Neurodegenerative Diseases Journal Impact Factor & Information

Publisher: Karger

Journal description

Neurodegenerative Diseases is a bimonthly, multidisciplinary journal for the publication of advances in the understanding of neurodegenerative diseases, including Alzheimer disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington disease and related neurological and psychiatric disorders. Neurodegenerative Diseases publishes results from basic and clinical scientific research programs designed to better understand the normal functions of genes and proteins involved in neurodegenerative diseases, to characterize their role in pathogenic disease mechanisms, to model their functions in animals and to explore their roles in the diagnosis, treatment and prevention of neurodegenerative diseases. It is our firm belief that successful strategies for novel treatments of neurodegenerative diseases will emerge from the intelligent integration of basic neurobiology with clinical sciences. Therefore, Neurodegenerative Diseases will accept high-quality papers from a broad spectrum of scientific research areas ranging from molecular and cell biology to neuroscience, pharmacology, genetics and the clinical sciences.

Current impact factor: 3.45

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 3.454
2012 Impact Factor 3.41
2011 Impact Factor 3.056
2010 Impact Factor 3.791
2009 Impact Factor 3.496
2008 Impact Factor 2.989

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.02
Cited half-life 3.90
Immediacy index 0.92
Eigenfactor 0.00
Article influence 0.86
Website Neurodegenerative Diseases website
Other titles Neuro-degenerative diseases
ISSN 1660-2862
OCLC 260107464
Material type Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Karger

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • On author's server or institutional server
    • Server must be non-commercial
    • Publisher's version/PDF cannot be used
    • Publisher copyright and source must be acknowledged
    • Must link to publisher version
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: β-Synuclein (β-Syn) is a member of the highly homologous synuclein protein family. The most prominent family member, α-synuclein (α-Syn), abnormally accumulates in so-called Lewy bodies, one of the major pathological hallmarks of α-synucleinopathies. Notably, parts of the peptide backbone, called the nonamyloid component, are also found in amyloid plaques. However, β-Syn seems to have beneficial effects by reducing α-Syn aggregation, and amyloid antiaggregatory activity has been described. The aim of the study was to analyze if wild-type β-Syn can counteract functional and pathological changes in a murine Alzheimer model over different time periods. At the onset of pathology, lentiviral particles expressing human β-Syn were injected into the hippocampus of transgenic mice overexpressing human amyloid precursor protein with Swedish and London mutations (APPSL). An empty vector served as the control. Behavioral analyses were performed 1, 3 and 6 months after injection followed by biochemical and histological examinations of brain samples. β-Syn expression was locally concentrated and rather modest, but nevertheless changed its effect on APP expression and plaque load in a time- and concentration-dependent manner. Interestingly, the phosphorylation of glycogen synthase kinase 3 beta was enhanced in APPSL mice expressing human β-Syn, but an inverse trend was observed in wild-type animals. The initially reported beneficial effects of β-Syn could be partially reproduced, but locally elevated levels of β-Syn might also cause neurodegeneration. To enlighten the controversial pathological mechanism of β-Syn, further examinations considering the relationship between concentration and exposure time of β-Syn are needed. © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 06/2015; DOI:10.1159/000430952
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    ABSTRACT: The sporadic form of the disease affects the majority of amyotrophic lateral sclerosis (ALS) patients. The role of glutamate (Glu) excitotoxicity in ALS has been extensively documented and remains one of the prominent hypotheses of ALS pathogenesis. In light of this evidence, the availability of a method to remove excess Glu from brain and spinal cord extracellular fluids without the need to deliver drugs across the blood-brain barrier and with minimal or no adverse effects may provide a major therapeutic asset, which is the primary aim of this study. The therapeutic efficacy of the combined treatment with recombinant Glu-oxaloacetate-transaminase (rGOT) and its co-factor oxaloacetic acid (OxAc) has been tested in an animal model of sporadic ALS. We found that OxAc/rGOT treatment provides significant neuroprotection to spinal cord motor neurons. It also slows down the development of motor weakness and prolongs survival. In this study we bring evidence that the administration of Glu scavengers to rats with sporadic ALS inhibited the massive death of spinal cord motor neurons, slowed the onset of motor weakness and prolonged survival. This treatment may be of high clinical significance for the future treatment of chronic neurodegenerative diseases. © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 06/2015; DOI:10.1159/000382034
