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PubMed1998

The role of NMDA receptors in the slow neuronal degeneration of Parkinson's disease.

Parkinson's disease is a disorder, in which neurons of various neuronal systems degenerate. Furthermore, in such degenerating neurons, the cytoskeleton seems to be affected. In this respect, Parkinson's disease resembles Alzheimer's disease. Since it has been shown, that elevated levels of intracellular calcium can disrupt the cytoskeleton and that the stimulation of glutamate (NMDA) receptors can cause high intracellular concentrations of calcium, it has been suggested, that the stimulation of glutamate receptors plays a role in the slow degeneration in Alzheimer's and Parkinson's disease. In case of the degeneration of the dopaminergic nigrostriatal system in Parkinson's disease, neurons that contain calcium binding protein appear to be less vulnerable than the neurons that lack it, suggesting that calcium binding protein might protect these neurons from degeneration by preventing that cytosolic calcium concentrations increase excessively. And, since there is in the nigrostriatal system a glutamatergic afferent pathway (the prefrontonigral projection) and since dopaminergic nigrostriatal neurons contain postsynaptic NMDA receptors, glutamatergic excitation may play a role in the degeneration of the nigrostriatal system in Parkinson's disease. If so, it may be possible to protect the neurodegeneration of these dopaminergic neurons by NMDA receptor antagonists.

Alzheimer Disease↗

PubMed1996

Effect of Nd:YAG laser on experimental disc degeneration. Part I. Biochemical and radiographical analysis.

Intervertebral disc herniation is an important health problem from both the social and economic aspect. It is often accompanied by a decrease in the content of water and proteoglycan (PG). The present study was undertaken to elucidate the effect of neodymium-yttrium-aluminum-garnet (Nd:YAG) laser on degenerated disc tissue. In this study a ventral disc herniation model in guinea pigs was performed to study the effects of ND:YAG laser on degenerated disc with low water and PG content. Effect of ND:YAG laser on degenerated cervical disc tissue is examined from the aspects of biochemistry and radiology. In the acute period water, PG, and collagen content decreased due to the ablative effect of ND:YAG laser on disc tissue. When changes in the degenerated disc in the post-laser chronic period were compared with degenerated disc findings, statistically significant changes could not be be found. From the results of this study, there is no question that the Nd:YAG laser offers many potential benefits, it remains to be proven whether or not this is of real benefit in the treatment of patients with degenerated disc disease.

Analysis of Variance↗

PubMed2005

Internal derangements of the knee associated with patellofemoral joint degeneration.

The objective of the present study was to evaluate whether internal derangements of the knee joint are associated with patellofemoral joint (PFJ) degeneration. Data were collected prospectively from 1,000 consecutive knee arthroscopies. Chondral lesions were observed in 854 patients, and these patients were included in this study. Patients' details (age, sex, duration of symptoms, injuries, and possible mechanism of injury), operative details (types and number of portals, equipment used), intra-articular findings (articular, meniscal and synovial lesions, and stability characteristics) and procedures performed were recorded. Articular lesions were noted on anatomic articular maps of the different functional zones, using a system which presaged the current ICRS system. Using this zoning system, it was easy for the authors to separate the patients with isolated patellofemoral degeneration and arthritis and to do the statistical analysis. Increased incidence of isolated patellofemoral degeneration was noted in patients with synovial shelves, in comparison with patients without shelves (24.7% vs. 15.5%, respectively; P=0.001). Patients with severe patellofemoral maltracking were found to have increased incidence of isolated patellofemoral degeneration in comparison with patients without patella maltracking (64.7% vs. 18% respectively; P<0.001). In conclusion, patellofemoral maltracking and synovial shelves of the knee are highly associated with PFJ degeneration. On the contrary, meniscal tears and ligamentous injuries are associated mainly with degeneration of other compartments of the knee joint and not the PFJ.

Adult↗

PubMed2003

The role of muscles in joint adaptation and degeneration.

