Search Criteria: Research Area is "Neurobiology Research: Parkinson's Disease: synuclein mutants"

Additional Register Interest Strains

JAX® Mice Strains

Stock
Number
Strain Name
 
Strain Description
Standard Supply
024338 B6.Cg-Sncatm1Rosl Tg(SNCA*A30P)192Rwm/J
Repository- Live
The A30P mutation of the human SNCA gene has been linked to familial Parkinsonís disease. These mutant mice carry a transgene containing a human SNCA gene with the A30P mutation and a knock out allele of the mouse Snca gene. Western blot analysis of brain tissue reveals human α-synuclein protein at levels significantly lower than endogenous wildtype C57BL/6 mouse α-synuclein protein levels. The transgene expression pattern is similar to the endogenous mouse Snca expression pattern. The transgene was detected at a single site of integration near the telomere on one copy of chromosome 15 by fluorescence in situ hybridization analysis. Electrically evoked dopamine release is reduced in the striatal caudate putamen, but not in the nucleus accumbens, of SNCA-A30P mice, when compared to Snca KO mice. Mutant mice exhibit increased anxiety with age and an increase in activity during the dark phase of a 12 hour- 12 hour light-dark cycle. Mice .....
For more information please see the full phenotype on the strain data sheet
006823 B6.Cg-Tg(Prnp-SNCA*A53T)23Mkle/J
Repository- Live
The donating investigator reports that homozygous mice are not viable. Mice hemizygous for the MoPrP-Hualpha-Syn(A53T) transgene are viable and fertile, but the donating investigator reports that female carriers do not breed well. These Hualpha-Syn(A53T) mice (also called G2-3(A53T), Hualpha-Syn(A53T), PrPsynA53T, or A53TαS Tg mice [line G2-3(A53T)]) express the familial Parkinson's disease-associated A53T missense mutant form of human alpha-synuclein (alpha-Syn or αS). Northern blot analysis shows high transgene expression in brain tissues is directed primarily to the hindbrain by the mouse prion protein promoter. Transgenic mice from line G2-3(A53T) express the A53T mutant alpha-Syn protein at approximately six times the level of endogenous mouse alpha-Syn. Hemizygous mice spontaneously develop adult-onset neurodegenerative disease between 9-16 months of age (mean age of onset is approximately 13 months, approximately 90% penetrant), with a progressive motoric dysfunction .....
For more information please see the full phenotype on the strain data sheet
003692 B6;129X1-Sncatm1Rosl/J
Repository- Live
Homozygous null mice are viable, fertile, normal in size and do not display any gross abnormalities. No gene product (mRNA or protein) is detected in brain tissue. A wild-type complement of dopamine neurons, fibers and synaptic terminals is present and the overall brain architecture appears to be intact. They suffer from a reduction in total striatal dopamine and exhibit an attenuated locomotor response when given amphetamine. Normal dopamine release is observed upon stimulation of the nigrostriatal terminal with a single electrical pulse. When multiple stimuli are applied however, null mice exhibit an accelerated recovery of dopamine release. A similar acceleration is seen in wildtype mice in the presence of increased extracellular calcium. The phenotype observed in homozygous Snca-null mice suggests that Snca is an activity-dependent negative regulator of dopamine neurotransmission.
004479 B6;C3-Tg(Prnp-SNCA*A53T)83Vle/J
Repository- Live
Mice homozygous for the transgenic insert are viable and normal in size. These transgenic mice express human A53T variant alpha-synuclein (full-length, 140 amino acid isoform) under the direction of the mouse prion protein promoter. At eight months of age, some homozygous mice develop a progressively severe motor phenotype. Presentation of the phenotype may manifest at 14-15 months of age (on average). Lax grooming, weight loss and diminished mobility precede movement impairment, partial limb paralysis, trembling and inability to stand. Immunohistochemistry analysis of mutants between eight to 12 months of age reveals widely distributed alpha-synuclein inclusions, with dense accumulation in the spinal cord, brainstem, cerebellum and thalamus. The appearance of alpha-synuclein aggregate inclusions parallels the onset of the motor impairment phenotype. Axons and myelin sheaths exhibit progressive ultrastructural degeneration. Immunoelectron microscopy and biochemical analysis show the in .....
