Pathology

@article{dao1984human,
    author = "Dao, Anh H. and Netsky, Martin G.",
    title = "Human tails and pseudotails",
    year = "1984",
    journal = "Human Pathology",
    url = "https://doi.org/10.1016/s0046-8177(84)80079-9",
    doi = "10.1016/s0046-8177(84)80079-9",
    number = "5",
    pages = "449-453",
    volume = "15"
}

@misc{dao1984human2,
    author = "Dao, A. H. and Netsky, M. G",
    title = "Human Tails and Pseudotails",
    year = "1984",
    howpublished = "Human Pathology, v. 15, p. 449-453",
    note = "talkorigins\_source = {true}; raw\_reference = {Dao, A. H., and Netsky, M. G., 1984, Human Tails and Pseudotails: Human Pathology, v. 15, p. 449-453.}"
}

@article{hogg1985airways,
    author = "Hogg, James C. and Wright, Joanne L. and Pare, Peter D.",
    title = "Airways disease: evolution, pathology, and recognition",
    year = "1985",
    journal = "Medical Journal of Australia",
    url = "https://doi.org/10.5694/j.1326-5377.1985.tb113531.x",
    doi = "10.5694/j.1326-5377.1985.tb113531.x",
    number = "11",
    pages = "605-607",
    volume = "142"
}

@book{boyd1989on1,
    author = "Boyd, G. W",
    title = "On Stress Disease and Evolution",
    year = "1989",
    publisher = "Hobart, University of Tasmania, 246 p",
    note = "talkorigins\_source = {true}; raw\_reference = {Boyd, G. W., 1989, On Stress Disease and Evolution: Hobart, University of Tasmania, 246 p.}"
}

@article{nixon1990on,
    author = "Nixon, P G F",
    title = "On Stress Disease and Evolution",
    year = "1990",
    journal = "Postgraduate Medical Journal",
    url = "https://doi.org/10.1136/pgmj.66.780.883-b",
    doi = "10.1136/pgmj.66.780.883-b",
    number = "780",
    pages = "883-884",
    volume = "66"
}

@article{reshetnikov2001tidal,
    author = "Reshetnikov, V. P. and Sotnikova, N. Ya.",
    title = "Tidal tails and galaxy evolution",
    year = "2001",
    journal = "Astronomical \& Astrophysical Transactions",
    url = "https://doi.org/10.1080/10556790108208195",
    doi = "10.1080/10556790108208195",
    number = "1",
    pages = "111-114",
    volume = "20"
}

@article{a2003evolution,
    author = "A, Sessa and M, Meroni and G, Battini and M, Righetti and M, Nebuloni and A, Tosoni and GL, Vago",
    title = "Evolution of renal pathology in Fabry disease",
    year = "2003",
    journal = "Acta Paediatrica",
    url = "https://doi.org/10.1080/08035320310000375",
    doi = "10.1080/08035320310000375",
    number = "0",
    pages = "6-8",
    volume = "92"
}

Fabry disease is a rare lysosomal storage disorder which results from deficient activity of the enzyme α‐galactosidase A. The resultant deposition and progressive accumulation of glycosphingolipids in all types of body tissue leads to severe clinical manifestations involving the heart, CNS and kidney. Renal manifestations are observed relatively early in the course of the disease, and progression to end‐stage renal failure is common in hemizygous males in the third to fifth decades of life. Renal biopsy specimens reveal evidence of diffuse intracytoplasmic glycosphingolipid accumulation, mainly affecting podocytes and epithelial cells of distal tubules, which are strikingly enlarged and vacuolated. On electron microscopy the deposits appear as typical osmiophilic inclusion bodies in the cytoplasm of all kinds of renal cells, and show a characteristic ‘onion skin’ or ‘zebra’ appearance. These pathological features are also evident in heterozygous females. Deposits occur before the development of renal impairment. As patients age, the disease progresses in cells throughout the kidney, and is associated with increasing glycosphingolipid accumulation. Conclusion: The age‐related evolution of renal pathology in Fabry disease is closely correlated with progressive intracellular deposition of glycosphingolipid and ultimately leads to end‐stage renal failure.