BACKGROUND: Muscles are the primary contributors to joint loading. Loading is typically associated with the onset and progression of joint degeneration, and in turn, joint degeneration is known to affect negatively the control of muscle forces and co-ordination patterns. Nevertheless, the role of muscles in joint adaptation and degeneration has been largely ignored. Here, we review some of our research on the in vivo changes in muscular forces and joint loading in animal models of osteoarthritis and in patients with joint injury and disease. We attempt to emphasize the close dependence of muscle forces, joint loading and degeneration and, vice versa, try to point out how joint degeneration affects muscle forces and joint loading. MATERIAL AND METHODS: We measured the forces and electromyographic signals in normal and anterior cruciate ligament transected feline knees and measured (1) a consistent decrease in the knee extensor and ankle extensor muscle forces for weeks following intervention; (2) a corresponding decrease in the static and dynamic external ground reaction forces; and (3) a change in the electromyographic signals (in terms of the firing patterns of individual muscles and of the co-ordination of extensors and flexors during locomotion). We introduced results on the biosynthetic response of articular cartilage to controlled, in vivo, loading and discuss preliminary results from an experimental animal model of muscle weakness. In contrast to much of the published literature, loading, in our case, is introduced by controlled nerve stimulation and the corresponding muscular forces that load the joint in its in vivo configuration. RESULTS: We found that short-term loading (30-60 min) in the cat knee produces distinct up-regulation of mRNA of specific metalloproteinases (MMPs) and some of the MMP inhibitors. In our newly developed muscle-weakness model, we confirmed that controlled Botox injections in the rabbit knee extensor muscles cause a 60-80% decrease in muscle force, and that these changes in muscle force are associated with changes in the external ground reaction forces, and most importantly, that muscle weakness seems to be associated with degeneration of the knee in the absence of joint instability or any other intervention. CONCLUSION: From the results of our research, we conclude that muscle health and muscle rehabilitation are key components for the successful prevention of, and recovery from, joint injury and disease.

Adaptation, Physiological↗

PubMed2001

Correlation between sagittal plane changes and adjacent segment degeneration following lumbar spine fusion.

Adjacent segment degeneration following lumbar spine fusion remains a widely acknowledged problem, but there is insufficient knowledge regarding the factors that contribute to its occurrence. The aim of this study is to analyse the relationship between abnormal sagittal plane configuration of the lumbar spine and the development of adjacent segment degeneration. Eighty-three consecutive patients who underwent lumbar fusion for degenerative disc disease were reviewed retrospectively. Patients with spondylolytic spondylolisthesis and degenerative scoliosis were not included in this study. Mean follow-up period was 5 years. Results were analysed to determine the association between abnormal sagittal configuration and post operative adjacent segment degeneration. Thirty-one out of 83 patients (36.1%) showed radiographic evidence of adjacent segment degeneration. Patients with normal C7 plumb line and normal sacral inclination in the immediate post operative radiographs had the lowest incidence of adjacent level change compared with patients who had abnormality in one or both of these parameters. The difference was statistically significant (P<0.02). There was no statistically significant difference in the incidence of adjacent level degeneration between male and female patients; between posterior fusion alone and combined posterolateral and posterior interbody fusions; and between fusions extending down to the sacrum and fusions stopping short of the sacrum. It was concluded was that normality of sacral inclination is an important parameter for minimizing the incidence of adjacent level degeneration. Retrolisthesis was the most common type of adjacent segment change. Patients with post operative sagittal plane abnormalities should preferably be followed-up for at least 5 years to detect adjacent level changes.

Female↗

PubMed1982

Reduced deposition of collagen in the degenerated articular cartilage of dogs with degenerative joint disease.

Collagen metabolism in the focal degenerated cartilage from immature dogs with degenerative joint disease was compared with that in the adjacent 'normal' cartilage of the same joint surface. The deposition of collagen into the cartilage in vitro as measured by accumulation of hydroxy[14C]proline was decreased in the early and in advanced stages of cartilage degeneration. The deposition of collagen into cartilage in vivo as measured by the accumulation of hydroxy[3H]proline (intravenously injected [3H]proline) also was reduced in the degenerated cartilages of a dog with degenerative joint disease. Gel electrophoretic analysis revealed that degenerated cartilage contained less alpha 1 II collagen chains, but increased amounts of larger proteins. Degenerated cartilage contained more water, increased amounts of unidentified, non-collagenous protein, increased collagenolytic enzyme activity and fewer chondrocytes. Decreased deposition of collagen would result in collagen depletion in the foci of degenerated cartilage in joints of dogs with degenerative joint disease.