For more information please see the full phenotype on the strain data sheet
008239 C57BL/6J-Tg(Th-SNCA*A30P*A53T)39Eric/J
Repository- Live
These hm2α-SYN-39 mice express a doubly-mutant form of human alpha-synuclein (hα-SYN) containing the A30P and A53T human mutations associated with autosomal dominant Parkinson's disease, under the control of the rat tyrosine hydroxylase promoter. Expression of hα-SYN is detected in cell bodies, axons, and terminals of the nigrostriatal system (mRNA expression in midbrain, eye, and adrenal gland, with high levels of protein expression in the cell bodies of dopaminergic neurons in the midbrain and striatum). Hemizygous mice exhibit several Parkinson's disease-related characteristics including increased density of the dopamine transporter, impairments of the ubiquitin-proteasome system, and age-related progressive loss of locomotor activity and substantia nigra pars compacta dopaminergic neurons. The Parkinson's disease-related phenotype of hm2α-SYN-39 mice is more severe than that of the control strain (hwα-SYN-5, see Stock .....
For more information please see the full phenotype on the strain data sheet
016123 C57BL/6N-Sncatm1Mjff/J
Repository- Live
These mice carry a targeted mutation of the Snca (synuclein, alpha) gene. Mice that are homozygous for the targeted mutation are viable and fertile. Expression of the targeted mutation allele has not been examined. Mutations in human SNCA that result in aberrant polymerization and fibrillar aggregations are associated with neurodegenerative synucleinopathies, such as Alzheimer's and Parkinson's diseases.
016936 C57BL/6N-Tg(Thy1-SNCA)12Mjff/J
Repository- Live
mThy1-hSNCA transgenic mice have the mouse thymus cell antigen 1 (Thy-1) promoter directing expression of the human α-synuclein (SNCA) gene. Hemizygotes are viable, fertile, and normal in size. This line carries ~23 copies of the transgene; expression is relatively high in the cerebral cortex and hippocampus, and relatively low in the kidneys. These mice may be useful for studying the Parkinson's disease pathogenesis and neurodegeneration elicited by the toxic effects of aggregation and somatic accumulation of SNCA.

There is a different founder line with the same construct available, stock number 17682, which has about 2-fold higher expression of the transgenic protein in the striatum and cortex.

017682 C57BL/6N-Tg(Thy1-SNCA)15Mjff/J
Repository- Live
mThy1-hSNCA transgenic mice express the human α-synuclein gene under the direction of the mouse thymus cell antigen 1 promoter. Hemizygotes are viable, fertile, and normal in size. This line carries 1-2 copies of the transgene. These mice may be useful for studying Parkinson's disease pathogenesis and neurodegeneration elicited by the toxic effects of aggregation and somatic accumulation of SNCA.
010710 FVB;129S6-Sncatm1Nbm Tg(SNCA)1Nbm/J
Repository- Live
These PAC-Tg(SNCAWT);Snca-/- mice are viable and fertile, harboring a Snca knockout allele and a transgene encoding the human α-synuclein. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by human α-synuclein from the two total insertions of the PAC-Tg(SNCAWT). While brain RNA expression of SNCAWT is more than 50-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAWT are ~100-fold greater than normal endogenous mouse α-synuclein. PAC-Tg(SNCAWT);Snca-/- mice do not show any enteric nervous system abnormalities or widespread α-synuclein aggregation in brain or colon. No detectable motor behavior impairments, autonomic abnormalities, olfactory dysfunction, dopaminergic deficits, Lewy body inclusions or neurodegeneration are .....
