Journal articles: 'Degeneration (Pathology)'

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Murali, Aishwarya, Subramanian Krishnakumar, Anuradha Subramanian, and Sowmya Parameswaran. "Bruch’s membrane pathology: A mechanistic perspective." European Journal of Ophthalmology 30, no. 6 (April 28, 2020): 1195–206. http://dx.doi.org/10.1177/1120672120919337.

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Bruch’s membrane, an extracellular matrix located between the retinal pigment epithelium and the choroid, plays a vital role as structural and functional support to the retinal pigment epithelium. Dysfunction of Bruch’s membrane in both age-related macular degeneration and other ocular diseases is caused mostly by extracellular matrix degeneration, deposit formation, and angiogenesis. Although these factors are dealt in greater detail with respect to the cells that are degenerated such as the retinal pigment epithelium and the endothelial cells, the pathology involving the Bruch’s membrane is often underrated. Since in most of the macular degenerations early degenerative changes are also observed in the Bruch’s membrane, addressing only the cellular component without the underlying membrane will not yield an ideal clinical benefit. This review aims to discuss the factors and the mechanisms affecting the integrity of the Bruch’s membrane, which would aid in developing an effective therapy for these pathologies.

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Ikeda, Kenji. "Basic pathology of corticobasal degeneration." Neuropathology 17, no. 2 (June 1997): 127–33. http://dx.doi.org/10.1111/j.1440-1789.1997.tb00026.x.

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Behzadi, Fardad, Peter J. Fiester, and Dinesh Rao. "Bilateral Hypertrophic Olivary Degeneration Following Brainstem Insult: A Retrospective Review and Examination of Causative Pathology." Neuroscience Insights 16 (January 2021): 263310552110074. http://dx.doi.org/10.1177/26331055211007445.

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Hypertrophic olivary degeneration is a rare condition caused by a lesion in the Guillain-Mollaret triangle which leads to trans-synaptic degeneration resulting in the degenerative hypertrophy of the inferior olivary nucleus. This condition presents clinically with palatal tremor but can also produce ocular myoclonus or cerebellar signs. While any lesion that occurs within the Guillian-Mollaret triangle and results in the deafferentation of the inferior olive can lead to hypertrophic olivary degeneration, the most common etiologies include ischemic and hemorrhagic stroke, vascular malformation, neoplasm, and iatrogenic injury related to surgery. We report a series of 7 patients who presented with this condition bilaterally on MRI imaging, including 1 case which represents the first report of toxoplasmosis leading to the development of bilateral hypertrophic olivary degeneration and only the third reported case, unilateral or bilateral, related to an infectious etiology.

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Hales, Chadwick M., and William T. Hu. "From frontotemporal lobar degeneration pathology to frontotemporal lobar degeneration biomarkers." International Review of Psychiatry 25, no. 2 (April 2013): 210–20. http://dx.doi.org/10.3109/09540261.2013.776522.

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Bohnert, Kathryn L., Mary K. Hastings, David R. Sinacore, Jeffrey E. Johnson, Sandra E. Klein, Jeremy J. McCormick, Paul Gontarz, and Gretchen A. Meyer. "Skeletal Muscle Regeneration in Advanced Diabetic Peripheral Neuropathy." Foot & Ankle International 41, no. 5 (February 14, 2020): 536–48. http://dx.doi.org/10.1177/1071100720907035.

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Background: Decreased lean muscle mass in the lower extremity in diabetic peripheral neuropathy (DPN) is thought to contribute to altered joint loading, immobility, and disability. However, the mechanism behind this loss is unknown and could derive from a reduction in size of myofibers (atrophy), destruction of myofibers (degeneration), or both. Degenerative changes require participation of muscle stem (satellite) cells to regenerate lost myofibers and restore lean mass. Determining the degenerative state and residual regenerative capacity of DPN muscle will inform the utility of regeneration-targeted therapeutic strategies. Methods: Biopsies were acquired from 2 muscles in 12 individuals with and without diabetic neuropathy undergoing below-knee amputation surgery. Biopsies were subdivided for histological analysis, transcriptional profiling, and satellite cell isolation and culture. Results: Histological analysis revealed evidence of ongoing degeneration and regeneration in DPN muscles. Transcriptional profiling supports these findings, indicating significant upregulation of regeneration-related pathways. However, regeneration appeared to be limited in samples exhibiting the most severe structural pathology as only extremely small, immature regenerated myofibers were found. Immunostaining for satellite cells revealed a significant decrease in their relative frequency only in the subset with severe pathology. Similarly, a reduction in fusion in cultured satellite cells in this group suggests impairment in regenerative capacity in severe DPN pathology. Conclusion: DPN muscle exhibited features of degeneration with attempted regeneration. In the most severely pathological muscle samples, regeneration appeared to be stymied and our data suggest that this may be partly due to intrinsic dysfunction of the satellite cell pool in addition to extrinsic structural pathology (eg, nerve damage). Clinical Relevance: Restoration of DPN muscle function for improved mobility and physical activity is a goal of surgical and rehabilitation clinicians. Identifying myofiber degeneration and compromised regeneration as contributors to dysfunction suggests that adjuvant cell-based therapies may improve clinical outcomes.

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Mimuro, Maya, and Yasushi Iwasaki. "Age-Related Pathology in Corticobasal Degeneration." International Journal of Molecular Sciences 25, no. 5 (February 27, 2024): 2740. http://dx.doi.org/10.3390/ijms25052740.

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Elderly human brains are vulnerable to multiple proteinopathies, although each protein has a different transmission pathway. Tau-immunoreactive astrocytes are well-known in elderly brains. In contrast, astrocytic plaques, a hallmark in corticobasal degeneration (CBD), rarely occur in aging and neurodegenerative disease other than CBD. To elucidate the clinicopathological correlation of aging-related pathology in CBD, we examined 21 pathologically proven CBD cases in our institute (12 males and 9 females, with a mean age of death 70.6 years). All CBD cases showed grains and neurofibrillary tangles (NFTs). Fifteen cases (71.4%) showed beta-amyloid deposition such as senile plaques or cerebral amyloid angiopathy. Three cases (14.3%) had Lewy body pathology. One case was classified as amygdala-predominant Lewy body disease, although no cases met the pathological criteria for Alzheimer’s disease. Five cases (23.8%) displayed Limbic-predominant and age-related TDP-43 encephalopathy (LATE). NFTs, grains, and TDP-43-positive neuronal inclusions were widely distributed throughout the limbic system of CBD patients, but their densities were low. CBD might a have similar cell vulnerability and transmission pathway to that of multiple proteinopathy in aging brains.

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TAN, CELIA I. C., SWITHIN SONG, STEPHEN J. EDMONDSTON, and KEVIN P. SINGER. "PATTERNS OF THORACIC DISC DEGENERATION FROM MRI: AGE, GENDER AND SPINAL LEVEL INFLUENCES." Journal of Musculoskeletal Research 05, no. 04 (December 2001): 269–78. http://dx.doi.org/10.1142/s0218957701000635.