Animals↗

PubMed1989

Aluminum-induced neurofibrillary degeneration affects a subset of neurons in rabbit cerebral cortex, basal forebrain and upper brainstem.

Neurofibrillary tangles in Alzheimer's disease show a predilection for cortical pyramidal and subcortical projection neurons. The antigenic composition, neuronal specificity and distribution of aluminum-induced neurofibrillary degeneration were examined in regions of rabbit brain analogous to those that develop neurofibrillary tangles in Alzheimer's disease. Neurofibrillary degeneration was induced by intraventricular instillation of aluminum chloride. In aluminum-treated rabbits, intensely immunoreactive filamentous aggregates were seen in affected neuronal perikarya after staining with an antiphosphorylated neurofilament antibody (SMI 31), while in controls immunoreactivity was confined to axon-like elements. Monoclonal antibodies against Microtubule-associated protein 2 and tau, which stain human neurofibrillary tangles, did not stain aluminum-induced neurofibrillary degeneration. Pyramidal neurons exhibiting neurofibrillary degeneration formed a discrete linear pattern in layers III and V of cortex. Cortical somatostatin and nicotinamide adenine dinucleotide phosphate diaphorase-reactive neurons identified in double-stained sections were unaffected. Large perikarya in the vicinity of the globus pallidus, some of which contained acetylcholinesterase, were frequently SMI 31-immunoreactive. Among the cell groups affected in the upper brainstem were the nucleus raphe dorsalis and locus coeruleus. These findings show that aluminum-induced neurofibrillary degeneration differs antigenically from neurofibrillary tangles in Alzheimer's disease. Nevertheless, many neuronal subsets that are particularly susceptible to Alzheimer's disease, including cortical pyramidal neurons, basal forebrain cholinergic neurons and upper brainstem catecholaminergic neurons, are also affected by aluminum-induced neurofibrillary degeneration.

Aluminum↗

PubMed2004

Mucoid degeneration of the anterior cruciate ligament.

PURPOSE: Mucoid degeneration of the anterior cruciate ligament (ACL) is not a well-known entity. Only 1 case of mucoid degeneration of the ACL has been reported in the English-language literature. This article describes 5 cases of mucoid degeneration of the ACL with clinical features, magnetic resonance imaging (MRI) findings, and a method of arthroscopic management of these cases. TYPE OF STUDY: Case series. METHODS: Over a period of 21 months from 1999 to 2001, 5 patients were diagnosed to be suffering from mucoid degeneration of the ACL using MRI, histopathologic, and arthroscopic criteria. All patients presented with progressive knee pain and restriction of flexion without history of a significant trauma or instability preceding the symptoms. MRI showed an increased signal in the substance of the ACL both in the T1- and T2-weighted images, with a mass-like configuration that was reported as a partial or complete tear of the ACL by most radiologists. At arthroscopy, the ACL was homogenous, bulbous, hypertrophied, and taut, occupying the entire intercondylar notch. The ligamentum mucosum was absent in all patients. A debulking of the ACL was performed by a judicious excision of the degenerate mucoid tissue, taking care to leave behind as much of the intact ACL as possible. Releasing it and performing a notchplasty treated impingement of the ACL to the roof and lateral wall. The ACL was not fully excised in any of the patients. RESULTS: All patients were pain free and had recovered full flexion except one who experienced painful flexion beyond 120 degrees. None of the patients showed symptoms of instability. Postoperative MRI performed after at least 12 months in 2 patients showed some intact ACL fibers in a now-thinned ACL mass. CONCLUSIONS: Mucoid degeneration of the ACL is a clinical condition afflicting active middle-aged people without a single significant traumatic episode with a specific MRI picture. They respond well to a judicious arthroscopic release of the ACL with notchplasty. LEVEL OF EVIDENCE: Level IV.