For more information please see the full phenotype on the strain data sheet
010799 FVB;129S6-Sncatm1Nbm Tg(SNCA*A53T)1Nbm Tg(SNCA*A53T)2Nbm/J
Repository- Live
These double transgenic homozygous mice (dbl-PAC-Tg(SNCAA53T);Snca-/- mice) are viable and fertile, harboring a Snca knockout allele and two independently inserted transgenes encoding the human A53T-mutant α-synuclein associated with autosomal dominant Parkinson's disease. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by α-synuclein*A53T from the four total insertions of the PAC-Tg(SNCAA53T). While brain RNA expression of SNCAA53T is ~10-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAA53T are ~80-fold greater than normal endogenous mouse α-synuclein. By three months of age, dbl-PAC-Tg(SNCAA53T);Snca-/- mice show robust abnormalities in enteric nervous system function (impaired colonic motility [males only] and prolonge .....
For more information please see the full phenotype on the strain data sheet
017000 STOCK Tg(SNCA*E46K)3Elan/J
Repository- Live
These transgenic mice express the mutant human SNCA, synuclein, alpha (non A4 component of amyloid precursor), with the E46K mutation in exon 3. Mice hemizygous for the transgenic insert are viable, fertile, and normal in size. Transgenic mice accumulate alpha synuclein and develop age-dependent dopaminergic (TH) fiber degeneration. Hemizygous mice display the loss of striatal tyrosine hydroxylase positive fibers by 6 months of age. The Donating Investigator recommends avoiding crossing to C57BL/6J because the Nnt deletion may have an effect on phenotype. This allele is also available on a congenic C57BL/6NJ background, which does not carrying the Nnt, see stock number 18768.
023837 B6.Cg-Tg(SNCA)OVX37Rwm Sncatm1Rosl/J
Under Development - Now Accepting Orders
These mutant mice carry a transgene containing human SNCA gene and a knock out allele of the mouse Snca gene. Human α-synuclein protein levels in the striatum of mutant mice is 1.9-fold higher than levels of endogenous mouse α-synuclein protein. Transgene expression is detected in the striatum (caudate putamen and nucleus accumbens). Mice that are homozygous for the targeted mutation and the transgene are viable and fertile. Male mice have an increased dry stool weight. SNCA-OVX mice, aged 18 months, exhibit age-related impairment of motor coordination, and loss of nigrostriatal dopamine neurons. Diminishment of motor coordination and firing rate of dopamine neurons of the substantia nigra pars compacta is age-dependent. Dopamine transmission in the dorsal striatum is reduced as early as 3-4 months of age. The transgene was detected at a single site of integration near the centromere of chromosome 4 by fluorescence in situ hybridization analysis.
008133 B6.129-Sncbtm1Sud/J
Cryopreserved - Ready for recovery
These mice possess loxP sites on either side of exon 2 of the targeted gene. Mice that are homozygous for this allele are viable, normal in size and do not display any gross physical or behavioral abnormalities, but breed very poorly. Protein levels are normal.

When bred to a strain expressing Cre recombinase, this mutant mouse strain may be useful in studies of presynaptic proteins and synaptic vesicles.

008843 B6.129P2-Sncgtm1Vlb/J
Cryopreserved - Ready for recovery
Mice homozygous for this γ-synuclein mutant allele are viable and fertile with no obvious abnormalities in development, behavior, or gross morphology of the nervous system. No RNA or protein expression from the targeted gene is observed. Slight upregulation of β-synuclein is reported in the midbrain of homozygous mice. Homozygous mice are also resistant to the inflammatory/apoptotic Parkinson's disease-like pathology that results following MPTP neurotoxin administration (the active form of which (MPP+) gains entry into dopaminergic cells via the dopamine transporter (DAT)). These γ-synuclein mutant mice may be useful in studying synuclein function in neurodegenerative diseases, such as Parkinson's disease.
012265 B6.Cg-Tg(THY1-SNCA*A30P)TS2Sud/J
Cryopreserved - Ready for recovery
The A30P mutation in this transgenic strain is associated with the development of familial Parkinson's disease. The onset of hind limb mobility problems occurs around 12 months of age (sometimes earlier), induced by a loss of motor neurons and associated with the formation of insoluble alpha synuclein aggregates. This strain may be useful in studies of Parkinson's disease. Hemizygous mice are viable and fertile.