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The present retrospective study reviewed and examined the prevalence of thoracic disc degeneration, end-plate lesions and osteophytes in the thoracic spine using T2-weighted sagittal magnetic resonance images (MRI). The sample comprised 216 thoracic spine cases (101 males and 115 females), aged from 1 to 85 years (mean age = 42±19.7 years). Nuclear and anular degeneration, end-plate lesions and osteophytes were graded using a 3-point scale. The prevalence of degeneration was highest in the nucleus (86%) and lowest in the end-plates (63%). Males had a higher prevalence of degeneration in the nucleus, anulus and end-plates, and a lower prevalence of osteophytes compared to females. Increasing cranio-caudal trends in the prevalence of degeneration in the nucleus, anulus and end-plates were observed, and these trends were statistically significant (p<0.01). Vertebral body osteophytes were most prevalent in the mid thoracic region. Osteophytes and degenerative changes in the nucleus and anulus increased significantly with age (p<0.05). These regional and age-related degenerative trends may influence the interpretation of thoracic spine pathology from MRI investigations.

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Ashinsky, B., HE Smith, RL Mauck, and SE Gullbrand. "Intervertebral disc degeneration and regeneration: a motion segment perspective." European Cells and Materials 41 (March 24, 2021): 370–87. http://dx.doi.org/10.22203/ecm.v041a24.

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Back and neck pain have become primary reasons for disability and healthcare spending globally. While the causes of back pain are multifactorial, intervertebral disc degeneration is frequently cited as a primary source of pain. The annulus fibrosus (AF) and nucleus pulposus (NP) subcomponents of the disc are common targets for regenerative therapeutics. However, disc degeneration is also associated with degenerative changes to adjacent spinal tissues, and successful regenerative therapies will likely need to consider and address the pathology of adjacent spinal structures beyond solely the disc subcomponents. This review summarises the current state of knowledge in the field regarding associations between back pain, disc degeneration, and degeneration of the cartilaginous and bony endplates, the AF-vertebral body interface, the facet joints and spinal muscles, in addition to a discussion of regenerative strategies for treating pain and degeneration from a whole motion segment perspective.

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Tfayli, Yehia, Joseph E. Nassar, Ahmad Salaheddine Naja, and Muhyeddine Al-Taki. "Arthroscopic Meniscus Trephination: A Novel Technique for the Treatment of Symptomatic Meniscal Degeneration: Surgical Technique and Literature Review." Journal of Orthopaedic Case Reports 13, no. 10 (2023): 141–44. http://dx.doi.org/10.13107/jocr.2023.v13.i10.3968.

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Introduction: Meniscal pathology constitutes a major reason for a vast number of patients suffering from knee pain. It is, in general, attributed either to meniscal tearing or degeneration. Debridement and partial meniscectomy, or repair, when possible, is the mainstay surgical approach for refractory knee pain from meniscal degeneration or tears. Sometimes, the patient has clinical symptoms of meniscal pathology, but despite those highly suggestive clinical symptoms, the patient turns out, during knee arthroscopy, to have meniscal degeneration and hardening of the meniscus without frank tearing of the meniscus Surgical Technique: To initiate meniscal trephination, we first conduct a diagnostic knee arthroscopy to examine the suprapatellar space, the gutters, and the anterior knee space for any pathologies. Following this, both menisci are inspected for any signs of tearing or hardening. For the purposes of our study, the medial meniscus is considered pathological if it shows signs of degeneration or hardening, which then justifies our intervention. An 18-gauge spinal needle, manually bent for the procedure, is inserted through the portal to perform trephination on the hardened menisci. Care is taken to adequately space the needle insertion points to prevent accidental tearing. Our trephination technique aims to soften the meniscus, facilitating its ability to compact and compress when patients ambulate. Additionally, the needle insertion points help attract blood flow to the meniscus, thereby enriching it with growth factors and stem cells that may aid in improving the degenerative condition. Conclusion: Meniscal trephination is benign and effective for meniscal degenerative pathologies. The procedure allows for a healthier meniscus, free from degeneration, that would otherwise disable patients. The intervention does not have long-term adverse effects. To this end, more comparative trials are required to confirm the effectiveness of the technique and to ensure minimal to no associated side effects. Keywords: Trephination, Meniscus, Knee, Degeneration

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Zhang, Chao, Sigurd H. Berven, Maryse Fortin, and Michael H. Weber. "Adjacent Segment Degeneration Versus Disease After Lumbar Spine Fusion for Degenerative Pathology." Clinical Spine Surgery 29, no. 1 (February 2016): 21–29. http://dx.doi.org/10.1097/bsd.0000000000000328.

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Lee, K. P., and L. A. Kinney. "The infrastructure and Reversibility of Testicular Atrophy Induced by Ethylene Glycol Monomethyl Ether (EGME) in the Rat." Toxicologic Pathology 17, no. 4_part_2 (April 1989): 759–73. http://dx.doi.org/10.1177/0192623389017004204.

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Inhalation exposure to 300 ppm ethylene glycol monomethyl ether (EGME) for 3 days produced degenerative changes in spermatocytes of pachytene and meiotic division at spermatogenic stage XIV in rats. However, a wide range of germ cell types including spermatogonia was affected and the stage-specific damage was not discernible after 2 weeks exposure to 300 ppm EGME. The stage-specific damage was related to exposure concentration-time course. In early stages, degenerating spermatocytes showed nuclear chromatin clumping around synaptonemal complexes, cytoplasmic vesiculation with electron-dense material deposition, and disruption of the plasma membrane. Chromosomal microtubules in the meiotic division of spermatocytes were discontinued with deposition of electron-dense chromatin material. Sertoli cells showed cytoplasmic vacuolization, contact loss to germ cells, and cytoplasmic processes fragmentation with disrupted microtubules. Degenerative pachytene or meiotic spermatocytes were associated with disrupted Sertoli-germ cell relationship, chromosomal microtubules, and synaptonemal complexes. Spermatid degeneration and giant cell formation were observed after spermatocyte degeneration. Spermatid degeneration appeared to be a secondary change resulting from disrupted Sertoli-to-germ cell association. After 14 days post-exposure (PE) following 2 weeks exposure, some tubules were lined with regenerating spermatocytes with or without round spermatids. By 42 days PE, many tubules regained normal germinal epithelium, but some tubules were still atrophic even after 84 days PE. Reversibility of testicular atrophy was inversely proportional to severity of damaged stem cells.

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Grunz, Jan-Peter, Carsten Herbert Gietzen, Georgios Christopoulos, Jörg van Schoonhoven, Florian Goehtz, Rainer Schmitt, and Nina Hesse. "Osteoarthritis of the Wrist: Pathology, Radiology, and Treatment." Seminars in Musculoskeletal Radiology 25, no. 02 (April 2021): 294–303. http://dx.doi.org/10.1055/s-0041-1730948.

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AbstractOsteoarthritis (OA) is a degenerative disease that can manifest in any synovial joint under certain conditions. It leads to destruction of articular cartilage and adjacent bone, as well as formation of osteophytes at the edges of afflicted joint surfaces. Regarding the wrist, typical degenerative arthritis affects particular joints at a specific patient age, due to asymmetric load distribution and repetitive microtrauma. However, in the presence of instability or systemic diseases, early-onset degeneration can also impair the range of motion and grip strength in younger patients. Although advanced stages of OA display characteristic signs in radiography, the detection of early manifestations frequently requires computed tomography or magnetic resonance imaging (in some cases with additional arthrography). If a wrist becomes unstable, timely diagnosis and precise treatment are essential to prevent rapid disease progression. Therefore, close collaboration between radiologists and hand surgeons is obligatory to preserve the carpal function of patients.