Adult↗

PubMed2005

Vertebral fractures and separations of endplates after traumatic loading of adolescent porcine spines with experimentally-induced disc degeneration.

BACKGROUND: Abnormalities of the intervertebral discs have been found in a high frequency among young elite athletes. Several studies have also reported that the adolescent spine, especially the vertebral growth zones, is vulnerable to trauma. However, there is incomplete knowledge regarding the injury mechanism of the growing spine. In this study, the injury patterns of the adolescent porcine spine with disc degeneration were examined. METHODS: Twenty-four male pigs were used. A degenerative disc was created by drilling a hole through the cranial endplate of a lumbar vertebra into the disc. Two months later the animals were sacrificed and the degenerative functional spinal units (segments) were harvested. The segments were divided into three groups and exposed to axial compression, flexion compression or extension compression to failure. The load and angle at failure were measured for each group. The segments were examined with magnetic resonance imaging and plain radiography before and after the loading and finally examined macroscopically and histologically. FINDINGS: The degenerated segments required considerably more compressive load to failure than non-degenerated segments. Creating a flexion injury required significantly more load than an extension injury. Fractures and/or separations of the endplates from the vertebral bodies were seen at the margins of the endplates and in the growth zone. Only severe separations and fractures could be seen on plain radiography and magnetic resonance imaging. INTERPRETATION: The weakest part of the adolescent porcine lumbar spine with experimentally-induced degeneration, when loaded in axial compression, flexion compression or extension compression, was the growth zone, and, to a lesser extent, the endplate. Degenerated discs seem to withstand higher mechanical loads than non-degenerated discs, probably due to altered stress distribution.

Aging↗

PubMed2004

Simulated influence of osteoporosis and disc degeneration on the load transfer in a lumbar functional spinal unit.

As life expectancy increases, age-related disorders and the search for related medical care will expand. Osteoporosis is the most frequent skeletal disease in this context with the highest fracture risk existing for vertebrae. The aging process is accompanied by systemic changes, with the earliest degeneration occurring in the intervertebral discs. The influence of various degrees of disc degeneration on the load transfer was examined using the finite element method. The effect of different possible alterations of the bone quality due to osteoporosis was simulated by adjusting the corresponding material properties and their distribution and several loadings were applied. An alteration of the load transfer, characterised by changed compression stiffness and strain distributions as well as magnitudes, due to osteoporotic bone and degenerated discs was found. When osteoporosis was simulated, the stiffness was substantially decreased, larger areas of the cancellous bone were subjected to higher strains and strain maxima were increased. Increasing ratios of transverse isotropy in the osteoporotic bone yielded smaller effects than reduced bone properties. Including a degenerated disc mainly altered the strain distribution. Combining osteoporosis and degenerated discs reduced the areas of cancellous bone subjected to substantial strain. Based on these results, it can be concluded that the definition of a healthy disc in osteoporotic spines might be considered as a worst-case scenario. One attempt to evaluate the progress of osteoporosis can be made by introducing increasing degrees of anisotropy. If several parameters in a model are changed to simulate degeneration, it should be pointed out how each individual definition influences the overall result.

Bone Density↗

PubMed2005

Analysis of the influence of disc degeneration on the mechanical behaviour of a lumbar motion segment using the finite element method.

Compared to a healthy intervertebral disc, the geometry and the material properties of the involved tissues are altered in a degenerated disc. It is not completely understood how this affects the mechanical behaviour of a motion segment. In order to study the influence of disc degeneration on motion segment mechanics a three-dimensional, nonlinear finite element model of the L3/L4 functional unit was used. Different grades of disc degeneration were simulated by varying disc height and bulk modulus of the nucleus pulposus. The model was loaded with pure moments of 10Nm in the three main anatomic planes. The finite element model predicted the same trends for intersegmental rotation and intradiscal pressure as described in the literature for in vitro studies. A comparison between calculated intersegmental rotation and experimental data showed a mean difference of 1.9 degrees while the mean standard deviation was 2.5 degrees . A mildly degenerated disc increases intersegmental rotation for all loading cases. With further increasing disc degeneration intersegmental rotation is decreased. For axial rotation the decrease takes place in the final stage. Intradiscal pressure is lower while facet joint force and maximum von Mises stress in the annulus are higher in a degenerated compared to a healthy disc.

