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Contursi Terme | |
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Comune di Contursi Terme | |
Coordinates: 40°38′N15°14′E / 40.633°N 15.233°E | |
Country | Italy |
Region | Campania |
Province | Salerno (SA) |
Frazioni | Bagni di Contursi, Pagliarini, Toppe, Piana, Monte di Pruno, Iannamici, Prato, Ponte Mefita, Saginara, San Pietro, Serroni |
Government | |
• Mayor | Antonio Briscione |
Area | |
• Total | 28.90 km2 (11.16 sq mi) |
Elevation | 250 m (820 ft) |
Population (31 August 2007) [2] | |
• Total | 3,281 |
• Density | 110/km2 (290/sq mi) |
Demonym | Contursani |
Time zone | UTC+1 (CET) |
• Summer (DST) | UTC+2 (CEST) |
Postal code | 84024 |
Dialing code | 0828 |
Patron saint | Saint Donatus |
Saint day | 7 August |
Website | Official website |
Contursi Terme (Contursano: Cundurs) is a village and comune in the province of Salerno in the Campania region of south-western Italy.
No secure identification of Contursi Terme, where ancient remains confirm a settlement at the confluence of the Tanagro (ancient Tanager) with the Sele, is likely. The Roman Ursentum noted in Pliny's Natural History (III.2), is more usually identified with Caggiano. [3] The local historian A. Filomarino, [4] based on etymologies of toponyms, placed the commune's origins as early as the fourth century AD, the result of efforts by the inhabitants of the former Saginara and Contursi to fortify a site that was destroyed by Alaric's Goths at the end of the fourth century. Under the Lombards it appears to have belonged to the gastaldate of Conza, [5] when a fortress was built in 840 by Orso, count of Conza, from whom the stronghold probably took its name Castrum comitis Ursi, the "castle of count Orso") [6] Orso took the part of his kinsman Siconulf of Salerno (839-51) in internecine wars with Radelchis I of Benevento, who had been a former gastaldo of Conza.
The later history of Contursi Termi [7] formed a local part of the Principality of Salerno, which was retained as a title until the territory was divided in three by Charles II of Naples in 1287, Contursi passing to the prince of Citerione (or Citra) and held by the family Sanseverino. In 1348, Contursi was taken by Louis of Taranto, king of Naples by right of his wife Joanna; he passed the title to his adherents, the Origlia. In 1448 Antonio Sanseverino succeeded in reclaiming title to Contursi, but the Sanseverino heirs held it only until the early sixteenth century, under the Viceroys of Naples. From the seventeenth century the commune passed successively through a number of families, the Bernalli, Pepe, Ludovisi and Parisani Bonanno. The last to hold the contado before the reunification of Italy were the Pisani di Tolentino, marchesi di Caggiano.
The thermal baths, insecurely linked to notices by Roman writers, were described in a manuscript Balnea Contursi of 1231; [8] The fifteen thermal springs, with varying mineral content, have retained their curative reputation, for bathing, both in warm pools and in a cold plunge, and for drinking.
Families from the village have played an important role in the understanding of Parkinson's disease. In 1986, Larry Golbe, a doctor based at the University of Medicine and Dentistry of New Jersey, came across a family with six Parkinson's patients, and found that they had originated in Contursi. [9] A few months later he found a second family with several Parkinson's patients, who also had ancestors from the village. [9] This prompted Golbe to collaborate with Giuseppe DiIorio at the University of Naples, to analyse the DNA from Contursani and people who had emigrated from the village across the world. [9] They identified three families in Italy and three families in the US, all of whom were descendants from a single couple who lived in Contursi in the late 17th and early 18th centuries. [9] Of 400 members of this extended family, known as the "Contursi kindred", 61 are known to have had Parkinson's. [9] This showed for the first time that Parkinson's could be inherited. [10]
Geneticists Alice Lazzarini and William Johnson worked through the early 1990s trying to isolate the mutation that caused the disease. [9] In 1996, a team led by Mihael Polymeropoulos at the National Institutes of Health located by linkage analysis the Parkinson's disease gene of the Contursi kindred on the long arm of human chromosome 4. [11] In 1997, the same team identified a point mutation in the alpha-synuclein gene in the Contursi kindred as well as Greek pedigrees with Parkinson's disease. [12] [13] The NIH team and a team led by Maria Grazia Spillantini reported on alpha-synuclein deposits in Lewy bodies as well as alpha-synuclein inclusions in other neurodegenerative disorders. [14] [15]
Dementia with Lewy bodies (DLB) is a type of dementia characterized by changes in sleep, behavior, cognition, movement, and regulation of automatic bodily functions. Memory loss is not always an early symptom. The disease worsens over time and is usually diagnosed when cognitive impairment interferes with normal daily functioning. Together with Parkinson's disease dementia, DLB is one of the two Lewy body dementias. It is a common form of dementia, but the prevalence is not known accurately and many diagnoses are missed. The disease was first described by Kenji Kosaka in 1976.
Lewy bodies are the inclusion bodies – abnormal aggregations of protein – that develop inside nerve cells affected by Parkinson's disease (PD), the Lewy body dementias, and some other disorders. They are also seen in cases of multiple system atrophy, particularly the parkinsonian variant (MSA-P).