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Shnayder, N. A., V. V. Trefilova, A. V. Ashkhotov, and O. A. Ovdienko. "Modern views on the pathogenesis of intervertebral disc degeneration." Clinician 18, no. 1 (June 24, 2024): 37–48. http://dx.doi.org/10.17650/1818-8338-2024-18-1-k705.

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Introduction. Intervertebral disc (IVD) degeneration is defined as a multifactorial degenerative disease of the spine, starting from the structures of the nucleus pulposus of the IVD, spreading to the fibrous ring and other elements of the spinal motion segment. Unlike natural aging, a pathological degenerative process that occurs in IVDs as a result of the additive effect of genetic predisposition and external environmental factors leads to the formation of chronic back pain and reduces the patient’s quality of life. Despite many years of studying the problem of the pathogenesis of IVD degeneration, it is far from being resolved, which encourages us to further study the pathogenetic mechanisms of the development of this pathology.Aim. To update the knowledge of practicing neurologists about the results of modern studies of the leading mechanisms of development of IVD degeneration in humans and their role in the development of promising biomarkers of this pathology and new strategies for pathogenetic therapy.Materials and methods. A search and analysis of publications was carried out in Russian-language (e-Library) and Englishlanguage databases (PubMed, Oxford Press, Clinical Keys, Springer, Elsevier, Google Scholar). Search depth – 5 years (2018–2023).Results. The analyzed and generalized results of studies of the molecular mechanisms influencing the development and progression of this pathology are presented. The leading pathogenetic mechanisms for the development of IVD degeneration, such as oxidative stress and the NO system, cytokine imbalance, increased activity of matrix metalloproteinases, dysfunction of fibrillar collagens and proteoglycan, as well as their relationship with each other, were considered.Conclusion. The review provides a broader look at the pathogenetic mechanisms of IVD degeneration, which makes it possible to set new goals for future development of promising therapeutic strategies.

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Ding, Xiaoyan, Mrinali Patel, and Chi-Chao Chan. "Molecular pathology of age-related macular degeneration." Progress in Retinal and Eye Research 28, no. 1 (January 2009): 1–18. http://dx.doi.org/10.1016/j.preteyeres.2008.10.001.

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Cazzanelli, Petra, and Karin Wuertz-Kozak. "MicroRNAs in Intervertebral Disc Degeneration, Apoptosis, Inflammation, and Mechanobiology." International Journal of Molecular Sciences 21, no. 10 (May 20, 2020): 3601. http://dx.doi.org/10.3390/ijms21103601.

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Intervertebral disc (IVD) degeneration is a multifactorial pathological process associated with low back pain, the leading cause of years lived in disability worldwide. Key characteristics of the pathological changes connected with degenerative disc disease (DDD) are the degradation of the extracellular matrix (ECM), apoptosis and senescence, as well as inflammation. The impact of nonphysiological mechanical stresses on IVD degeneration and inflammation, the mechanisms of mechanotransduction, and the role of mechanosensitive miRNAs are of increasing interest. As post-transcriptional regulators, miRNAs are known to affect the expression of 30% of protein-coding genes and numerous intracellular processes. The dysregulation of miRNAs is therefore associated with various pathologies, including degenerative diseases such as DDD. This review aims to give an overview of the current status of miRNA research in degenerative disc pathology, with a special focus on the involvement of miRNAs in ECM degradation, apoptosis, and inflammation, as well as mechanobiology.

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Stanishevskaya, O. M., M. A. Glock, M. A. Safronova, A. I. Belyaeva, and D. V. Chernykh. "Classifications of peripheral retinal dystrophies." Fyodorov journal of ophthalmic surgery, no. 3 (October 20, 2023): 119–24. http://dx.doi.org/10.25276/0235-4160-2023-3-119-124.

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Purpose. To analyze the existing classifications of peripheral retinal dystrophies. Material and methods. While writing a literature review, a search was made for data from domestic and foreign literature, mostly in the last 20 years. The search was carried out using the following keywords: «peripheral retinal dystrophies», «retinal detachment», «laser coagulation», «lattice degeneration». In total, 20 articles were selected that relate to the topic of this literature review. Results. Retinal detachment is a severe pathology leading to a significant reduction or loss of vision. Peripheral retinal dystrophies play a leading role in the development of retinal detachment. The leading role in the development of rhegmatogenous forms of peripheral degenerations is assigned to changes in the vitreous body with a traction effect on the retina. The question of the incidence of retinal detachment in its dystrophies remains debatable. In publications, we came across a large number of classifications of peripheral retinal dystrophies, covering from 8 to 20 different clinical forms. The question of which retinal dystrophies are predisposing or not predisposing to retinal detachment remains open. Visualization of the vitreoretinal interface in peripheral degenerations is relevant for determining treatment tactics. Optical coherence tomography is highly informative in the early diagnosis of the traction component, visualization of retinal tears and detachment, and determination of indications for laser coagulation of the retina. Conclusion. Retinal detachment is a severe pathology leading to a significant reduction or loss of vision. Peripheral retinal dystrophies play a leading role in the development of retinal detachment. The question of the incidence of retinal detachment in its dystrophies remains debatable. The issue of creating a working classification that reflects the morphology of the degenerative process and indications for laser treatment remains relevant. Key words: peripheral retinal dystrophy, retinal detachment, retinal laser treatment, lattice degeneration

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Ohm, Daniel T., Katheryn A. Q. Cousins, Sharon X. Xie, Claire Peterson, Corey T. McMillan, Lauren Massimo, Katya Raskovsky, et al. "Signature laminar distributions of pathology in frontotemporal lobar degeneration." Acta Neuropathologica 143, no. 3 (January 8, 2022): 363–82. http://dx.doi.org/10.1007/s00401-021-02402-3.

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AbstractFrontotemporal lobar degeneration (FTLD) with either tau (FTLD-tau) or TDP-43 (FTLD-TDP) inclusions are distinct proteinopathies that frequently cause similar frontotemporal dementia (FTD) clinical syndromes. FTD syndromes often display macroscopic signatures of neurodegeneration at the level of regions and networks, but it is unclear if subregional laminar pathology display patterns unique to proteinopathy or clinical syndrome. We hypothesized that FTLD-tau and FTLD-TDP accumulate pathology in relatively distinct cortical layers independent of clinical syndrome, with greater involvement of lower layers in FTLD-tau. The current study examined 170 patients with either FTLD-tau (n = 73) or FTLD-TDP (n = 97) spanning dementia and motor phenotypes in the FTD spectrum. We digitally measured the percent area occupied by tau and TDP-43 pathology in upper layers (I–III), lower layers (IV–VI), and juxtacortical white matter (WM) from isocortical regions in both hemispheres where available. Linear mixed-effects models compared ratios of upper to lower layer pathology between FTLD groups and investigated relationships with regions, WM pathology, and global cognitive impairment while adjusting for demographics. We found lower ratios of layer pathology in FTLD-tau and higher ratios of layer pathology in FTLD-TDP, reflecting lower layer-predominant tau pathology and upper layer-predominant TDP-43 pathology, respectively (p < 0.001). FTLD-tau displayed lower ratios of layer pathology related to greater WM tau pathology (p = 0.002) and to earlier involved/severe pathology regions (p = 0.007). In contrast, FTLD-TDP displayed higher ratios of layer pathology not related to either WM pathology or regional severity. Greater cognitive impairment was associated with higher ratios of layer pathology in FTLD-tau (p = 0.018), but was not related to ratios of layer pathology in FTLD-TDP. Lower layer-predominant tau pathology and upper layer-predominant TDP-43 pathology are proteinopathy-specific, regardless of clinical syndromes or regional networks that define these syndromes. Thus, patterns of laminar change may provide a useful anatomical framework for investigating how degeneration of select cells and corresponding laminar circuits influence large-scale networks and clinical symptomology in FTLD.