Biomechanical Phenomena↗

PubMed2005

Cartilage degeneration in post-collapse cases of osteonecrosis of the human femoral head: altered mechanical properties in tension, compression, and shear.

Osteonecrosis, or avascular necrosis, is a painful and debilitating condition characterized by progressive joint degeneration subsequent to collapse of necrotic regions of trabecular bone. A clear understanding of the mechanism of cartilage degeneration in osteonecrosis is critical to the development of treatment strategies aimed at sparing the femoral head. An analysis of 13 post-collapse osteonecrotic (ON) human femoral heads was performed relative to 24 non-ON controls to determine quantitatively the biomechanical and histological properties of post-collapse osteonecrotic cartilage. Cartilage mechanical properties were measured in tension, compression, and shear at different sites on the femoral head and correlated to histologic measures of cartilage degeneration using a semi-quantitative grading scale. Decreasing cartilage tensile strength correlated with histologic evidence of degeneration in the ON group; however, less correlation was noted with shear and compressive properties. After statistical correction for the more severe histologic degeneration in the ON group, the non-ON samples were found to exhibit significantly smaller loss angles during shear testing, while samples from the ON group were found to have greater tensile strength. Similarly, the ON group was found to exhibit significantly greater proteoglycan loss while the non-ON group showed significantly increased surface fibrillation. This study provides evidence that the changes occurring in post-collapse cases of osteonecrosis may involve mechanisms other than those typically attributed to osteoarthritic degeneration. One potential explanation is that decreased loading of cartilage overlying collapsed ON lesions leads to proteoglycan loss similar to that occurring with cartilage disuse. Unlike degenerative changes, some articular cartilage changes caused by disuse may be reversible. The presence of reversible changes would likely increase the chances of success of head sparing treatment strategies that rely on the viability and mechanical integrity of the articular cartilage.

Adult↗

PubMedDate not supplied

Quantitative analysis of gene expression in a rabbit model of intervertebral disc degeneration by real-time polymerase chain reaction.