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    ABSTRACT: Prion diseases are known as neurodegenerative diseases of the central nervous system with a long incubation period. Alzheimer's disease (AD) and prion diseases share the hallmark of severe neuronal loss, although their pathogenic mechanisms are similarly incomplete. It appears that these two neurodegenerative diseases share a complex deterioration of function involved in the onset of neuronal loss. To investigate presymptomatic biochemical changes indicative of the initial stage of prion diseases and decipher the pathophysiological mechanisms of these two neurodegenerative diseases, we performed a differential proteomic analysis on brain tissues of 263K-infected hamsters during the presymptomatic period and transgenic APPSWE, PSEN1dE9 mice (a mouse model of AD). We identified 7 differentially expressed proteins including the β-soluble N-ethylmaleimide-sensitive factor attachment protein (β-SNAP) by 2-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. The β-SNAP expression patterns in the brains of cases and controls were further quantified by Western blotting. β-SNAP showed an early decrease followed by a progressive depletion. The expression of β-SNAP was also significantly downregulated in the mouse model of AD. β-SNAP is brain-specific and known to bind to the SNAP receptors and is therefore involved in the control of neurotransmitter release as well as in constitutive vesicular transport. Our results suggest that presynaptic failure and abnormalities in neurotransmission may be early events in the development of neuronal dysfunction. © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 05/2015; DOI:10.1159/000371553
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    ABSTRACT: Voice abnormalities are among the symptoms occurring in patients with amyotrophic lateral sclerosis (ALS). They are divergent and range from hoarseness, through the excessive adduction of false folds, up to the weakness of the vocal folds. The aim of the study was to analyze the phonatory function of the larynx in ALS patients. Seventeen patients with ALS were evaluated with subjective perceptual voice assessment (including the GRBAS scale), videolaryngostroboscopy including voice range and maximum phonation time (MPT), and objective acoustic voice analysis with IRIS software (including evaluation of jitter, shimmer, mean fundamental frequency, and noise-to-harmonics ratio (NHR)). Examinations were performed three times at 6-month intervals. Hoarseness, roughness, and breathiness of voice were all found more frequently in the majority of these patients. Voice range, amplitude of vibration, mucosal wave, and glottal closure showed significant abnormalities with repeated examinations. MPT was shortened especially among women with ALS. Acoustic analysis of voice among men showed increased jitter value in the first examination only, while jitter, shimmer, and NHR in women with ALS were increased in all examinations. Analysis of voice qualities among patients with ALS allows for the detection of various abnormalities associated with the natural progression of the disease. © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 05/2015; DOI:10.1159/000381956
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    ABSTRACT: Trends in disease incidence and mortality can provide clues to disease etiology. Previously, we described a town in New Hampshire (N.H.), USA, with 25 times the expected incidence rate of amyotrophic lateral sclerosis (ALS). This study aimed to describe the incidence and mortality of ALS across the state to assess rates relative to other states and industrialized nations. A retrospective review of records from regional ALS centers, clinics and ALS organizations was conducted to obtain demographics and diagnostic details for patients diagnosed with ALS or primary lateral sclerosis in N.H. from January 2004 to December 2007. Data on mortality from review of death certificates were obtained for a similar time frame. We identified 113 N.H. residents diagnosed with ALS in 2004-2007, yielding an age-standardized incidence rate ranging from 1.3 to 2.2 per 100,000 of the population per year. During the same period, the standardized mortality rate per 100,000 varied from 2.6 to 3.5. ALS was more common among men (ratio 1.6:1), who were more likely than women to have an earlier age at onset (59 ± 14.2 vs. 65 ± 11.8 years, p = 0.01). While localized areas in N.H. with high ALS incidence rates have been reported previously, the overall incidence and mortality rates of ALS in N.H. are similar to those in other industrialized nations. © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 04/2015; DOI:10.1159/000374117
