inhibit the macro biophysical physiological mind operational kinetics. It replaces non-automatic into automatic velocity-reduced BOR regulation at sleep phases to sustain homeostatic balance and human life-supporting properties. Nighttime sleep phases carry on fundamental homeostatic functions on resynchronizing cellular and tissues systems, stabilizing intellectual memory with closure of memory storages and activating sexual organs from adolescence on with vivid erotic dreams influencing heterosexual wakeful orientation effects.

1. At sleep stage IV homeostatic tuning of the overall body cells and tissues with an automatic biophysical engraving genetic program to tune the life span timing scale for every circadian cycle events.
2. At sleep, stage IV under the least metabolic energy usage and low-rate kinetics hermetic closure of all daily working memory repositories occur to tuning stabilizing intellectual memory potentials for given circadian cycles.
3. At REM sleep stage II, sexual organs potentiate orgasmic sensation linked with erotic dreams tuning homeostatic heterosexual pairing.
   

Complementary fixed biochemical and biophysical parameters at sleep stage IV, may serve as an individual’s database for comparison in health and pathology, severely influencing all kinds at sleep disturbances.

Keywords
Body-brain-biophysical mind unity; Circadian diurnal and nocturnal cycles; Evolutionary sleep control over mutated genetics

Figure 1: MRI of brain showing infract on Pons

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Apoplexy along with Spinal Cord Injury - A rare Combination

Article Information

Article Type: Case Report

Citation: Khanal D (2015) Apoplexy along with Spinal Cord Injury - A rare Combination. J Neurol Neurobiol 1(2): doi. http://dx.doi.org/10.16966/2379-7150.106

Copyright: ©2015 Khanal D. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Publication history:

 Received date: 28 March, 2015

 Accepted date: 28 May, 2015;

 Published date: 31 May, 2015

Authors :

Dildip Khanal*
Siddhi Vinayak Aspatal & Prasuti Griha Pvt. Ltd, Gongabu Chowk, Kathmandu, Nepal

*Corresponding author: Dildip Khanal, HOD of Physiotherapy Department, Siddhi Vinayak Aspatal & Prasuti Griha Pvt. Ltd, Gongabu Chowk, Kathmandu, Nepal, E-mail: dildip17@gmail.com

Abstract

Apoplexy and the spinal cord injury are the most common neurological disorder, representing foremost causes of disability. Nevertheless, a combination of the diseases is a rare life-threatening condition requiring a team of rehabilitation for management.

Keywords
Apoplexy; Spinal cord injury; Therapeutic rehabilitation

Figure 1: MRI of brain showing infract on Pons



Figure 2: MRI of Spinal Cord showing mild degenerative disc disease at C3-5 and L5-S1 levels and C5-6 disectomy and fusion

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The Unisex Brain: The Next Stage in Human Evolution

Article Information

Article Type: Editorial

Citation: Rajalakshmi K (2015) The Unisex Brain: The Next Stage in Human Evolution. J Neurol Neurobiol 1(2): doi http://dx.doi.org/10.16966/2379-7150.e103

Copyright: ©2015 Rajalakshmi K. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Publication history:

 Received date: 28 May, 2015

 Accepted date: 30 May, 2015

 Published date: 31 May, 2015

Authors :

Rajalakshmi K

Autism Expert, Authentic Autism and ADHD Solutions, Energy Medicine Consultant, PioneerIntent Healing Featured On CNNIBN, Chennai, India

*Corresponding author: Rajalakshmi K, Autism Expert, Authentic Autism and ADHD Solutions, Energy Medicine Consultant, Pioneer-Intent Healing Featured On CNN-IBN, Chennai, India. E-mail: snowy123@gmail.com

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Previous Injury and Chronic Pain are Associated with Side of Onset in Parkinson’s Disease