BACKGROUND CONTEXT: Serial analysis of gene expression during the course of intervertebral disc degeneration (IDD) could elucidate valuable insight into pathophysiology and provide a basis for identification of potential targets for the development of novel cellular- and gene-based therapies. However, very few previous studies described the changes in gene expression through the process of IDD using a suitable animal model. PURPOSE: To use a recently developed rabbit annular stab model and the technique of real-time reverse transcriptase-polymerase chain reaction (RT-PCR) to quantify the change in expression of key rabbit-specific mRNA sequences encoding for selected extracellular matrix (ECM) products, catabolic, anabolic, and anti-catabolic factors in normal and stabbed discs. STUDY DESIGN: Gene expression analyses were performed to characterize a slowly progressive and reproducible animal model of IDD using real-time RT-PCR. METHODS: Twelve rabbits underwent an annular stab with a 16-gauge needle to the L2-L3, L3-L4, and L4-L5 discs, and three rabbits served as sham controls. Nucleus pulposus tissues were harvested from the stabbed discs at 3, 6, 12 and 24 weeks after confirmation of degenerative changes by magnetic resonance imaging (MRI) scan. Real-time RT-PCR was performed with the use of rabbit-specific primers for 1) extracellular matrix (ECM) component genes: collagen type Ia and IIa, and aggrecan; 2) catabolic genes: matrix metalloprotease-3 (MMP-3), inducible nitric oxide synthase (iNOS), and interleukin-1beta (IL-1beta); 3) anabolic growth genes: bone morphogenic protein-2, and -7 (BMP-2, -7), transforming growth factor-beta1 (TGF-beta1), and insulin-like growth factor-1 (IGF-1); and 4) anti-catabolic gene: tissue inhibitor of metalloprotease-1 (TIMP-1). These data were normalized to mRNA levels of glyceraldehyde phosphate dehydrogenase (GAPDH), a constitutively expressed gene. RESULTS: The MRI images confirmed progressive decline in the nucleus pulposus area of high T2 signal and in the signal intensity of the stabbed discs over the 24-week study period consistent with IDD. The ECM components, aggrecan and collagen type IIa mRNA levels had decreased markedly by week 3 and never recovered, whereas type Ia collagen mRNA gradually increased throughout course of degeneration. BMP-2, BMP-7 and IGF-1 mRNA were relatively decreased from weeks 3 to 6 but then increased at weeks 12 and 24 to end at a level near the preoperative level. The TIMP-1 expression fell dramatically to approximately one tenth of the preoperative level by week 3 and remained low throughout the degenerative process. The remaining results, including those from TGF-beta1 and the catabolic genes (MMP-3, IL-1beta, iNOS) demonstrated a double peak characteristic. The gene expression increased by week 3, decreased to a low level at weeks 6 and 12 and then had a second, late peak at 24 weeks. CONCLUSIONS: The gene expression profiles of ECM components and anabolic, catabolic, and anti-catabolic factors demonstrate many characteristics similar to the findings in human disc degeneration and suggest an inability of the intervertebral disc (IVD) to mount an early anabolic response to injury, thereby offering a possible explanation for the disc's lack of reparative capabilities. Catabolic genes are strongly up-regulated both early and late in degeneration, lending strong support to the hypothesis that an anabolic or catabolic imbalance plays a primary role in IDD. According to the resultant patterns, augmenting early production of BMP-2, BMP-7, IGF-1 or TIMP-1 by gene transfer techniques might possibly alter the progressive course of degeneration as seen in the stab model. The next step will be to transfer these therapeutic genes to regulate the biologic processes and ideally alter the progressive course of disc degeneration.

Animals↗

PubMedDate not supplied

Molecular pathogenic factors in symptomatic disc degeneration.

BACKGROUND CONTEXT: Although symptomatic disc degeneration is thought to be the leading cause of chronic low back pain, no available biologic therapy is yet available to treat this highly prevalent condition. PURPOSE: In this article, the cellular, biomechanical and molecular alterations that occur during disc degeneration are reviewed to provide a better understanding of this pathologic process. STUDY DESIGN: The cellular and molecular aspects of disc degeneration are reviewed. METHODS: The available studies detailing the molecular and cellular changes during disc degeneration are reviewed in an effort to provide a basis for understanding the biologic strategies for disc repair. RESULTS: Disc degeneration begins early in life and involves a cascade of changes at the cellular and molecular level that results in degradation of the extracellular matrix of the disc, leading to biomechanical failure of this complex structure. CONCLUSION: With a thorough understanding of the cellular and molecular events causing degeneration of the intervertebral disc, rational strategies for disc repair can be understood and evaluated. It appears that biologic disc repair will be feasible in the future although challenges remain in this blossoming field.

Adult↗

PubMed1998

Phosphorylation of specific sets of tau isoforms reflects different neurofibrillary degeneration processes.

Tau proteins are the basic components of filaments that accumulate within neurons during neurofibrillary degeneration, a degenerating process with disease-specific phenotypes. This specificity is likely to be sustained by both phosphorylation state and isoform content of tau aggregates that form neuronal inclusions. In the present study, characterization of tau isoforms involved in neurofibrillary degeneration in Alzheimer's disease, Pick's disease, corticobasal degeneration and progressive supranuclear palsy was performed. Both analyses by immunoblotting using specific tau antibodies and cell transfection by tau isoform cDNAs allowed us to demonstrate the aggregation of (1) the six hyperphosphorylated tau isoforms in Alzheimer's disease, (2) tau isoforms without exon 10-encoding sequence in Pick's disease and (3) hyperphosphorylated exon 10-tau isoforms in corticobasal degeneration and progressive supranuclear palsy. Thus, neurofibrillary degeneration phenotypes are likely to be related to the phosphorylation of different combinations of tau isoforms (with and/or without exon 10-encoding sequence) in subpopulations of neurons.

