1639 - First description of a "sago spleen" by Nicholaus Fontanus
| 1639 - First description of a "sago spleen" by Nicholaus Fontanus |
| 1789 - Description of a lardeceous liver by Antoine Portal. Later he also describes an enlarged liver in an 8-year-old boy with tuberculosis |
| 1842 - "Lardeceous-gelatinous"-like firm greyish material in the liver of patients with tuberculosis, syphilis and mercury poisoning described by Carl Rokitansky |
| 1856 - Probably the first description of a patient with "primary" amyloidosis by Samuel Wilks. In 1865 he described five similar cases |
| 1872 - Adams and Dowse describe amyloid in patients with multiple myeloma |
| 1932 - Ostertag describes the first family with hereditary amyloidosis (of the kidneys) |
| 1945 - Siegal describes patients with familial benign paroxysmal peritonitis, currently known as familial Mediterranean fever (FMF). Amyloidosis is in this disease a frequent (in about 40% of cases) late complication. |
| 1952 - Corine Andrade describes 74 patients, members of many families all originating from the same area around a small coast village in Portugal. All patients suffering from a familial amyloidotic polyneuropathy (FAP) |
| 1956 - Rukavina decribes familial amyloid polyneuropathy in Indiana |
| 1967 - First international Symposium on Amyloid and Amyloidosis, held in Groningen, organised by Enno Mandema, Luuk Ruinen, Jan Scholten and Alan Cohen |
| 1967 - Jan Scholten describes in The Netherlands a family with hereditary amyloidotic polyneuropathy |
| 1968 - Meretoja describes in Finland an hereditary form of systemic amyloidosis characterised by cornea lattice dystrofie, cutis laxa, and a cranial neuropathy |
| 1968 - Shukuro Araki describes in Japan familial amyloidotic polyneuropathy |
| 1969 - Van Allen describes a family with renal amyloidosis in Iowa |
| 1970 - Rune Andersson describes in Sweden familial amyloidotic polyneuropathy |
| 1977 - Warren describes a high frequency of carpal tunnel syndrome (CTS) in patients who are on longstanding dialysis. Gradually thereafter, since about 1984, it becomes clear that deposition of amyloid is the cause of the CTS as well as other joint problems |
| 1993 - Alan Cohen becomes editor-in-chief of a new medical journal called AMYLOID, The International Journal of Protein Folding Disorders |
| 1854 - The name "amyloid" is coined by Rudolph Virchow to describe material deposited in tissue, based upon the colour reaction with iodine and sulphuric acid (from brown to blue) similar to starch (amylum) |
| 1859 - Friedreich and Kekule show that amyloid is composed of proteins instead of carbohydrates |
| 1875 - Methylviolet stain is more useful to detect amyloid than the iodine sulphuric acod test. This finding was described independently from each other by André-Victor Cornil (Parijs), Richard Heschl (Wenen), and Rudolph Jürgens (Berlijn) |
| 1907 - Alzheimer describes fibrillar argyrophyl deposits in cortical neurons |
| 1922 - Hermann Bennhold introduces the Congo red stain for amyloid. In 1927 describes Divry the characteristic apple-green birefringence (e.g. in cortical neurons in Alzheimers's disease) |
| 1959 - Alan Cohen and Evan Calkins describe the fibrillar structure of amyloid when studied electron microscopically |
| 1961 - Ehrlich detects localised deposits of amyloid in the islands of Langerhans in the pancreas of patients with diabetes mellitus type II |
| 1966 - Bladen and Glenner describe the pentagonal protein serum amyloïd P component |
| 1968 - Eanes and Glenner show that the beta-pleated sheet is the basic structure of amyloid fibrils |
| 1968 - Mordechai Pras introduces a method to extract proteins from fibrils with water. This method turned out to be a big step forward in the chemical characterisation of amyloid proteins, as can be seen in the following years |
| 1971 - George Glenner shows that some amyloid fibrils are derived from the variable portion of a kappa or lambda light chaint |
| 1972 - Earl Benditt describes AA amyloid as the newly characterised typical protein in "secundary" amyloidosis |