008859 B6.Cg-Tg(THY1-SNCA*A53T)F53Sud/J
Cryopreserved - Ready for recovery
These mice are transgenic for the A53T mutation of the human SNCA (synuclein, alpha) gene under the control of a human THY1 (thymus cell antigen 1, theta) promoter. Hemizygotes are viable and fertile and develop a Parkinson-like phenotype upon aging. Hind limb paralysis due to loss of motor neurons and a resting tremor are initially seen at about eight months of age. No Lewy body-like pathology is noted. Cell death in the spinal cord (extensive) and brain are observed. Expression of the transgene is 10-fold increased in the brain and 20-fold in the spinal cord.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become availa .....
For more information please see the full phenotype on the strain data sheet

008135 B6.Cg-Tg(THY1-SNCA*A53T)M53Sud/J
Cryopreserved - Ready for recovery
Hemizygous transgenic mice are viable and fertile and develop a Parkinson-like phenotype upon aging. Hind limb paralysis due to loss of motor neurons and a resting tremor are initially seen at about six months of age. No Lewy body-like pathology is noted. Cell death in the spinal cord (extensive) and brain are observed.
008883 B6;129-Gt(ROSA)26Sortm1(SNCA*A53T)Djmo/TmdJ
Cryopreserved - Ready for recovery
Homozygous ROSA26-Syn-A53T mice are viable and fertile, with the familial Parkinson's disease-associated A53T missense mutant form of human alpha-synuclein (human A53T α-Syn or SYNA53T) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of human A53T α-Syn is blocked by an upstream loxP-flanked STOP sequence (in the absence of Cre recombinase, no human A53T α-Syn protein is observed in brain regions). When bred to cre expressing mice, the STOP sequence is deleted in the tissues of offspring where Cre recombinase is present; resulting in human A53T α-Syn expression. In particular, Stock No. 008601 B6.Cg-Tg(Th-cre)1Tmd/J may be useful for this application. These ROSA26-Syn-A53T mice allow inducible expression of a human mutation associated with familial Parkinson's disease and may be useful for studying the progressive dopaminergic neurodegeneration of Parkinson's dise .....
For more information please see the full phenotype on the strain data sheet
008889 B6;129-Gt(ROSA)26Sortm2(SNCA*119)Djmo/TmdJ
Cryopreserved - Ready for recovery
Homozygous ROSA26-Syn119 mice are viable and fertile, with the familial Parkinson's disease-associated Syn119 C-terminal truncation of human alpha-synuclein (human α-Syn119 or SynCT119) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of human α-Syn119 is blocked by an upstream loxP-flanked STOP sequence (in the absence of Cre recombinase, no human α-Syn119 protein is observed in brain regions). When bred to cre expressing mice, the STOP sequence is deleted in the tissues of offspring where Cre recombinase is present; resulting in human α-Syn119 expression. In particular, Stock No. 008601 B6.Cg-Tg(Th-cre)1Tmd/J may be useful for this application. These ROSA26-Syn119 mice allow inducible expression of a human mutation associated with familial Parkinson's disease and may be useful for studying the progressive dopaminergic neurodegeneration of Parkinson's disease and .....
For more information please see the full phenotype on the strain data sheet
008886 B6;129-Gt(ROSA)26Sortm3(SNCA*E46K)Djmo/TmdJ
Cryopreserved - Ready for recovery
Homozygous ROSA26-Syn-E46K mice are viable and fertile, with the E46K missense mutant form of human alpha-synuclein (human E46K α-Syn or SYNE46K; associated with familial Parkinson's disease, dementia, and visual hallucinations) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of human E46K α-Syn is blocked by an upstream loxP-flanked STOP sequence (in the absence of Cre recombinase, no human E46K α-Syn protein is observed in brain regions). When bred to cre expressing mice, the STOP sequence is deleted in the tissues of offspring where Cre recombinase is present; resulting in human E46K α-Syn expression. In particular, Stock No. 008601 B6.Cg-Tg(Th-cre)1Tmd/J may be useful for this application. These ROSA26-Syn-E46K mice allow inducible expression of a human mutation associated with familial Parkinson's disease, dementia, and visual hallucinations and may be usefu .....