Alzheimer Disease↗

PubMed2002

Neural- and endocrine control of flight muscle degeneration in the adult cricket, Gryllus bimaculatus.

Neural- and endocrine mechanisms controlling degeneration of a dorsal longitudinal flight muscle, M112a, have been studied in adult Gryllus bimaculatus (Orthoptera: Gryllidae). Decapitation completely prevented muscle degeneration. Implantation of a pair of corpora allata or injection of juvenile hormone III into decapitated crickets caused muscle degeneration. Denervation of M112a resulted in reduction of muscle mass compared with that in sham-operated crickets. Denervation of M112a in decapitated crickets, however, did not affect muscle mass. Birefringence and ultrastructure of M112a showed an obvious regional difference in the onset of degeneration. Fibrillar structures of M112a always disappeared from the ventral to dorsal part. Distribution of axon terminals of motor neurons and mechanical responses to the motor nerve stimuli showed that M112a is composed of five motor units with similar twitch properties. When M112a was fully denervated, regional differences in degeneration disappeared. Partial denervation resulted in denervated muscle fibers losing birefringence earlier than innervated fibers. These results suggest that juvenile hormone causes breakdown of flight muscles, and neural factors control degeneration of flight muscles to some extent under the presence of the juvenile hormone.

Journal Article↗

PubMed2003

Pathological heterogeneity of clinically diagnosed corticobasal degeneration.

Two patients fulfilling suggested clinical diagnostic criteria for corticobasal degeneration (CBD) are presented, who were found at postmortem to have alternative pathological diagnoses not suspected during life, namely, Alzheimer's disease and Pick's disease, respectively. The nosological position of these cases is considered in light of a literature review of previous reports of clinically diagnosed corticobasal degeneration with atypical (not corticobasal degeneration) pathology. Since such phenocopies may be common, we suggest that all clinically diagnosed cases of corticobasal degeneration should initially be labelled as "corticobasal degeneration syndrome" (CBDS) to emphasize that this is a diagnosis based on clinical phenotype, with the term corticobasal degeneration being reserved for the specific neuropathological phenotype, which itself may have a variety of clinical presentations.

Alzheimer Disease↗

PubMed2003

Transplantation of mesenchymal stem cells embedded in Atelocollagen gel to the intervertebral disc: a potential therapeutic model for disc degeneration.

Intervertebral disc degeneration is considered to be one of the major causes of low back pain. Despite this irreversible phenomenon, attempts to decelerate disc degeneration using various techniques have been reported. However, to date there has been no proven technique effective for broad clinical application. Based on previous studies, we hypothesize that maintenance of proteoglycan content in the disc is achieved by avoiding the depletion of nucleus pulposus and preserving the structure of the annulus is a primary factor in decelerating disc degeneration. One novel approach to solve the dilemma of intervertebral disc degeneration is found at the stem cell level. Mesenchymal stem cells (MSCs) are known to possess the ability to differentiate into various kinds of cells from mesenchymal origin. Although the majority of cells that contribute to disc formation are known to obtain chondrocyte-like phenotypes, no reported study has emphasized the correlation with mesenchymal stem cells. To evaluate the possible potential of MSCs in disc cell research and treatment of degenerative disc disease, autologous MSCs embedded in Atelocollagen gel were transplanted into the discs of rabbits which had undergone a procedure proven to induce degeneration. The results suggest that MSC transplantation is effective in decelerating disc degeneration in experimental models and provided new hopes for treatment of degenerative disc disease in humans. Atelocollagen gel served as an important carrier of MSCs in transplantation, permitting proliferation, matrix synthesis and differentiation of MSCs. This study strengthens the viable efficacy of practical application of MSCs in treatment of intervertebral disc disease.

Animals↗