@article{sessa2003evolution,
    author = "Sessa, A and Meroni, M and Battini, G and Righetti, M and Nebuloni, M and Tosoni, A and Vago, GL",
    title = "Evolution of renal pathology in Fabry disease",
    year = "2003",
    journal = "Acta Paediatrica",
    abstract = "Fabry disease is a rare lysosomal storage disorder which results from deficient activity of the enzyme α‐galactosidase A. The resultant deposition and progressive accumulation of glycosphingolipids in all types of body tissue leads to severe clinical manifestations involving the heart, CNS and kidney. Renal manifestations are observed relatively early in the course of the disease, and progression to end‐stage renal failure is common in hemizygous males in the third to fifth decades of life. Renal biopsy specimens reveal evidence of diffuse intracytoplasmic glycosphingolipid accumulation, mainly affecting podocytes and epithelial cells of distal tubules, which are strikingly enlarged and vacuolated. On electron microscopy the deposits appear as typical osmiophilic inclusion bodies in the cytoplasm of all kinds of renal cells, and show a characteristic ‘onion skin’ or ‘zebra’ appearance. These pathological features are also evident in heterozygous females. Deposits occur before the development of renal impairment. As patients age, the disease progresses in cells throughout the kidney, and is associated with increasing glycosphingolipid accumulation. Conclusion: The age‐related evolution of renal pathology in Fabry disease is closely correlated with progressive intracellular deposition of glycosphingolipid and ultimately leads to end‐stage renal failure.",
    url = "https://doi.org/10.1111/j.1651-2227.2003.tb00212.x",
    doi = "10.1111/j.1651-2227.2003.tb00212.x",
    number = "s443",
    pages = "6-8",
    volume = "92"
}

@article{teixeira2006evolution,
    author = "Teixeira, Antonio RL and Nascimento, Rubens J and Sturm, Nancy R",
    title = "Evolution and pathology in Chagas disease: a review",
    year = "2006",
    journal = "Memórias do Instituto Oswaldo Cruz",
    url = "https://doi.org/10.1590/s0074-02762006000500001",
    doi = "10.1590/s0074-02762006000500001",
    number = "5",
    pages = "463-491",
    volume = "101"
}

Introduction Extracellular accumulation of amyloid‐β protein and intracellular accumulation of tau in brain tissues have been described in animal models of Alzheimer's disease (AD) and mechanical stress‐based diseases of different mechanisms, such as traumatic brain injury (TBI), arterial hypertension (HTN), and normal pressure hydrocephalus (NPH). Methods We provide a brief overview of experimental models of TBI, HTN, and NPH showing features of tau‐amyloid pathology, neuroinflammation, and neuronal loss. Results “Alzheimer‐like” hallmarks found in these mechanical stress‐based models were compared with AD features found in transgenic models. Discussion The goal of this review is, therefore, to build on current concepts of onset and progression of AD lesions. We point to the importance of accumulated mechanical stress in brain as an environmental and endogenous factor that pushes protein deposition and neuronal injury over the disease threshold. We further encourage the development of preventing strategies and drug screening based on mechanical stress models.

@article{levynogueira2016mechanical,
    author = "Levy Nogueira, Marcel and Epelbaum, Stéphane and Steyaert, Jean‐Marc and Dubois, Bruno and Schwartz, Laurent",
    title = "Mechanical stress models of Alzheimer's disease pathology",
    year = "2016",
    journal = "Alzheimer's \& Dementia",
    abstract = "Introduction Extracellular accumulation of amyloid‐β protein and intracellular accumulation of tau in brain tissues have been described in animal models of Alzheimer's disease (AD) and mechanical stress‐based diseases of different mechanisms, such as traumatic brain injury (TBI), arterial hypertension (HTN), and normal pressure hydrocephalus (NPH). Methods We provide a brief overview of experimental models of TBI, HTN, and NPH showing features of tau‐amyloid pathology, neuroinflammation, and neuronal loss. Results “Alzheimer‐like” hallmarks found in these mechanical stress‐based models were compared with AD features found in transgenic models. Discussion The goal of this review is, therefore, to build on current concepts of onset and progression of AD lesions. We point to the importance of accumulated mechanical stress in brain as an environmental and endogenous factor that pushes protein deposition and neuronal injury over the disease threshold. We further encourage the development of preventing strategies and drug screening based on mechanical stress models.",
    url = "https://doi.org/10.1016/j.jalz.2015.10.005",
    doi = "10.1016/j.jalz.2015.10.005",
    number = "3",
    pages = "324-333",
    volume = "12"
}

@article{sompol2022oxidative,
    author = "Sompol, Pradoldej and Kraner, Susan and Arthiushin, Irina and TANGPONG, J.I.T.B.A.N.J.O.N.G. and Norris, Christopher and Nelson, Peter",
    title = "Oxidative stress-associated cerebrovascular pathology in Alzheimer’s disease",
    year = "2022",
    journal = "Free Radical Biology and Medicine",
    url = "https://doi.org/10.1016/j.freeradbiomed.2022.10.065",
    doi = "10.1016/j.freeradbiomed.2022.10.065",
    pages = "44",
    volume = "192"
}

@incollection{halder2024apoptosis,
    author = "Halder, Satyajit and Jana, Shraman and Majumder, Chirantan and Jana, Kuladip",
    title = "Apoptosis: ER Stress and Disease Pathology",
    year = "2024",
    booktitle = "Apoptosis and Human Health: Understanding Mechanistic and Therapeutic Potential",
    url = "https://doi.org/10.1007/978-981-97-7905-5\_6",
    doi = "10.1007/978-981-97-7905-5\_6",
    pages = "127-139"
}