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Yamashita, Haruhiro, Mark J. Hoenerhoff, Shyamal D. Peddada, Robert C. Sills, and Arun R. Pandiri. "Chemical Exacerbation of Light-induced Retinal Degeneration in F344/N Rats in National Toxicology Program Rodent Bioassays." Toxicologic Pathology 44, no. 6 (July 11, 2016): 892–903. http://dx.doi.org/10.1177/0192623316650050.

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Retinal degeneration due to chronic ambient light exposure is a common spontaneous age-related finding in albino rats, but it can also be related to exposures associated with environmental chemicals and drugs. Typically, light-induced retinal degeneration has a central/hemispherical localization whereas chemical-induced retinal degeneration has a diffuse localization. This study was conducted to identify and characterize treatment-related retinal degeneration in National Toxicology Program rodent bioassays. A total of 3 chronic bioassays in F344/N rats (but not in B6C3F1/N mice) were identified that had treatment-related increases in retinal degeneration (kava kava extract, acrylamide, and leucomalachite green). A retrospective light microscopic evaluation of the retinas from rats in these 3 studies showed a dose-related increase in the frequencies of retinal degeneration, beginning with the loss of photoreceptor cells, followed by the inner nuclear layer cells. These dose-related increased frequencies of degenerative retinal lesions localized within the central/hemispherical region are suggestive of exacerbation of light-induced retinal degeneration.

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Vialle, Emiliano Neves, Luiz Roberto Gomes Vialle, Christiano Esteves Simões, and Phelipe de Souza Menegaz. "CLINICAL-RADIOGRAPHIC CORRELATION OF DEGENERATIVE CHANGES OF THE SPINE - SYSTEMATIC REVIEW." Coluna/Columna 15, no. 4 (December 2016): 325–29. http://dx.doi.org/10.1590/s1808-185120161504157006.

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ABSTRACT Systematic review of the literature on the evaluation of images of degenerative changes of the spine and its clinical correlation. A systematic literature review was conducted, and the results evaluated for the presence of clinical correlation, as well as the type of imaging method used. The search terms were "Intervertebral Disc Degeneration", "Intervertebral disc", "Classification", "Anulus fibrosus", "Nucleus pulposus", "Lumbar spine", "Degenerative disc disease", "Degeneration", "Zygapophyseal Joint". We also assessed whether there were inter- and intraobserver agreement in the selected works and possible guidelines regarding the treatment and prognosis of patients. Of the 91 reviewed abstracts, 31 articles were selected that met the inclusion criteria. Six articles were related to the cervical spine, 13 to the lumbar spine and 12 were about changes not related specifically to a single segment of the spine. Articles that determined limiting values considered normal were also included, since variations were considered signs of degeneration or pathology. It was not possible to establish the relationship between the changes identified in imaging and the clinical history of patients, either define treatment and prognosis guidelines.

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Runwal, Gautam, and Robert H. Edwards. "The Membrane Interactions of Synuclein: Physiology and Pathology." Annual Review of Pathology: Mechanisms of Disease 16, no. 1 (January 24, 2021): 465–85. http://dx.doi.org/10.1146/annurev-pathol-031920-092547.

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Specific proteins accumulate in neurodegenerative disease, and human genetics has indicated a causative role for many. In most cases, however, the mechanisms remain poorly understood. Degeneration is thought to involve a gain of abnormal function, although we do not know the normal function of many proteins implicated. The protein α-synuclein accumulates in the Lewy pathology of Parkinson's disease and related disorders, and mutations in α-synuclein cause degeneration, but we have not known its normal function or how it triggers disease. α-Synuclein localizes to presynaptic boutons and interacts with membranes in vitro. Overexpression slows synaptic vesicle exocytosis, and recent data suggest a normal role for the endogenous synucleins in dilation of the exocytic fusion pore. Disrupted membranes also appear surprisingly prominent in Lewy pathology. Synuclein thus interacts with membranes under both physiological and pathological conditions, suggesting that the normal function of synuclein may illuminate its role in degeneration.

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Patel, Hershel R., and Curtis E. Margo. "Pathology of Ischemic Optic Neuropathy." Archives of Pathology & Laboratory Medicine 141, no. 1 (January 1, 2017): 162–66. http://dx.doi.org/10.5858/arpa.2016-0027-rs.

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Ischemic optic neuropathy (ION) describes a state of hypoxic injury of the optic nerve. Clinically, ION is divided into anterior and posterior forms defined by the presence or absence of optic disc swelling, respectively. It is further classified as arteritic when secondary to vasculitis, and nonarteritic when not. The site of vascular occlusion for anterior ION from giant cell arteritis is the short posterior ciliary arteries, but mechanical vascular obstruction does not play a role in most nonarteritic cases. Histologically, ION is characterized by axon and glial necrosis, edema, and a sparse mononuclear response. Like other ischemic injuries, the morphologic alternations in the nerve are time dependent. A variant of ION called cavernous degeneration (of Schnabel) features large cystic spaces filled with mucin. Several conditions can histologically mimic cavernous degeneration of the optic nerve. The scarcity of cases of ION examined histologically has contributed to an incomplete understanding of its pathogenesis.

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Sakae, Nobutaka, Octavio A. Santos, Otto Pedraza, Irene Litvan, Melissa E. Murray, Ranjan Duara, Ryan J. Uitti, et al. "Clinical and pathologic features of cognitive-predominant corticobasal degeneration." Neurology 95, no. 1 (June 9, 2020): e35-e45. http://dx.doi.org/10.1212/wnl.0000000000009734.

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ObjectiveTo describe clinical and pathologic characteristics of corticobasal degeneration (CBD) with cognitive predominant problems during the disease course.MethodsIn a series of autopsy-confirmed cases of CBD, we identified patients with cognitive rather than motor predominant features (CBD-Cog), including 5 patients thought to have Alzheimer disease (AD) and 10 patients thought to have behavioral variant frontotemporal dementia (FTD). We compared clinical and pathologic features of CBD-Cog with those from a series of 31 patients with corticobasal syndrome (CBD-CBS). For pathologic comparisons between CBD-Cog and CBD-CBS, we used semiquantitative scoring of neuronal and glial lesion types in multiple brain regions and quantitative assessments of tau burden from image analysis.ResultsFive of 15 patients with CBD-Cog never had significant motor problems during their disease course. The most common cognitive abnormalities in CBD-Cog were executive and visuospatial dysfunction. The frequency of language problems did not differ between CBD-Cog and CBD-CBS. Argyrophilic grain disease, which is a medial temporal tauopathy associated with mild cognitive impairment, was more frequent in CBD-Cog. Apathy was also more frequent in CBD-Cog. Tau pathology in CBD-Cog was greater in the temporal and less in perirolandic cortices than in CBD-CBS.ConclusionA subset of patients with CBD has a cognitive predominant syndrome than can be mistaken for AD or FTD. Our findings suggest that distribution of tau cortical pathology (greater in temporal and less in perirolandic cortices) may be the basis of this uncommon clinical variant of CBD.