For more information please see the full phenotype on the strain data sheet
006390 B6;129-Sncatm1Sud Sncbtm1.1Sud/J
Cryopreserved - Ready for recovery
Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. No protein product from these targeted genes is detected in brain tissue. Overall brain morphology and structure appears normal. No significant changes in the ultrastructure, short- or long-term synaptic plasticity, or in the pool size or replenishment of recycling synaptic vesicles is detected. Dopamine levels in the double targeted mice are decreased by approximately 20%, but dopamine uptake and release from isolated nerve terminals is normal. Serotonin levels are unchanged. This mutant mouse strain represents a model that may be useful in studies of synaptic function and neurodegenerative disease.
012450 B6;D2-Tg(tetO-SNCA)1Cai/J
Cryopreserved - Ready for recovery
Mice hemizygous for the human synuclein (alpha-syn) transgene, (SNCA) are viable and fertile. Expression of the transgene is regulated by the tetracycline operator (tetO); also called tetracycline-responsive element (TRE, TetRE) or tet-operator). When mated to a strain expressing tetracycline-controlled transactivator protein (tTA), expression of the SNCA protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. The formation of alpha-syn aggregates is a key step in the pathogenesis of Parkinson's disease. These aggregates cause formation of fibrillar aggregates causing various forms of cytotoxicity, including impairment of proteasomal and lysosomal activities, disruption of ER-Golgi traffic and microtubule-based transport, and dysfunction of mitochondria. SNCA mice develop age-dependent, progressive neurodegeneration. These mice may be useful for studying the Parkinson's disease pathogenesis and n .....
For more information please see the full phenotype on the strain data sheet
008473 B6;SJL-Tg(THY1-SNCA*A30P)M30Sud/J
Cryopreserved - Ready for recovery
The A30P mutation in this transgenic strain is associated with the development of familial Parkinson's disease. The onset of hind limb mobility problems and a resting tremor phenotype occur around 10 months of age due to a loss of motor neurons. No Lewy body-like pathology has been observed. Extensive cell death in the spinal cord and brain are seen. This strain may be useful in studies of Parkinson's disease. Expression of the transgene is 5-fold higher in the brain and 10-fold higher in the spinal cord. Hemizygous mice are viable and fertile, and survive to approximately 14 months of age.
008134 B6;SJL-Tg(THY1-SNCA*A30P)TS2Sud/J
Cryopreserved - Ready for recovery
The A30P mutation in this transgenic strain is associated with the development of familial Parkinson's disease. The onset of hind limb mobility problems occurs around 12 months of age (sometimes earlier), induced by a loss of motor neurons and associated with the formation of insoluble alpha synuclein aggregates. This strain may be useful in studies of Parkinson's disease. Hemizygous mice are viable and fertile.
016976 B6C3-Tg(tetO-SNCA*A53T)33Vle/J
Cryopreserved - Ready for recovery
Mice hemizygous for the human synuclein (α-SYN) mutant transgene, (SNCA*A53T) are viable and fertile. Expression of SNCA*A53T is regulated by the tetracycline operator (tetO); also called tetracycline-responsive element (TRE, TetRE) or tet-operator). When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of SNCA*A53T protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. α-syn is localized mainly in synapses where it regulates synaptic transmission, neuronal plasticity, synaptic vesicle release, and protein folding. Mutations in α-syn cause autosomal dominantly inherited familial Parkinson's disease (PD) by accelerating the formation of fibrillar aggregates causing various forms of cytotoxicity, including impairment of proteasomal and lysosomal activities, disruption of ER-Golgi traffic and microtubule-based transport, a .....