Article Information

Aritcle Type: Short Communication

Citation: Tekin I, Vgontzas A, Lewis MM, Kothari S, Kong L, et al. (2015) Previous Injury and Chronic Pain are Associated with Side of Onset in Parkinson’s Disease. J Neurol Neurobiol 1(1): doi http://dx.doi. org/10.16966/2379-7150.109

Copyright: © 2015 Tekin I, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Publication history:

 Received date: 3 July 2015

 Accepted date: 20 July 2015

 Published date: 25 July 2015

Authors :

Izel Tekin¹   Angeliki Vgontzas²   Mechelle M Lewis^1,3   Saira Kothari³    Lan Kong⁶   Yue Lu⁸   Kent E Vrana¹   Xuemei Huang<sup>1,3,4,5,7*

1</sup>Department of Pharmacology, Pennsylvania State University College of Medicine, Hershey, PA, USA²Department of Medicine, Pennsylvania State University College of Medicine, Hershey, PA, USA³Department of Neurology, Pennsylvania State University College of Medicine, Hershey, PA, USA⁴Department of Radiology, Pennsylvania State University College of Medicine, Hershey, PA, USA⁵Department of Neurosurgery, Pennsylvania State University College of Medicine, Hershey, PA, USA⁶Department of Public Health Sciences Pennsylvania State University College of Medicine, Hershey, PA, USA⁷Department of Kinesiology, Pennsylvania State University, University Park, PA, USA⁸Department of Kinesiology, Statistics8 Pennsylvania State University, University Park, PA, USA*Corresponding author: Xuemei Huang, MD, PhD, Departments of Neurology, Penn State University-Hershey Medical Center, H037 500 University Drive, Hershey, PA 17033-0850, USA Tel: 717-531-0003-287082; E-mail: Xuemei@psu.edu


Abstract

Background

Parkinson’s disease (PD) motor symptoms are frequently asymmetric and the factors that influence the side of onset are unclear.

Objective

To explore whether peripheral injury and associated chronic limb pain may influence the side of onset.

Methods

We administered a questionnaire to 128 PD patients in a tertiary movement disorder clinic. Handedness, date and type of limb injury(s) and duration of associated pain, and date and side of onset were ascertained.

Results

Sixty-two subjects reported limb injuries prior to the onset of PD symptoms, 30 with and 32 without chronic pain (i.e., ≥ 2 months). There was no association between injury and PD onset side overall (p=0.334). In subjects with chronic pain associated with limb injuries, however, side of injuries was associated with the side of PD symptom onset (p=0.030).

Conclusions

Limb injury with chronic pain may be related to the side of PD symptom onset. Future studies may shed light on the nature of this observation.

Keywords

Parkinson’s disease; Peripheral limb injury; Side of onset; Handedness

Figure 1: Distribution of subjects with a history of peripheral injury and PD side of onset. The numbers on top of the columns indicate the number of subjects in each group. The upper panel describes all PD subjects separated by right side injury, left side injury, and no history of injury. The bottom panel shows the distribution of subjects according to their chronic injury side and whether they have suffered chronic pain due to injury.

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Clinical Presentation along with Imaging Features of Superficial Peroneal Nerve Shwannoma: A Rare Case Report

Article Information

Aritcle Type: Case Report

Citation: Cellina M, Orsi M, Fetoni V, Oliva G (2015) Clinical Presentation along with Imaging Features of Superficial Peroneal Nerve Shwannoma: A Rare Case Report. J Neurol Neurobiol 1(3): doi http://dx.doi. org/10.16966/2379-7150.111

Copyright: © 2015 Cellina M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Publication history:

 Received date: 24 June 2015

 Accepted date: 24 July 2015

 Published date: 29 July 2015

Authors :

Michaela Cellina^1*   Marcello Orsi¹   Vincenza Fetoni²   Giancarlo Oliva<sup>1

1</sup>Radiological Department, Azienda Ospedaliera Fatebenefratelli e Oftalmico, Corso di Porta Nuova 23, 20121, Milan, Italy
²Neurological Department, Azienda Ospedaliera Fatebenefratelli e Oftalmico, Corso di Porta Nuova 23, 20121, Milan, Italy