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Bettiol, Nicole Barbosa, Simone Cecilio Hallak Regalo, Flávia Argentato Cecilio, Ligia Maria Napolitano Gonçalves, Paulo Batista de Vasconcelos, Claire Genoveze Gauch Lopes, Lilian Mendes Andrade, Isabela Hallak Regalo, Selma Siéssere, and Marcelo Palinkas. "Intervertebral Disc Degeneration: Functional Analysis of Bite Force and Masseter and Temporal Muscles Thickness." Prague Medical Report 123, no. 2 (2022): 101–12. http://dx.doi.org/10.14712/23362936.2022.11.

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Intervertebral disc degeneration is a pathological condition associated with the intervertebral disc and is related to functional alterations in the human body. This study aimed to evaluate the maximum molar bite force and masseter and temporal muscles thickness in individuals with intervertebral disc degeneration. Thirty-two individuals were divided into two groups: those with degeneration of intervertebral discs (n=16) and those without degeneration (n=16). The maximum molar bite force (on the right and left sides) was measured using a dynamometer. Masseter and temporal muscle thickness during mandibular task rest and dental clenching in maximum voluntary contraction were analysed using ultrasound. Significant differences in the left molar bite force (p=0.04) were observed between the groups (Student’s t-test, p<0.05). The intervertebral disc degeneration group had a lower maximum molar bite force. No significant differences in muscle thickness were observed between the masseter and temporal muscles in either group. However, based on clinical observations, the group with intervertebral disc degeneration presented less masseter muscle thickness and greater temporal muscle thickness in both mandibular tasks. Degenerative disease of the intervertebral discs promoted morphofunctional changes in the stomatognathic system, especially in maximum molar bite force and masticatory muscle thickness. This study provides insight into the interaction between spinal pathology and the stomatognathic system, which is important for healthcare professionals who treat patients with functional degeneration.

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Suryadevara, Manasa, Gaurav Mishra, Pratapsingh Parihar, and Anshul Sood. "MRI-based evaluation of lower back pain with reference to ligamentum flavum hypertrophy." F1000Research 12 (September 4, 2023): 1105. http://dx.doi.org/10.12688/f1000research.139565.1.

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Introduction The lower back ache or lumbago is a common musculoskeletal complaint patients present with, especially among the elderly. It can be caused mostly by degenerative changes like ligamentum flavum hypertrophy associated with aging and physical strain, first causing spinal canal narrowing and leading to stenosis later. MRI provides excellent high-resolution images of structures including the spinal canal, vertebral body, discs, joints, and other structures. Aim and objective This study aims to bring out the relation between degenerative disc changes and LF hypertrophy in patients presenting with lower back pain and helps in earlier discovery of degeneration and in understanding the underlying pathology better. Methods A descriptive prospective study will be done at Acharya Vinoba Bhave Rural Hospital, Sawangi, involving 30 patients who are referred to the department of Radiodiagnosis, AVBRH, Sawangi with lower back pain will be subjected to the study – purposive sampling. Expected results After an appropriate statistical analysis, we expect to assess the role of MRI which provides excellent high-resolution images of structures including the spinal canal, vertebral body, discs, joints, and other structures. This study aims to bring out the relation between degenerative disc changes and LF hypertrophy in patients presenting with lower back pain and helps in earlier discovery of degeneration and in understanding the underlying pathology better. CTRI registration: REF/2023/05/067795

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Sosnovskii, S. V., and K. V. Penzeva. "Vitreoretinal pathology in neovascular age-related macular degeneration." Modern technologies in ophtalmology, no. 2 (April 27, 2020): 349–54. http://dx.doi.org/10.25276/2312-4911-2020-2-349-354.

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Videman, Tapio, Laura E. Gibbons, and Michele C. Battié. "Age- and Pathology-Specific Measures of Disc Degeneration." Spine 33, no. 25 (December 2008): 2781–88. http://dx.doi.org/10.1097/brs.0b013e31817e1d11.

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Whitwell, Jennifer L., and Keith A. Josephs. "Neuroimaging in frontotemporal lobar degeneration—predicting molecular pathology." Nature Reviews Neurology 8, no. 3 (January 31, 2012): 131–42. http://dx.doi.org/10.1038/nrneurol.2012.7.

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Brown, Jeremy N., Simon N. J. Roberts, Michael G. Hayes, and Andrew D. Sales. "Shoulder pathology associated with symptomatic acromioclavicular joint degeneration." Journal of Shoulder and Elbow Surgery 9, no. 3 (May 2000): 173–76. http://dx.doi.org/10.1067/mse.2000.103618.

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Brosnahan, Donal M., Susan M. Kennedy, Carolyn A. Converse, William R. Lee, and Harold M. Hammer. "Pathology of Hereditary Retinal Degeneration Associated with Hypobetalipoproteinemia." Ophthalmology 101, no. 1 (January 1994): 38–45. http://dx.doi.org/10.1016/s0161-6420(94)31358-3.

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Hsieh, Sung-Tsang, Hou-Yu Chiang, and Whei-Min Lin. "Pathology of Nerve Terminal Degeneration in the Skin." Journal of Neuropathology & Experimental Neurology 59, no. 4 (April 2000): 297–307. http://dx.doi.org/10.1093/jnen/59.4.297.

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Bayram, Ece, Dennis W. Dickson, Stephen G. Reich, and Irene Litvan. "Pathology‐Proven Corticobasal Degeneration Presenting as Richardson's Syndrome." Movement Disorders Clinical Practice 7, no. 3 (February 14, 2020): 267–72. http://dx.doi.org/10.1002/mdc3.12900.

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Kitab, Sameer, Ghaith Habboub, Salam B. Abdulkareem, Muthanna B. Alimidhatti, and Edward Benzel. "Redefining lumbar spinal stenosis as a developmental syndrome: does age matter?" Journal of Neurosurgery: Spine 31, no. 3 (September 2019): 357–65. http://dx.doi.org/10.3171/2019.2.spine181383.