Alpha-synuclein(aSyn) is a protein that, in humans, is encoded by the SNCA gene. Alpha-synuclein is a neuronal protein that regulates synaptic vesicle trafficking and subsequent neurotransmitter release.
Multiple system atrophy (MSA) is a rare neurodegenerative disorder characterized by autonomic dysfunction, tremors, slow movement, muscle rigidity, and postural instability and ataxia. This is caused by progressive degeneration of neurons in several parts of the brain including the basal ganglia, inferior olivary nucleus, and cerebellum.
Ubiquitin carboxy-terminal hydrolase L1 is a deubiquitinating enzyme.
Parkin is a 465-amino acid residue E3 ubiquitin ligase, a protein that in humans and mice is encoded by the PARK2 gene. Parkin plays a critical role in ubiquitination – the process whereby molecules are covalently labelled with ubiquitin (Ub) and directed towards degradation in proteasomes or lysosomes. Ubiquitination involves the sequential action of three enzymes. First, an E1 ubiquitin-activating enzyme binds to inactive Ub in eukaryotic cells via a thioester bond and mobilises it in an ATP-dependent process. Ub is then transferred to an E2 ubiquitin-conjugating enzyme before being conjugated to the target protein via an E3 ubiquitin ligase. There exists a multitude of E3 ligases, which differ in structure and substrate specificity to allow selective targeting of proteins to intracellular degradation.
A neurodegenerative disease is caused by the progressive loss of structure or function of neurons, in the process known as neurodegeneration. Such neuronal damage may ultimately involve cell death. Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, tauopathies, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation. Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assemblies and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.
Synucleins are a family of soluble proteins common to vertebrates, primarily expressed in neural tissue and in certain tumors.
Beta-synuclein is a protein that in humans is encoded by the SNCB gene.
Gamma-synuclein is a protein that in humans is encoded by the SNCG gene.
Protein deglycase DJ-1, also known as Parkinson disease protein 7, is a protein which in humans is encoded by the PARK7 gene.
Synphilin-1 is a protein that in humans is encoded by the SNCAIP gene. SNCAIP stands for "synuclein, alpha interacting protein" and can be signified by SNCAP_HUMAN, synphilin 1, synuclein, alpha interacting protein (synphilin), and SYPH1.
Parkinson's disease (PD), or simply Parkinson's, is a chronic degenerative disorder of the central nervous system that affects both the motor system and non-motor systems. The symptoms usually emerge slowly, and as the disease progresses, non-motor symptoms become more common. Early symptoms are tremor, rigidity, slowness of movement, and difficulty with walking. Problems may also arise with cognition, behaviour, sleep, and sensory systems. Parkinson's disease dementia is common in advanced stages.
The history of Parkinson's disease expands from 1817, when British apothecary James Parkinson published An Essay on the Shaking Palsy, to modern times. Before Parkinson's descriptions, others had already described features of the disease that would bear his name, while the 20th century greatly improved knowledge of the disease and its treatments. PD was then known as paralysis agitans. The term "Parkinson's disease" was coined in 1865 by William Sanders and later popularized by French neurologist Jean-Martin Charcot. Paralysis
Parkinson's disease (PD) is a degenerative disorder of the central nervous system. Most people with PD have idiopathic Parkinson's disease. A small proportion of cases, however, can be attributed to known genetic factors. Other factors such as environmental toxins, herbicides, pesticides, and fungicides, have been associated with the risk of developing PD, but no causal relationships have been proven.
Maria Grazia Spillantini, is Professor of Molecular Neurology in the Department of Clinical Neurosciences at the University of Cambridge. She is most noted for identifying the protein alpha-synuclein as the major component of Lewy bodies, the characteristic protein deposit found in the brain in Parkinson's disease and dementia with Lewy bodies. She has also identified mutations in the MAPT gene as a heritable cause for frontotemporal dementia.
Alice M. Lazzarini is a scientist, author and researcher on neurogenetic disorders, including Huntington's disease and Parkinson's disease. She is an assistant professor of Neurology at Rutgers Robert Wood Johnson Medical School, where her work helped establish the genetic basis of Parkinson's. Later in life, she was diagnosed with Parkinson's—the very disease she had spent decades researching.
Synucleinopathies are neurodegenerative diseases characterised by the abnormal accumulation of aggregates of alpha-synuclein protein in neurons, nerve fibres or glial cells. There are three main types of synucleinopathy: Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Other rare disorders, such as various neuroaxonal dystrophies, also have α-synuclein pathologies. Additionally, autopsy studies have shown that around 6% of sporadic Alzheimer's Disease exhibit α-synuclein positive Lewy pathology, and are sub-classed as Alzheimer's Disease with Amygdalar Restricted Lewy Bodies (AD/ALB).
Proprotein convertase subtilisin/kexin type 1 inhibitor is a protein by the name of proSAAS that in humans is encoded by the PCSK1N gene.
The Parkinson's Foundation is a national organization that funds research and provides educational resources to Parkinson’s disease patients and caregivers. The Parkinson's Foundation was established in 2016 through the merger of the National Parkinson Foundation and the Parkinson's Disease Foundation. The Parkinson's Foundation has headquarters in Miami and New York City, in addition to 17 chapters throughout the United States.