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    ABSTRACT: Frontotemporal lobar degeneration (FTLD) is the second most common early-onset dementia. Over the last few decades, a growing number of evidence suggests mitochondrial involvement in neurodegeneration, namely modifications of mitochondrial DNA (mtDNA) contributing to energy impairment. To sequence the 7 mitochondrially encoded complex I (MT-ND) genes in 70 FTLD patients and investigate mitochondrial respiratory chain (MRC) complex I activity. A sample of 70 patients was studied (39 females and 31 males; age range: 38-82 years, mean ± SD: 63 ± 11 years) with a probable diagnosis of FTLD. Total DNA was extracted from peripheral blood, and sequencing analysis of 7 MT-NDn (1, 2, 3, 4L, 4, 5, 6) genes was performed. Variants identified were submitted to in silico study. Spectrophotometric evaluation of MRC activity in lymphocytes was performed, and results were compared with age-matched controls. A total of 358 (161 different) alterations were found in 92.9% of patients. According to in silico analysis of nonsynonymous variants, only 5 variations are possibly or probably damaging. Complex I activity is significantly decreased in patients. To our knowledge, this is the first report of the complete sequence of the MT-ND genes in FTLD patients and correlation with MRC activity. The high number of mtDNA variations identified and a significant decrease in complex I activity suggest a possible involvement of mtDNA alterations in FTLD. Although the majority of these alterations are not primarily pathogenic, an interaction with other mutations may occur, leading to the disease, worsening its expression or influencing age of onset. © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 04/2015; DOI:10.1159/000380766
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    ABSTRACT: Almost all patients with amyotrophic lateral sclerosis (ALS) develop bulbar symptoms; therefore, it is important to have valid animal models that accurately reflect these features. While the SOD1-G93A rat is extensively used as an ALS model, bulbar symptoms in this model are not well characterized. In the present study, we aimed to better characterize bulbar dysfunction in terms of histology to determine whether the SOD1-G93A rat is a useful model for bulbar-onset ALS. Sixty-day-old SOD1-G93A rats on a Sprague-Dawley background and age-matched wild-type controls were assessed weekly for global motor function, facial nerve function, and vagal nerve function. The study endpoint was determined when an SOD1-G93A rat could not right itself within 30 s of being placed on its side. At that point, neuronal counts were assessed in different brainstem cranial nerve nuclei. In addition, the masseter muscle, posterior belly of the digastric muscle, and tongue muscle were evaluated for intact neuromuscular junctions. Our data demonstrate decreases in the number of motor neurons in the trigeminal, facial, and hypoglossal nuclei, as well as compromised neuromuscular junction integrity in the muscles they innervate. These findings suggest that, from a histological standpoint, the SOD1-G93A rat is a valid model of ALS bulbar symptoms. © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 03/2015; 15(2). DOI:10.1159/000377725
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    ABSTRACT: Background: Cerebral deposition of amyloid-β (Aβ) is the beginning of amyloid cascade leading to Alzheimer’s disease (AD). Approximately 95% of AD accounts from SAD during aging. Aβ42-peptides and plaques, generate from APP through sequential actions of β- and γ-secretases, whereas cleavage by α-and γ- secretases prevent toxic Aβ formation. Objectives: Although localization of APP and secretases (ADAM10, BACE1 and PS1) are key proteins for regulating amyloidogenic pathway, it is unclear, whether aging promotes altered levels of expression and its subcellular distribution. Present study thus aimed to elucidate the cellular effect of resveratrol, on localization of AD related proteins during aging. Methods: Using double immunofluorescence technique, the expression and subcellular localization (ER, Golgi and Mitochondria) of ADAM10, BACE1, PS1, APP and Aβ were examined in young and aged wistar rat brain regions with and without resveratrol. Results: Absolute weight of the aged brain was increased (~26.5%), whereas the relative weight was decreased (~52%). We further identified decreased levels of ADAM10 (~50%) and elevated levels of BACE1 in aged rats. Although cell surface PS1 level was reduced, total expression remains unchanged, providing clue for enhanced Amyloidogenic pathway facilitating extracellular Aβ accumulation during aging. Resveratrol treatment significantly reduced BACE1 elevation and increased the expression of ADAM10 levels, further normalized cell surface PS1 expression. Conclusion: From our results we conclude that aging promotes altered expression and subcellular distribution of secretases that may favor SAD, while resveratrol treatment exhibited positive influence on non-amyloidogenic pathway.
    Neurodegenerative Diseases 03/2015; 15(Suppl. 1):676.