| 1973 - Franklin and Levin show the presence in blood of serum amyloid A protein (SAA), which later turns out to be an acute phase protein |
| 1978 - Pedro Costa describes prealbumin (transthyretin) as the protein characterististic of amyloid in familial amyloidotic polyneuropathy |
| 1980 - Knut Sletten describes prealbumin (transthyretin) as the characteristic protein of amyloid in a patient with senile systemic amyloidosis |
| 1983 - Alan Cohen describes cystatin-C as the protein characterististic of amyloid in Icelandic familial cerebral amyloid angiopathy |
| 1984 - Tawara and Araki describe a point mutation in the transthyretin gene, resulting in a substitution of methionine instead of valine at position 30, in patients with familial amyloidotic polyneuropathy |
| 1985 - Fumitake Gejyo describes β-2-microglobulin as the protein characterististic of amyloid in dialysis-related amyloid arthropathy |
| 1988 - Nichols and Benson describe apolipoprotein AI as the protein characterististic of amyloid in a familial form of systemic amyloidotic polyneuropathy in Iowa |
| 1990 - Peter Maury describes gelsolin as the protein characterististic of amyloid in the Finnish form of hereditary amyloid polyneuropathy |
| 1993 - Merrill Benson describes fibrinogen Aα chain as the protein characterististic of amyloid in a familial form of renal (as prominent manifestation of systemic) amyloidosis |
| 1993 - Mark Pepys describes lysozyme as the protein characterististic of amyloid in a familial form of renal (as prominent manifestation of systemic) amyloidosis |
| 2001 - Merrill Benson describes apolipoprotein AII as the protein characterististic of amyloid in a familial form of renal (as prominent manifestation of systemic) amyloidosis |
| 1986 - Zemer shows that treatment of familial Mediterranean fever (FMF) with colchicine is not only effective to prevent attacks of the disease, but also prevents AA amyloidosis as a late complication |
| 1988 - Philip Hawkins and Mark Pepys introduce 123I-SAP scintigraphy as a clinical method to visualise the presence of amyloid in organs of patients with systemic amyloidosis |
| 1991 - Holmgren introduces liver transplantation as treatment modality of patients with familial ATTR amyloidosis |
| 1996 - Martha Skinner shows that the combination of prednisolone, melphalan, and colchicine has a favourable effect on survival of patients with AL amyloidosis compared to colchicine alone |
| 1996 - Ray Comenzo shows in patients with AL amyloidosis the promising first results of high dose melphalan followed by autologous stem cell support |
| 1997 - Bob Kyle confirms the observation of Martha Skinner that the combination of prednisolone and melphalan has a favourable effect on survival of patients with AL amyloidosis and that addition of colchicine has no additional benefit in this group of patients |
| 2001 - Julian Gillmore shows that effective reduction of the serum concentration of serum amyloid A protein (SAA) has a favourable effect on the disease course and survival of AA amyloidosis |
| 2004 - Martha Skinner and Angela Dispenzieri both confirm the favourable effect of high dose melphalan with stem cell support in larger groups of patients with AL amyloidosis |
| 2005 - Morie Gertz describes on behalf of a number of clinical research
groups in patients with AL amyloidosis a common set of criteria for organ
involvement and criteria for improvement and worsening during therapy
|
Since the end of the sixties considerable progress has been made and new developments in various areas of amyloid research have changed the overall picture of this group of diseases. Many proteins have been detected to be building bricks or related to the genesis of amyloid fibrils. Biochemists, chemists, pathologists, geneticists, clinicians, and many other researchers have tried to unravel the genesis of the various types of amyloidosis, to improve the detection of amyloid in the individual patient, and to search for more effective ways of treatment.