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OBJECTIVEAge is commonly thought to be a risk factor in defining lumbar spinal stenosis (LSS) degenerative or developmental subtypes. This article is a follow-up to a previous article (“Redefining Lumbar Spinal Stenosis as a Developmental Syndrome: An MRI-Based Multivariate Analysis of Findings in 709 Patients Throughout the 16- to 82-Year Age Spectrum”) that describes the radiological differences between developmental and degenerative types of LSS. MRI-based analysis of “degeneration” variables and spinal canal morphometric characteristics of LSS segments have been thought to correlate with age at presentation.METHODSThe authors performed a re-analysis of data from their previously reported prospective MRI-based study, stratifying data from the 709 cases into 3 age categories of equal size (instead of the original < 60 vs ≥ 60 years). Relative spinal canal dimensions, as well as radiological degenerative variables from L1 to S1, were analyzed across age groups in a multivariate mode. The total degenerative scale score (TDSS) for each lumbar segment from L1 to S1 was calculated for each patient. The relationships between age and qualitative stenosis grades, TDSS, disc degeneration, and facet degeneration were analyzed using Pearson’s product-moment correlation and multiple regression.RESULTSMultivariate analysis of TDSS and spinal canal dimensions revealed highly significant differences across the 3 age groups at L2–3 and L3–4 and a weaker, but still significant, association with changes at L5–S1. Age helped to explain only 9.6% and 12.2% of the variance in TDSS at L1–2 and L2–3, respectively, with a moderate positive correlation, and 7.8%, 1.2%, and 1.9% of the variance in TDSS at L3–4, L4–5, and L5–S1, respectively, with weak positive correlation. Age explained 24%, 26%, and 18.4% of the variance in lumbar intervertebral disc (LID) degeneration at L1–2, L2–3, and L3–4, respectively, while it explained only 6.2% and 7.2% of the variance of LID degeneration at L4–5 and L5–S1, respectively. Age explained only 2.5%, 4.0%, 1.2%, 0.8%, and 0.8% of the variance in facet degeneration at L1–2, L2–3, L3–4, L4–5, and L5–S1, respectively.CONCLUSIONSAge at presentation correlated weakly with degeneration variables and spinal canal morphometries in LSS segments. Age correlated with upper lumbar segment (L1–4) degeneration more than with lower segment (L4–S1) degeneration. The actual chronological age of the patients did not significantly correlate with the extent of degenerative pathology of the lumbar stenosis segments. These study results lend support for a developmental contribution to LSS.

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Ashok, Ajay, Neena Singh, Suman Chaudhary, Vindhya Bellamkonda, Alexander E. Kritikos, Aaron S. Wise, Neil Rana, Dallas McDonald, and Rithvik Ayyagari. "Retinal Degeneration and Alzheimer’s Disease: An Evolving Link." International Journal of Molecular Sciences 21, no. 19 (October 2, 2020): 7290. http://dx.doi.org/10.3390/ijms21197290.

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Age-related macular degeneration (AMD) and glaucoma are degenerative conditions of the retina and a significant cause of irreversible blindness in developed countries. Alzheimer’s disease (AD), the most common dementia of the elderly, is often associated with AMD and glaucoma. The cardinal features of AD include extracellular accumulation of amyloid β (Aβ) and intracellular deposits of hyper-phosphorylated tau (p-tau). Neuroinflammation and brain iron dyshomeostasis accompany Aβ and p-tau deposits and, together, lead to progressive neuronal death and dementia. The accumulation of Aβ and iron in drusen, the hallmark of AMD, and Aβ and p-tau in retinal ganglion cells (RGC), the main retinal cell type implicated in glaucoma, and accompanying inflammation suggest overlapping pathology. Visual abnormalities are prominent in AD and are believed to develop before cognitive decline. Some are caused by degeneration of the visual cortex, while others are due to RGC loss or AMD-associated retinal degeneration. Here, we review recent information on Aβ, p-tau, chronic inflammation, and iron dyshomeostasis as common pathogenic mechanisms linking the three degenerative conditions, and iron chelation as a common therapeutic option for these disorders. Additionally discussed is the role of prion protein, infamous for prion disorders, in Aβ-mediated toxicity and, paradoxically, in neuroprotection.

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Díaz-Delgado, Josué, Derick B. Whitley, Ralph W. Storts, Jill J. Heatley, Sharman Hoppes, and Brian F. Porter. "The Pathology of Wobbly Hedgehog Syndrome." Veterinary Pathology 55, no. 5 (April 19, 2018): 711–18. http://dx.doi.org/10.1177/0300985818768033.

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Wobbly hedgehog syndrome (WHS) is a leading cause of neurologic disease in African pygmy hedgehogs (APHs; Atelerix albiventris). This study describes the signalment, clinical signs, gross, microscopic, and ultrastructural lesions of WHS in a cohort of 12 pet APHs. Microscopically, lesions consisted of status spongiosus of the white matter, typically bilateral and symmetrical, with myelin degeneration and loss that was accompanied by neuronal/axonal degeneration plus reactive microgliosis and mild, focal astrocytosis and astrogliosis. Lesions were most severe in the cerebellum and medulla oblongata, as well as cervical and thoracic spinal cord. Less affected areas were the corona radiata, corpus callosum, corpus striatum, internal capsule, and the mesencephalon. Ultrastructurally, the lesions consisted of splitting of the myelin sheath at the intraperiod line with subsequent focal expansion, resulting in status spongiosus, disruption, dilatation, rhexis, and phagocytosis. Based on these results, WHS is best described as a “spongy myelinopathy” with widespread central nervous system involvement.

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Ovchinnikova, E. V., E. E. Vaiman, N. A. Shnayder, A. A. Ovchinnikova, and R. F. Nasyrova. "Classification and Clinical Heterogeneity of Hepatolenticular Degeneration." Personalized Psychiatry and Neurology 3, no. 2 (November 15, 2023): 15–24. http://dx.doi.org/10.52667/2712-9179-2023-3-2-15-24.

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Hepatolenticular degeneration (HLD) or Wilson-Konovalov disease (OMIM277900) is a hereditary monogenic autosomal recessive degenerative disease related to metabolic diseases - a category of storage diseases. HLD has been studied for more than 130 years. During this time, more classifications of this disease were proposed. In this review, we systematized all the proposed classifications of HLD. And we noticed, they are based on the following criteria: 1) clinical signs of the disease; 2) the sequence of their appearance as the pathology progresses (with the primary appearance of signs of liver or brain damage); 3) severity of the disease. This review also systematizes data on the clinical picture of HLD.

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Abraham, Thangapalam Jawahar, Harresh Adikesavalu, and Sayani Banerjee. "Pathology of systemic multiple bacterial infections and peritonitis in hatchery-produced African catfish Clarias gariepinus (Burchell, 1822) larvae." Journal of Fisheries 10, no. 1 (February 20, 2022): 101204. http://dx.doi.org/10.17017/j.fish.300.

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Diseases are the major problems that have a significant impact on African catfish Clarias gariepinus seed production. This study reports the necropsy, microscopy, bacteriology and histopathology of diseased catfish larvae that experienced mass mortalities (>80%). The gill filaments of diseased larvae revealed no ectoparasites. The intestines had no parasitic association. About 35 – 40% of the dead larvae had ruptured abdomen. The affected larvae had abdominal haemorrhages and disintegrated intestine with marked degenerative and inflammatory changes, which indicated peritonitis. Bacteria including Aeromonas veronii, Edwardsiella tarda and Pseudomonas putida were isolated from the haemorrhagic exudates of diseased catfish larvae. Histopathology demonstrated dense melanomacrophage aggregates in the spleen. The intestine had extensive degeneration, basophilic margination and disintegration of the mucosal layer. The kidney section suggested a suppurative infection with necrosis of haematopoietic tissue, inflammation of the epithelial tissue, vacuolar degenerations and hypoplastic haematopoietic tissue. Aeromonas veronii and E. tarda immersion challenge at 5×106 cells mL–1 yielded no mortalities under laboratory conditions. Nevertheless, the hatchery management measures and the laboratory analyses supported peritonitis with systemic multiple bacterial infections in the observed large-scale motilities of excessively fed larvae.