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    ABSTRACT: Background/Objective: Present study aims at investigating, age-specific degeneration of neuronal-circuits in hippocampal formation (neural-layout of Subiculum-hippocampus proper-DG-EC) and resultant cognitive impairment during aging that forms major risk factor for SAD like pathology. Further, neuroprotective effect of resveratrol on age-specific pathological changes in the hippocampal neuronal-circuits were evaluated. Methods:Radial-Arm-Maze (RAM) was performed to evaluate hippocampal-dependent spatial and learning memory. Nissl Staining of FC, subiculum, Hippocampal-proper (CA1→CA2→CA3→CA4), DG, amygdala, cerebellum, thalamus, hypothalamus, layers of temporal and parietal lobe of the Neocortex were examined for pathological changes in young and aged wistar rats, with and without resveratrol. Results and Conclusion: Extensive loss of glutamatergic and inhibitory GABAergic neurons were observed during aging. Moreover, Trisynaptic (EC layerII→DG→CA3→CA1) circuit forming new memory and monosynaptic circuit (EC→CA1) that strengthens old memories was disturbed. Loss of Granular neuron in DG and polymorphic cells of CA4 lead to decreased mossy fibers disturbing neural-transmission (CA4→CA3) in perforant pathway. Further, intensity of Nissl granules (SLM-SR-SO) of CA3 pyramidal neurons was decreased, disturbing the communication in Schaffer collaterals (CA3-CA1) during aging. We also noticed disarranged neuronal cell layer in Subiculum (PrS-PaS), interfering output from hippocampus to PFC, EC, Hypothalamus, and amygdala that interrupt thinking process. We conclude from our observations that neuronal-circuits of hippocampus (DG-CA4-CA1-Sub) were damaged leading to memory impairment that was supported by RAM analysis. Interestingly, resveratrol induced neurogenesis in DG and culminated the pathological events proving as good as therapeutic drugs against age associated neurodegeneration and memory loss.
    Neurodegenerative Diseases 03/2015; 15(Suppl. 1):512.
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    ABSTRACT: Background: Parkinson's disease mainly affects the elderly population causing a progressive functional disability with motor, psychic, and cognitive deterioration. Objective: This study was carried out to evaluate disability caused by Parkinson's disease by analyzing the median time to reach Hoehn and Yahr stage III and to investigate predictor variables based on a 20-year longitudinal follow-up study. Methods: We examined 273 patients with Parkinson's disease recruited between 1978 and 1998. We performed a survival analysis using the Kaplan-Meier method to determine the time to disability and we used a Cox regression model to adjust prognosis factors. Results: The median time to reach Hoehn and Yahr stage III was 7.73 years (95% CI: 5.95-8.05). Independent predictors of disability were: age at onset, the hazard ratio (HR) = 1.10, 95% CI: 1.08-1.12; UPDRS II (activities of daily living) HR = 1.08, 95% CI: 1.03-1.14; and akinesia and rigidity at onset HR = 1.55, 95% CI: 1.07-2.24. Conclusions: Patients with Parkinson's disease evolve gradually toward disability, and prognostic factors of this evolution were identified. © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 01/2015; DOI:10.1159/000369531
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    ABSTRACT: The reason for regeneration in the adult spinal cord during motor neuron degeneration in amyotrophic lateral sclerosis (ALS) remains largely unknown. To this end, we studied the alteration of vimentin (a neural precursor cells marker in CNS)-containing cells (VCCs) in spinal cord during different stages of ALS used C57BL/6J G93A SOD1 transgenic mice mimicking ALS. Results showed that VCCs were mostly distributed in the ependymal zone (EZ) surrounding the central canal of spinal cord in SOD1 wild type mice; a few of VCCs were sparsely distributed in other regions. However, the number of VCCs significantly increased in the spinal cord during the onset and progression stages of ALS. They were extensively distributed in the EZ, the anterior, the lateral and the posterior horn of grey matter, particularly in the posterior horn region at the progression stage. A majority of VCCs in the anterior, the lateral and the posterior horn of grey matter (outside of EZ) generated astrocytes, but no neurons, oligodendrocytes and microgliocytes. Our results suggested that there was a potential astrocyte regenerative response to motor neuron degeneration in motor neurons-degenerated regions in the adult spinal cord during the onset and progression stages of ALS-like disease. The regenerative responses in the adult spinal cord of ALS-like mice may be a potential pathway in attempting to repair the degenerated motor neurons and restore the dysfunctional neural circuitry. © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 01/2015; 15(1). DOI:10.1159/000369466