For more information please see the full phenotype on the strain data sheet
018768 B6N.Cg-Tg(SNCA*E46K)3Elan/J
Cryopreserved - Ready for recovery
These transgenic mice express the mutant human SNCA, synuclein, alpha (non A4 component of amyloid precursor), with the E46K mutation in exon 3. Mice hemizygous for the transgenic insert are viable, fertile, and normal in size. Transgenic mice accumulate alpha synuclein and develop age-dependent dopaminergic (TH) fiber degeneration. The Donating Investigator recommends avoiding crossing to C57BL/6J because the Nnt deletion may have an effect on phenotype.
008389 C57BL/6-Tg(THY1-SNCA)1Sud/J
Cryopreserved - Ready for recovery
This transgenic strain carries a human THY1 promoter driving expression of the human synuclein, alpha (SNCA) gene. Levels of expression show a 5-fold increase in the brain and a 10-fold increase in the spinal cord. Hemizygotes are viable and fertile and unlike some similar mutant transgenic lines, do not display any Parkinson-like phenotype upon aging.
012769 C57BL/6-Tg(Thy1-Sncg)HvP36Putt/J
Cryopreserved - Ready for recovery
Thy1mγSN transgenic mice have the mouse thymus cell antigen 1 (Thy-1) promoter directing expression of the mouse γ-synuclein (Sncg) gene. Homozygous Thy1mγSN mice are viable, fertile, and normal in size. They develop a clasping reflex, abnormal posture and gait, and other symptoms of motor dysfunction around 6 months of age, develop limb paralysis by 9 months of age, and die by 16 months of age. Homozygotes also show a 7-fold increase of γ-synuclein mRNA in neurons compared with wild-type mice, leading to motor neuron impairment and premature death. Hemizygous mice develop this phenotype starting at 12 months of age. γ-synuclein aggregates form fibrils, much like α-synuclein, aggregates of which have been associated with neurodegeneration in diseases such as Parkinson's disease. These mice may be useful for studying the pathophysiology of Parkinson's disease, and other neurodegenerative disorders.
008245 C57BL/6J-Tg(Th-SNCA)5Eric/J
Cryopreserved - Ready for recovery
These hwα-SYN-5 mice express wildtype human alpha-synuclein (hα-SYN) under the control of the rat tyrosine hydroxylase promoter. Expression of hα-SYN is detected in cell bodies, axons, and terminals of the nigrostriatal system (mRNA expression in midbrain, eye, and adrenal gland, with high levels of protein expression in the cell bodies of dopaminergic neurons in the midbrain and striatum). Hemizygous mice exhibit several Parkinson's disease-related characteristics including increased density of the dopamine transporter, impairments of the ubiquitin-proteasome system, and age-related progressive loss of locomotor activity and substantia nigra pars compacta dopaminergic neurons. The Parkinson's disease-related phenotype of these hwα-SYN-5 mice is intermediate between that of the C57BL/6J wild-type controls and the severely affected hm2α-SYN-39 strain (see Stock No. 008239). As such, these h .....
For more information please see the full phenotype on the strain data sheet
017678 FVB;129-Pink1tm1Aub Tg(Prnp-SNCA*A53T)AAub/J
Cryopreserved - Ready for recovery
These double mutant mice overexpress the mutant A53T human SNCA, synuclein, alpha (non A4 component of amyloid precursor), and are deficient in endogenous mouse Pink1, PTEN induced putative kinase 1. Mice that are homozygous for both the transgene and the Pink1tm1Aub allele develop a behavior phenotype at 3 months of age, consisting of impaired spontaneous locomotion in open field tests for horizontal and vertical activity. This behaviour deficit appears much later also in the single mutant mice. In addition, the brain transcriptome profile in striatum of homozygous double mutants shows many consistent early alterations in the pathways of trophic signaling to mitochondria and apoptosis, which are not apparent in the transcriptome profiles of single mutants.