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Gong, Cheng-Xin, Fei Liu, Inge Grundke-Iqbal, and Khalid Iqbal. "Dysregulation of Protein Phosphorylation/Dephosphorylation in Alzheimer's Disease: A Therapeutic Target." Journal of Biomedicine and Biotechnology 2006 (2006): 1–11. http://dx.doi.org/10.1155/jbb/2006/31825.

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Studies during the last two decades have provided new insights into the molecular mechanism of Alzheimer's disease (AD). One of the milestone findings in AD research was the demonstration that neurofibrillary degeneration characterized by tau pathology is central to the pathogenesis of AD and other tauopathies and that abnormal hyperphosphorylation of tau is pivotal to neurofibrillary degeneration. This article reviews the recent research advances in tau pathology and the underlying dysregulation of the protein phosphorylation/dephosphorylation system. An updated model of the mechanism of neurofibrillary degeneration is also presented, and a promising therapeutic target to treat AD by correcting dysregulation of protein phosphorylation/dephosphorylation is discussed.

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Sekirnjak, Chris, Lauren H. Jepson, Pawel Hottowy, Alexander Sher, Wladyslaw Dabrowski, A. M. Litke, and E. J. Chichilnisky. "Changes in physiological properties of rat ganglion cells during retinal degeneration." Journal of Neurophysiology 105, no. 5 (May 2011): 2560–71. http://dx.doi.org/10.1152/jn.01061.2010.

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Retinitis pigmentosa (RP) is a leading cause of degenerative vision loss, yet its progressive effects on visual signals transmitted from the retina to the brain are not well understood. The transgenic P23H rat is a valuable model of human autosomal dominant RP, exhibiting extensive similarities to the human disease pathology, time course, and electrophysiology. In this study, we examined the physiological effects of degeneration in retinal ganglion cells (RGCs) of P23H rats aged between P37 and P752, and compared them with data from wild-type control animals. The strength and the size of visual receptive fields of RGCs decreased rapidly with age in P23H retinas. Light responses mediated by rod photoreceptors declined earlier (∼P300) than cone-mediated light responses (∼P600). Responses of ON and OFF RGCs diminished at a similar rate. However, OFF cells exhibited hyperactivity during degeneration, whereas ON cells showed a decrease in firing rate. The application of synaptic blockers abolished about half of the elevated firing in OFF RGCs, indicating that the remodeled circuitry was not the only source of degeneration-induced hyperactivity. These results advance our understanding of the functional changes associated with retinal degeneration.

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Elmore, Susan A., Famke Aeffner, Dinesh S. Bangari, Torrie A. Crabbs, Stacey Fossey, Shayne C. Gad, Wanda M. Haschek, et al. "Proceedings of the 2017 National Toxicology Program Satellite Symposium." Toxicologic Pathology 45, no. 7 (October 2017): 799–833. http://dx.doi.org/10.1177/0192623317733924.

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The 2017 annual National Toxicology Program Satellite Symposium, entitled “Pathology Potpourri,” was held in Montreal, Quebec, Canada at the Society of Toxicologic Pathology’s 36th annual meeting. The goal of this symposium was to present and discuss challenging diagnostic pathology and/or nomenclature issues. This article presents summaries of the speakers’ talks along with select images that were used by the audience for voting and discussion. Various lesions and other topics covered during the symposium included renal papillary degeneration in perinatally exposed animals, an atriocaval mesothelioma, an unusual presentation of an alveolar–bronchiolar carcinoma, a paraganglioma of the organ of Zuckerkandl (also called an extra-adrenal pheochromocytoma), the use of human muscle samples to illustrate the challenges of manual scoring of fluorescent staining, intertubular spermatocytic seminomas, medical device pathology assessment and discussion of the approval process, collagen-induced arthritis, incisor denticles, ameloblast degeneration and poorly mineralized enamel matrix, connective tissue paragangliomas, microcystin-LR toxicity, perivascular mast cells in the forebrain thalamus unrelated to treatment, and 2 cases that provided a review of the International Harmonization of Nomenclature and Diagnostic Criteria (INHAND) bone nomenclature and recommended application of the terminology in routine nonclinical toxicity studies.

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St. Iencean, Andrei, and Ion Poeata. "Three-level cervical disc herniation." Romanian Neurosurgery 29, no. 3 (September 1, 2015): 309–15. http://dx.doi.org/10.1515/romneu-2015-0041.

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Abstract Multilevel cervical degenerative disc disease is well known in the cervical spine pathology, with radicular syndromes or cervical myelopathy. One or two level cervical herniated disc is common in adult and multilevel cervical degenerative disc herniation is common in the elderly, with spinal stenosis, and have the same cause: the gradual degeneration of the disc. We report the case of a patient with two level cervical disc herniation (C4 – C5 and C5 – C6) treated by anterior cervical microdiscectomy both levels and fusion at C5 – C6; after five years the patient returned with left C7 radiculopathy and MRI provided the image of a left C6 – C7 disc herniation, he underwent an anterior microsurgical discectomy with rapid relief of symptoms. Three-level cervical herniated disc are rare in adults, and the anterior microdiscectomy with or without fusion solve this pathology.

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Rannou, François, Tzong-Shyuan Lee, Rui-Hai Zhou, Jennie Chin, Jeffrey C. Lotz, Marie-Anne Mayoux-Benhamou, Jacques Patrick Barbet, Alain Chevrot, and John Y. J. Shyy. "Intervertebral Disc Degeneration." American Journal of Pathology 164, no. 3 (March 2004): 915–24. http://dx.doi.org/10.1016/s0002-9440(10)63179-3.

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Kostina, D. A., V. E. Uspensky, D. S. Semenova, A. S. Kostina, N. V. Boyarskaya, O. B. Irtyuga, and A. B. Malashicheva. "Role of calcification in aortic degeneration." Translational Medicine 7, no. 1 (March 11, 2020): 6–21. http://dx.doi.org/10.18705/2311-4495-2020-7-1-6-21.

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Vascular calcification is a widely-spread pathology with high mortality. It is active bioregulated process that is observed in pathogenesis of different desires, associated with metabolic dysfunction, congenital tissue desires and aging. Signal pathways and transcription factors that are involved in vascular calcification are also takes place in normal osteogenesis and/or vascular development. In the review the main attention is payed to the role of signaling pathways BMP (bone morphogenic protein), Notch, Wnt and to the role of transcription factors BMP2, RUNX2, Msx2 in vascular calcification. Probably, dysfunction of osteogenic signal pathways and transdifferentiation of vascular cells to osteoblast-like cells is a common prosses not only for vascular calcification or mineralization, but is a way of vascular degradation in general. Proosteogenic changes at cellular and molecular level may play role in pathogenesis of a disease without manifestation of vascular mineralization, such as thoracic aortic aneurysm. Ability of vascular cells to change their phenotype to osteophenotype is very likely biologically important ability. Over weakness of calcific signaling pathways activity can also lead to vascular pathology. The aim of the review is to overlook the mechanisms of vascular calcification focusing at the role of signal pathways and vascular cells at this process with particular attention to aortic calcification. Understanding the mechanisms of biological regulation of pro- and antiosteogenic processes in pathology and normal conditions opens new opportunities to influence this prosess in order to correct vascular pathologies.

