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01.12.2013
The cause of prostate cancer is unknown but the risk factors for prostate cancer include genetics, advancing age, hormonal effects (testosterone), and some environmental factors which include toxins, industrial products and chemicals.
Age is the most evident risk factor as the chance of developing prostate cancer increases with the advancing age. It has been thought now that the growth of prostate cancer can be inhibited if the level of testosterone is decreased. Objective: Define the phenotype and genotype of a cluster of families with a relatively pure cerebellar ataxia referred to as Autosomal Recessive Cerebellar Ataxia type 1 (ARCA-1).
The hereditary ataxias can be divided based on their mode of inheritance into autosomal dominant, autosomal recessive, X-linked and the mitochondrial ataxias.
Subjects were referred to the study protocol by their treating physician based on a preliminary assessment consistent with the core features of ARCA-1 (ataxia and dysarthria of middle-age onset with cerebellar atrophy) and a recessive family history (parents unaffected).
ARCA-1 is thus a new recessive relatively pure cerebellar ataxia that is caused by various mutations in SYNE1. Please note: If you have a promotional code you'll be prompted to enter it prior to confirming your order.
If you subscribe to any of our print newsletters and have never activated your online account, please activate your account below for online access. When it comes to preventing and treating high blood pressure, one often-overlooked strategy is managing stress. Hip and knee pain can keep you from the activities you love, as well as make routine tasks difficult. Your hands perform countless small and large tasks each day—from pouring coffee, brushing teeth, and buttoning shirts to raking leaves or kneading bread. Food intolerance and food allergies often produce similar symptoms, but they're not the same.
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It is highly recommended that at the age of 40, all men should undergo yearly screening process for prostate cancer. However, genetic predispositions can be modified by diet, environment and other unknown factors.
Environmental factors which includes diets that are high in animal fat and cigarette smoking, increases the risk of prostate cancer while a diet high in vegetables and fruit decreases the risk. Some factors that have not been clarified yet include the risk of developing prostate cancer by additional toxins or substances in the environment or chemicals from industrial sources. An enlarged prostate may, in some cases, be a sign of prostate cancer but it does not necessarily predict it to be a sign of prostate cancer even then a person should be vigilant.
Methods: We ascertained 64 probands and affected members of 30 French-Canadian families all showing similar clinical features and originating from the same region of Quebec.
These disease categories share the prototypic feature of impaired walking, although they usually present a variety of other neurological symptoms such as pyramidal signs, peripheral neuropathy, extrapyramidal signs, cognitive loss, or retinopathy.
On her initial visit, she mentioned that around the age of 30 she started noticing that her speech was slurred.


ARCA-1 shows relative homogeneity of the phenotype, despite being caused by more than seven different mutations.
Like valves used in house plumbing, the heart valves open to allow fluid (blood) to be pumped forward, and they close to prevent fluid from flowing backward. A heart valve problem is classified as congenital when some factor during fetal development causes the valve to form abnormally.
After informed consent, we performed detailed clinical history, neurological examination, brain imaging, nerve conduction studies, and SYNE1 mutation detection of all available subjects. The autosomal recessive ataxias are also a heterogeneous group of disorders comprised mainly of Friedreicha€™s Ataxia, Ataxia Telangiectasia, Ataxia with Vitamin E Deficiency, Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay (ARSACS), Abetalipoproteinemia, Ataxia with Oculomotor Apraxia type 1 (AOA-1) and type 2 (AOA-2) (67).Over the last decade, we have identified a large cluster of French-Canadian families whose ancestors originate mostly from the same region of the Province of Quebec (Canada). All 64 available affected and unaffected members of the 30 recruited families underwent a thorough neurological examination, and were examined independently by at least two neurologists. Figure 2: Magnetic resonance imaging of a 43 years old ARCA-1 patient after 5 years of disease evolution. The age of onset does not vary significantly in function of given mutations like in trinucleotide repeat disorders, whereas the disease shows little associated features accompanying the core symptoms of dysarthria and dysmetria. This is because there is a higher risk of valve abnormalities in the parents and siblings of affected newborns, compared with the overall risk of less than in the general population. Sagittal T1 shows marked diffuse cerebellar atrophy with no cerebral cortical atrophy; no midbrain, pontine or bulbar atrophy. Sometimes, the heart defect is related to health or environmental factors that affected the mother during pregnancy. We identified a total of 7 mutations in our population, thereby providing evidence of genotypic heterogeneity. The affected individuals in these families all share similar clinical characteristics that define this new disease entity we named ARCA-1, also known as Recessive Ataxia of Beauce (RAB) (68), (69).