*Corresponding author: Michaela Cellina, Radiological Department, Azienda Ospedaliera Fatebenefratelli e Oftalmico, Corso di Porta Nuova 23, 20121, Milan, Italy, Tel: 0039- 0263632424; E-mail: michaela.cellina@fbf.milano.it

Abstract
Schwannomas are encapsulated, benign, slowly growing tumors arising from Schwann cells of peripheral nerve sheath. Although they represent the commonest benign peripheral nerve sheath tumors, the occurrence on the lower limbs and especially from the superficial peroneal nerve is exceptionally rare. We present the clinical manifestations and imaging findings of a superficial nerve Schwannoma presenting as a painful mass in the external compartment of the calf, which was confirmed histologically and we correlate our experience with previously reported cases.

Figure 1: Ultrasonography scan of the external compartment of the left leg Presence of a well-defined, ovoid-shaped, homogeneously hypoechoic, lesion in the peroneus longus muscle.

Figure 2: Contrast-enhanced MRI of the left leg Axial images: T2 weighted image with fat suppression (A) and T1 weighted image after contrast medium injection (B). Coronal images: STIR (C), T1 weighted image before (D) and after (E) contrast medium injection. Ovoid lesion with well-defined smooth margins in the peroneus longus muscle, hyperintense in basal acquisitions, especially in STIR and T2 weighted images, with a marked, homogeneous enhancement after contrast injection. After contrast medium injection (E) the continuity with superficial peroneal nerve, known as “tail sign”, is well visible.


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Traumatic Brain Injury: Is Neurofeedback the Best Available Therapy?

Article Information

Aritcle Type: Editorial Commentary

Citation: Koberda JL (2015) Traumatic Brain Injury: Is Neurofeedback the Best Available Therapy? J neurol Neurobiol 1(3): doi http://dx.doi.org/10.16966/2379-7150.110

Copyright:© 2015 Koberda JL. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Publication history:
 

 Received date: 23 July 2015

 Accepted date: 25 July 2015

 Published date: 28 July 2015

Authors :
 J Lucas Koberda^1,2*
1Director of Tallahassee NeuroBalance Center, Tallahassee, FL 32309, USA
²CEO-Brain Enhancement Inc., USA

*Corresponding author: J. Lucas Koberda, Director of Tallahassee NeuroBalance Center, Tallahassee, FL 32309, USA, E-mail: JLKoberda@yahoo.com

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Association of Cdk5 and Soluble Oligomeric Species of β-amyloid Induced Tau Hyperphosphorylation

Article Information

Aritcle Type: Research Article

Citation: Li S, Tian S, Sun L, Liang Z, Cheng X, et al. (2015) Association of Cdk5 and Soluble Oligomeric Species of β-amyloid Induced Tau Hyperphosphorylation. J Neurol Neurobiol 1(3): doi http://dx.doi.org/10.16966/2379-7150.108

Copyright: © 2015 Li S, et al. This is an openaccess article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Publication history:
 

 Received date: 8 July 2015

 Accepted date: 20 July 2015

 Published date: 25 July 2015


Authors :
 Shanshan Li^1#   Sumin Tian^2#   Lingzhi Sun¹   Zhihao Liang¹    Xiaohui Cheng¹   Han Wang¹   Yuxin Ma¹   Jing Liu¹   Guoying Li^1*   Qing Mei Wang<sup>3

1</sup>Department of Anatomy and Histology, School of Basic Medicine, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China
²Department of Physiology, School of Basic Medicine, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China
³Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Boston, MA, USA^#These authors contributed equally to this work.