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    ABSTRACT: Objective: Analyze indications for ordering DAT-SPECT scans and the clinical impact of scan results on patients evaluated in a movement disorders practice. Background: DAT-SPECT is FDA approved to evaluate cases of suspected presynaptic dopaminergic deficiency. Little data is available on clinical use and impact of these scans among movement disorders neurologists. Methods: DAT-SPECT scans ordered at the Northwestern University Parkinson's disease (PD) and movement disorders center from 2011-2013 were reviewed. Clinic notes were reviewed for information regarding the indication for ordering each scan, and to assess for any changes in clinical impression or management choices that followed the scan. Results: 83 scans were ordered by four specialists. Scans were commonly ordered to differentiate PD from Essential Tremor (21.7%, n = 18) or from drug-induced parkinsonism (21.7%, n = 18). In 59% (n = 49) of cases, a change in clinical diagnosis or medication regimen occurred within one visit after the scan. The strongest impact was seen for the indication of ET vs. PD in which 72.2% (n = 13) had a change in diagnosis, management, or both. Conclusions: Diagnostic uncertainty in cases of parkinsonism exists even in a tertiary referral center. DAT-SPECT has significant impact on clinical diagnosis and management even in the hands of movement disorders specialists. © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 01/2015; 15(2). DOI:10.1159/000370116
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    ABSTRACT: Neurodegenerative diseases are the result of progressive loss of neurons and axons in the central nervous system (CNS), which can lead to cognition and motor dysfunction. It is well known that CNS inflammation and immune activation play a major role in the pathophysiology of neurodegenerative diseases. Although the blood-brain barrier (BBB) is able to protect the CNS from immune activation, it becomes more permeable during inflammation, which renders the brain vulnerable to infections. A better understanding of the interaction between inflammatory mediators, such as cytokines, and the activated immune response, including astrocytes and microglia, is critical for the development of new therapeutic strategies for neurodegenerative diseases. This review first describes the role of innate immune activation in neurodegenerative diseases and illustrates the factors that contribute to the communication between the CNS and the immune system. A closer look is given at the role of the BBB in inflammation and immunity, as well as at the animal models used to study inflammation in neurodegenerative diseases. Finally, this review outlines the key pathways and biological mechanisms involved in CNS diseases, with a particular focus on multiple sclerosis (MS), Parkinson's disease (PD), and Alzheimer's disease (AD). © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 01/2015; 15(2). DOI:10.1159/000369933
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    ABSTRACT: Background: Senile plaques in Alzheimer's disease (AD) are composed of amyloid-β (Aβ), especially N-truncated forms including Aβ4-42. These are thought to be neurotoxic. However, individuals may live for decades with biomarker evidence of cerebral β-amyloidosis (positive amyloid PET imaging and/or low cerebrospinal fluid levels of the 42 amino acid form of Aβ) without cognitive impairment. This condition may be termed pathological ageing (PA). Objective: To investigate whether there is a difference in the cerebral Aβ fragment pattern in brain specimens from non-demented (PA) and demented (AD) individuals expressing the full neuropathological triad of AD (senile plaques, neurofibrillary tangles and neurodegeneration). Methods: We extracted Aβ using formic acid and hybrid (6E10 and 4G8) immunoprecipitation from fresh-frozen temporal cortex tissue of 6 elderly individuals (mean age ± SD: 89 ± 3.5 years) with PA and 10 patients with AD (mean age ± SD: 72 ± 8.5 years). The full spectrum of Aβ peptides was determined by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Results: AD patients had generally more N-terminally truncated and pyroglutamate-modified Aβ than PA patients, whereas PA patients had on average more Aβ1-40 than AD patients. Conclusion: Senile plaques in AD may have an Aβ fragment composition distinct from PA with more N-terminally and pyroglutamate-modified Aβ peptides that may be linked to neurotoxicity. © 2015 S. Karger AG, Basel.
    Neurodegenerative Diseases 01/2015; 15(1). DOI:10.1159/000369465
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    ABSTRACT: Background: Alzheimer's disease (AD) is characterized by the dynamic accumulation of extracellular amyloid deposits from the interplay between amyloid-β (Aβ) plaques, reactive astrocytes and activated microglia. Several immunotherapies against Aβ have been shown to reduce amyloid neuropathology. However, the role of the associated glia in the recovery process requires clarification. Previously, we described the safety and effectiveness in aged domestic canine with cognitive dysfunction syndrome of a new active vaccine candidate for the treatment of AD in humans. Objective: The aim of this article is to gain a better understanding of how immunotherapy modifies the amyloid burden and its effects on astroglial and microglial reactivity in immunized dogs. Methods: In order to achieve this, we compared and quantified amyloid plaques and astroglial and microglial reactions in the frontal cortex of unimmunized and immunized aged domestic dogs. Results: We found amyloid plaques from immunized dogs to be smaller and more compact than those from unimmunized dogs. In these new plaques, the associated astrocytes were closer and less immunoreactive to the β subunit of S100 protein (S100B). We also found no modification in the microglial reaction associated with immunization. Conclusion: The anti-Aβ immunotherapy developed in our laboratory modifies the equilibrium between soluble and insoluble Aβ in aged dogs in close correlation with S100B-negative astrocytosis and microglial reaction. © 2014 S. Karger AG, Basel.
    Neurodegenerative Diseases 12/2014; 15(1). DOI:10.1159/000368672