Twenty-two subjects underwent electrophysiological studies (D.B) including compound motor action potentials of median, ulnar, tibial and peroneal nerves, as well as sensory nerve action potentials of median, ulnar, radial and sural nerves, with standard values for filters, stimulus duration and electrode positioning. Strangers would sometimes wonder if she had been drinking alcohol, and her gait was becoming more wide-based with a tendency to fall if she did not pay more attention than usual during her movements.
Known ARCA-1 disease causing mutations are in black and newly identified mutations lie within boxes. The protein contains two N-terminal actin-binding regions that comprise tandem paired calponin-homology-domains, a transmembrane domain, multiple spectrin repeats and a C-terminal KASH domain.
Genome-wide linkage and fine-mapping analysis on selected families with ARCA-1 established a minimum candidate interval of about 0.5-Mb on chromosome 6q containing a single causal gene (SYNE1) (66). Although SYNE1 is expressed in multiple tissues, its greatest level in the central nervous system of mice is in the cell bodies of the Purkinje cells and in neurons of the olivary region of the brainstem, while in humans it is also expressed predominantly in the cerebellum; it is not expressed in glial cells. Interpretation: We identified a cluster of French-Canadian families with a new recessive ataxia of relatively pure cerebellar type caused by mutations in SYNE1. Spanning over 0.5-Mb of genomic DNA, SYNE1 is one of the biggest gene in the human genome formed of 147 exons that encodes a 27,652-kb mRNA and an 8797 amino acid long protein. Upon receipt of informed consent, blood samples were obtained from affected individuals in 30 families.
On neurological examination at age 42, she had normal fundoscopy, normal ocular saccades and pursuit, and no nystagmus. In the peripheral nervous system, SYNE-1 is involved in anchoring specialized myonuclei underneath the neuromuscular junctions (66). The function of SYNE-1 is thus critical in the maintenance of cerebellar structure in humans.
It was found in a muscle biopsy of an ARCA-1 patient that fewer myonuclei come to lie beneath the neuromuscular junction, although this has no consequences clinically, electrophysiologically, or ultrastructurally. We expect that this disease will be a common cause of middle-age onset recessive ataxia worldwide.
In the present paper, we report 2 novel mutations, also leading to premature termination of the protein, and define the full clinical and molecular spectrum of ARCA-1.
For mutation screening, a set of 154 PCR primer pairs were designed from genomic DNA to amplify each exon of the SYNE1 gene, including the flanking splice sites and the untranslated regions (66).
SYNE-1 is part of the spectrin family of structural proteins that share a common function of linking the plasma membrane to the actin cytoskeleton.


Products were PCR-amplified, checked on agarose gels, and then sequenced using the forward primers for all of the amplicons.Each fragments containing mutations were PCR-amplified a second time and sequenced with the reverse primer in order to confirm that the identified mutations are not due to PCR artefact. This family also includes dystrophin (Duchenne and Becker muscular dystrophies)(72), SPTBN2 (Spinocerebellar ataxia type 5 ) (73), PLEKHG4 (16q-Autosomal dominant cerebellar ataxia) (74) and Spnb4 (75). Sensory examination was normal to pain, temperature, vibration, proprioception, and light touch. Holmesa€™ type of hereditary ataxia (76) was described a century ago (1907) in a family of eight siblings, with four of them presenting with middle-age onset dysarthria, ataxia and hypogonadism (not present in ARCA-1).