*Corresponding author: Dr. Guoying Li, Department of Anatomy and Histology, Basic Medical College, Guangdong Pharmaceutical University, Guangzhou, Guangdong, 510006, China, Tel: +86-020-39352232; Fax:+86-020-39352186; E-mail: gzlgying820@sina.com

Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative disease with deteriorating memory loss in the aged population. Currently, its exact pathogenesis remains elusive. Some studies have shown that soluble oligomeric Aβ (β-amyloid), inducing hyperphosphorylation of tau, may be the initial link to AD pathogenesis. However, it is poorly known how Aβ influences tau phosphorylation; Results, in this study, soluble oligomeric Aβ42 peptide was injected into the hippocampus of mice with saline as a control. Hematoxylin and eosin (HE) staining showed that Aβ42 was mainly deposited in the Cornu Ammonis area 1 (CA1). Within 7 to 21 days after the operation, the area of Aβ42 decreased gradually. Compared to the control, the expression of phosphorylated tau (p-tau) was significantly increased, suggesting that soluble Aβ oligomers activated phosphorylation of tau and increased total tau. Meanwhile, we found that elevated Cdk5, mainly in the CA1 area and subgranular zone (SGZ), correlates with increased phosphorylation of tau. Conclusions, thus, the results suggest that hyperphosphorylation of tau induced by soluble amyloid Aβ is associated with an increased level of Cdk5.

Keywords
Alzheimer’s disease; β-amyloid; tau; Cdk5

Figure 1: Histological changes in the hippocampus. (A) HE staining in normal hippocampus of BALB/c mice. (C) HE staining in NS-injected hippocampus. (E) HE staining in Aβ42-injected hippocampus. (B, D, F), respectively, represent the region of high magnification in (A, C, E). (F) HE staining showed neuronal loss at the injection site surrounding Aβ peptide. Scale bar=200 μm in (A, C, E) and 50 μm in (B, D, F).



Figure 2: Immunostaining of Aβ in the hippocampus. (A) NS-injected group. (B, D), respectively, represent the region of high magnification in (A, C). (B) Higher magnification of negative Aβ aggregation at the injection site from NS-injected hippocampus. (C) Aβ42-injected group. (D) Aβ aggregation in SGZ of DG from Aβ42-injected hippocampus. Scale bar=200 μm in (A, C) and 100 μm in (B, D).



Figure 3: Immunofluorescence for expression of hyperphosphorylated tau in hippocampus. (A) Tau staining in control group (BALB / c + NS). (B, C) represent the region of high magnification in (A). (B) Negative au expression located in CA1. (C) Negative tau expression located in DG. (D) Tau staining in Aβ42-injected group (BALB / c + Aβ42). (E, F), respectively, represent the region of high magnification in (D). (E) p-tau located in CA1. (F) p-tau located in DG. Scale bar=100 μm in (A, D) and 50 μm in (B, C, E, F).



Figure 4: Immunofluorescence for expression of Cdk5 in the hippocampus. (A) Cdk5 staining in control group (BALB / c + NS). (B, C) represent the region of high magnification in (A). (B) Negative Cdk5 expression located in CA1. (C) Negative Cdk5 expression located in DG. (D) Cdk5 staining in Aβ42-injected group (BALB / c + Aβ42). (E, F), respectively, represent the region of high magnification in (D). (E) Cdk5 located in CA1. (F) Cdk5 located in DG. Scale bar=100 μm in (A, D) and 50 μm in (B, C, E, F).



Figure 5: Protein levels of tau and Cdk5 in hippocampus 7 days after Aβ42 injection. (A) Detection of protein levels of tau and Cdk5 using western blot. (B) Histograms represent the relative density of tau. Asterisks indicate data significantly different from those of NS injection (*P <0.01, student two-tailed t test). n=10 mice per group; error bars, SEM. (C) Histograms represent the relative density of Cdk5. Asterisks indicate data significantly different from those of NS injection (*P <0.01, student two-tailed t test). n=10 mice per group; error bars, SEM.

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