017744 FVB;129-Tg(Prnp-SNCA*A53T)AAub/J
Cryopreserved - Ready for recovery
These transgenic mice express the mutant A53T human alpha-synuclein (SNCA) under the direction of the mouse prion protein promoter in nigrostriatal and corticostriatal projection neurons, but not local striatal neurons. The A53T mutation is associated with early onset familial Parkinson's disease. Transgene expression levels are 1.5-2 fold greater than endogenous mouse gene expression levels. Homozygotes older than 6 months of age display progressively spontaneous vertical movement (rearing). At 7 months of age, dense alpha-synuclein immunoreactive resembling Lewy neurites is detected in the olfactory bulb. Ultrastructural examination of neurons reveals diffuse accumulation of human alpha-synuclein. A53T SCNA protein is detected in neuronal axons, dendrites, cell bodies, and nuclei throughout the CNS by immunohistochemical analysis (including: olfactory bulb, cerebral cortex, hippocampus, midbrain, pons, medulla oblongata). Mice 18 months of age and older display insoluble a .....
For more information please see the full phenotype on the strain data sheet
010788 FVB;129S6-Sncatm1Nbm Tg(SNCA*A30P)1Nbm Tg(SNCA*A30P)2Nbm/J
Cryopreserved - Ready for recovery
These double transgenic homozygous mice (dbl-PAC-Tg(SNCAA30P);Snca-/- mice) are viable and fertile, harboring a Snca knockout allele and two independently inserted transgenes encoding the human A30P-mutant α-synuclein associated with autosomal dominant Parkinson's disease. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by α-synuclein*A30P from the PAC-Tg(SNCAA30P). Because PAC-Tg(SNCAA30P) line 1 inserted on the X chromosome and line 2 inserted on a somatic chromosome, homozygous females have four total insertions and homozygous males have three total insertions. While brain RNA expression of SNCAA30P is more than 10-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAA30P are ~80-fold greater than normal endogenous mouse α-synuclein. .....
For more information please see the full phenotype on the strain data sheet
008474 STOCK Tg(THY1-SNCA*A53T)F53Sud/J
Cryopreserved - Ready for recovery
These mice are transgenic for the A53T mutation of the human SNCA (synuclein, alpha) gene under the control of a human THY1 (thymus cell antigen 1, theta) promoter. Hemizygotes are viable and fertile and develop a Parkinson-like phenotype upon aging. Hind limb paralysis due to loss of motor neurons and a resting tremor are initially seen at about eight months of age. No Lewy body-like pathology is noted. Cell death in the spinal cord (extensive) and brain are observed. Expression of the transgene is 10-fold increased in the brain and 20-fold in the spinal cord.
008132 STOCK Tg(THY1-Snca)M1mSud/J
Cryopreserved - Ready for recovery
Mice hemizygous for this transgene are viable and fertile and do not display any gross physical or behavioral abnormalities, even upon aging. This strain may be useful in studies of presynaptic proteins and synaptic vesicles.
012442 STOCK Tg(tetO-SNCA*A53T)E2Cai/J
Cryopreserved - Ready for recovery
Mice hemizygous for the human synuclein (alpha-syn) mutant transgene, (SNCA*A53T) are viable and fertile. Expression of SNCA*A53T is regulated by the tetracycline operator (tetO); also called tetracycline-responsive element (TRE, TetRE) or tet-operator). When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of SNCA*A53T protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. Mutations in alpha-syn greatly accelerate the formation of fibrillar aggregates causing various forms of cytotoxicity, including impairment of proteasomal and lysosomal activities, disruption of ER-Golgi traffic and microtubule-based transport, and dysfunction of mitochondria. SNCA*A53T mice develop age-dependent, progressive neurodegeneration. These mice may be useful for studying the Parkinson's disease pathogenesis and neurodegeneration elicited by the toxic effec .....
For more information please see the full phenotype on the strain data sheet

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Stock
Number
Strain Name
 
Strain Description
Standard Supply
025533C57BL/6N-Sncatm1Mjff Tg(Thy1-SNCA)15Mjff/J
In Progress
These double mutant mice carry a targeted mutation for the Snca (synuclein, alpha) gene and a transgene consisting of the human SNCA under the direction of a mouse Thy-1 promoter. Applications exist in studies related to Parkinson's disease and neurodegeneration elicited by the aggregation of SNCA.

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