There was significant dysmetria on finger-to-nose and heel-to-shin, as well as cerebellar hypotonia (Holmesa€™ sign) in the upper limbs. The inheritance pattern was most likely autosomal recessive, since the parents were not affected. Magnetic resonance imaging revealed diffuse cerebellar atrophy and nerve conduction studies were normal. Autopsy of one affected case showed diffuse cerebellar atrophy with no pontine or olivary involvement. To our knowledge, no linkage or gene defect responsible for this type of ataxia has been reported as yet. Over time, all patients develop significant dysarthria and ataxia, with other associated features such as dysmetria, brisk lower extremity tendon reflexes, and minor abnormalities in saccade and smooth pursuit. None of the subjects evaluated showed extrapyramidal signs, cognitive loss, retinopathy, cardiomyopathy, sensory abnormalities, or autonomic disturbances. ARSACS patients exhibit early onset signs of spasticity in the lower limbs usually observed at gait initiation (12-18 months) (28).
The clinical picture noticed by parents from early childhood is always that of a gait ataxia with a tendency to fall.
Nerve conduction studies performed on 22 affected individuals were always normal, showing therefore no sign of a peripheral sensory or motor neuropathy in this disease.
Single-fiber electromyography was also normal when performed on one subject, suggesting preserved function at the neuromuscular junction. It is characterized mainly by cerebellar atrophy, axonal sensory-motor neuropathy and elevated serum I±-fetoprotein (77). The main differences clinically between these other recessive ataxias common in Quebec and ARCA-1 is the earlier age of onset, the higher degree of disability, and the associated peripheral neuropathy. Of interest, 16q-Autosomal Dominant Cerebellar Ataxia is characterized by an age of onset >55 years and sensorineuroral hearing impairment (74), which is different from what we found in ARCA-1.
However, there are similarities in that it is also a relatively pure cerebellar syndrome caused by mutations in PLEKHG4, also part of the spectrin family of structural proteins. On pathology, 16q-Autosomal dominant cerebellar ataxia shows peculiar degeneration of Purkinje cells that undergo shrinkage and are surrounded by amorphous material. Spinocerebellar Ataxia type 5 is characterized by a slowly progressive cerebellar syndrome beginning mostly in the third decade (78), (79). Symptom progression is slow, and all patients remain ambulatory despite disease duration of up to 30 years. Again, this other ataxia caused by mutations in a spectrin family protein shows striking similarities with ARCA-1 in terms of the predominant cerebellar involvement, middle-age onset, relatively slow progression, and moderate degree of disability. In conclusion, ARCA-1, Spinocerebellar Ataxia type 5 and 16q-Autosomal Dominant Cerebellar Ataxia taken together allow us to define a new category of hereditary ataxias related to the spectrin family of structural proteins.
Despite significant genetic heterogeneity, this category of ataxia shares many common clinical features.
We expect that this new category of inherited ataxias may be more frequent than previously thought, mainly through the contribution of ARCA-1, since we have encountered important genetic heterogeneity even within a homogeneous founder population. We speculate that a significant proportion of yet undiagnosed recessive or a€?sporadica€? ataxias may be due to SYNE1 mutations, which would have great repercussions on our ability to diagnose more precisely these ataxia types in specialized clinics worldwide.ACKNOWLEDGEMENTSThis work was supported by the National Ataxia Foundation (Funding), the Canadian Genetic Disease Network (Funding), the Canadian Institute of Health Research (Scholarships of FGL and ND) and the Association des Ataxies Familiales (Scholarship of DV). France Gosselin and Madeleine Plante performed blood collection of patients and obtained their consent.



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