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Finol, H. J., A. Marquez, M. Pulido-Mendez, B. Muller, I. Montes de Oca, and P. Tonino. "Pericyte Ultrastructural Pathology in Autoimmune Inflammatory Myopathies." Microscopy and Microanalysis 4, S2 (July 1998): 1080–81. http://dx.doi.org/10.1017/s1431927600025526.

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Ultrastructural Pathology of capillary endothelial cells in autoimmune inflammatory myopathies has been intensively investigated in the last two decades, but much less is known about the alterations of capillary pericytes. In other diseases as diabetes and arterial hypertension perycites abnormalities have been reported. In this work we report the pericyte ultrastructural pathology in autoimmune inflammatory myopathies.Patients admitted to the study were attending the rheumatology clinics at the Caracas University Hospital. Diagnoses were systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, and muscle paraneoplastic phenomenon.Needle muscle biopsies were processed with routine techniques for transmission electron microscopy and observed in a Hitachi H-500 electron microscope.Two different processes were observed, pericyte hypertrophy and cell degeneration. In the first one cytoplasmic proliferation is evident (Fig. 1). Some capillaries embraced by the pericyte were found (Fig. 2). In the second one cytoplasmic vacuolation and capillary necrosis (Fig. 3) were evident. Usually, pericyte and endothelial degeneration were concomitant.

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Camelo, Serge. "Potential Sources and Roles of Adaptive Immunity in Age-Related Macular Degeneration: Shall We Rename AMD into Autoimmune Macular Disease?" Autoimmune Diseases 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/532487.

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Age-related macular degeneration (AMD) is the leading cause of vision loss in the elderly throughout the industrialized world. Its most prominent pathologic features are lesions involving the retinal pigment epithelium (RPE) the Bruch’s membrane, the degeneration of photoreceptors, and, in the most aggressive cases, choroidal neovascularization. Genetic associations between the risk of developing AMD and polymorphism within components of the complement system, as well as chemokine receptors expressed on microglial cells and macrophages, have linked retinal degeneration and choroidal neovascularization to innate immunity (inflammation). In addition to inflammation, players of the adaptive immunity including cytokines, chemokines, antibodies, and T cells have been detected in animal models of AMD and in patients suffering from this pathology. These observations suggest that adaptive immunity might play a role in different processes associated with AMD such as RPE atrophy, neovascularization, and retinal degeneration. To this date however, the exact roles (if any) of autoantibodies and T cells in AMD remain unknown. In this review we discuss the potential effects of adaptive immune responses in AMD pathogenesis.

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Krakora, Dan, Corey Macrander, and Masatoshi Suzuki. "Neuromuscular Junction Protection for the Potential Treatment of Amyotrophic Lateral Sclerosis." Neurology Research International 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/379657.

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Amyotrophic lateral sclerosis (ALS) is a neuromuscular disease characterized by the progressive degeneration of upper and lower motor neurons (MNs), leading to muscular atrophy and eventual respiratory failure. ALS research has primarily focused on mechanisms regarding MN cell death; however, degenerative processes in the skeletal muscle, particularly involving neuromuscular junctions (NMJs), are observed in the early stages of and throughout disease progression. According to the “dying-back” hypothesis, NMJ degeneration may not only precede, but actively cause upper and lower MN loss. The importance of NMJ pathology has relatively received little attention in ALS, possibly because compensatory mechanisms mask NMJ loss for prolonged periods. Many mechanisms explaining NMJ degeneration have been proposed such as the disruption of anterograde/retrograde axonal transport, irregular cellular metabolism, and changes in muscle gene and protein expression. Neurotrophic factors, which are known to have neuroprotective and regenerative properties, have been intensely investigated for their therapeutic potential in both the preclinical and clinical setting. Additional research should focus on the potential of preserving NMJs in order to delay or prevent disease progression

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Fanjul-Moles, María Luisa, and Germán Octavio López-Riquelme. "Relationship between Oxidative Stress, Circadian Rhythms, and AMD." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–18. http://dx.doi.org/10.1155/2016/7420637.

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This work reviews concepts regarding oxidative stress and the mechanisms by which endogenous and exogenous factors produce reactive oxygen species (ROS). It also surveys the relationships between oxidative stress, circadian rhythms, and retinal damage in humans, particularly those related to light and photodamage. In the first section, the production of ROS by different cell organelles and biomolecules and the antioxidant mechanisms that antagonize this damage are reviewed. The second section includes a brief review of circadian clocks and their relationship with the cellular redox state. In the third part of this work, the relationship between retinal damage and ROS is described. The last part of this work focuses on retinal degenerative pathology, age-related macular degeneration, and the relationships between this pathology, ROS, and light. Finally, the possible interactions between the retinal pigment epithelium (RPE), circadian rhythms, and this pathology are discussed.

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Liu, Kang, and Bolin Xie. "Today and Future of Age-Related Macular Degeneration." ISRN Ophthalmology 2012 (April 4, 2012): 1–9. http://dx.doi.org/10.5402/2012/480212.

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Age-related macular degeneration (AMD) is the leading cause of blindness in people over 50 in developed countries. Understanding of the pathologic process, genetic mechanisms, and risk factors of this disease has the benefit of seeking newer and more effective treatment options. Current clinical therapy for AMD shows a dramatic change from a decade ago. Anti-VEGF drug therapy is regarded as the more effective treatment for neovascular AMD now, especially combining PDT therapy. In the future, the genetic and biochemical therapies may be the promising treatments for AMD. This paper will focus on the progress of pathology, candidate genes of AMD, risk factors, and the existing drugs or surgical therapies available, in order to present some new directions of care with the prospect of improved vision in many patients suffered from AMD.

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Idland, Ane-Victoria, Torgeir Bruun Wyller, Randi Støen, Lars Magne Eri, Frede Frihagen, Johan Ræder, Farrukh Abbas Chaudhry, et al. "Preclinical Amyloid-β and Axonal Degeneration Pathology in Delirium." Journal of Alzheimer's Disease 55, no. 1 (November 1, 2016): 371–79. http://dx.doi.org/10.3233/jad-160461.

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Vattoth, S., F. Y. Ahmed, R. C. Telford, and G. H. Roberson. "Hypertrophic Olivary Degeneration: Review of Anatomy, Pathology, and Imaging." Neurographics 4, no. 3 (September 1, 2014): 114–22. http://dx.doi.org/10.3174/ng.3140085.

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Ling, Helen, Gabor G. Kovacs, Jean Paul G. Vonsattel, Karen Davey, Kin Y. Mok, John Hardy, Huw R. Morris, Thomas T. Warner, Janice L. Holton, and Tamas Revesz. "Astrogliopathy predominates the earliest stage of corticobasal degeneration pathology." Brain 139, no. 12 (October 25, 2016): 3237–52. http://dx.doi.org/10.1093/brain/aww256.

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Journal articles on the topic 'Degeneration (Pathology)'

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