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Showing 1 to 12 of 791 entries
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Abnormal cortical thickness connectivity persists in childhood absence epilepsy.

Annals of clinical and translational neurology

Curwood EK, Pedersen M, Carney PW, Berg AT, Abbott DF, Jackson GD.
PMID: 26000319
Ann Clin Transl Neurol. 2015 May;2(5):456-64. doi: 10.1002/acn3.178. Epub 2015 Apr 11.

OBJECTIVE: Childhood absence epilepsy (CAE) is a childhood-onset generalized epilepsy. Recent fMRI studies have suggested that frontal cortex activity occurs before thalamic involvement in epileptic discharges suggesting that frontal cortex may play an important role in childhood absence seizures....

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Curwood EK, Pedersen M, Carney PW, et al. Abnormal cortical thickness connectivity persists in childhood absence epilepsy. Ann Clin Transl Neurol. 2015;2(5):456-64doi: 10.1002/acn3.178.
Curwood, E. K., Pedersen, M., Carney, P. W., Berg, A. T., Abbott, D. F., & Jackson, G. D. (2015). Abnormal cortical thickness connectivity persists in childhood absence epilepsy. Annals of clinical and translational neurology, 2(5), 456-64. https://doi.org/10.1002/acn3.178
Curwood, Evan K, et al. "Abnormal cortical thickness connectivity persists in childhood absence epilepsy." Annals of clinical and translational neurology vol. 2,5 (2015): 456-64. doi: https://doi.org/10.1002/acn3.178
Curwood EK, Pedersen M, Carney PW, Berg AT, Abbott DF, Jackson GD. Abnormal cortical thickness connectivity persists in childhood absence epilepsy. Ann Clin Transl Neurol. 2015 May;2(5):456-64. doi: 10.1002/acn3.178. Epub 2015 Apr 11. PMID: 26000319; PMCID: PMC4435701.
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A second trigeminal CGRP receptor: function and expression of the AMY1 receptor.

Annals of clinical and translational neurology

Walker CS, Eftekhari S, Bower RL, Wilderman A, Insel PA, Edvinsson L, Waldvogel HJ, Jamaluddin MA, Russo AF, Hay DL.
PMID: 26125036
Ann Clin Transl Neurol. 2015 Jun;2(6):595-608. doi: 10.1002/acn3.197. Epub 2015 Apr 01.

OBJECTIVE: The trigeminovascular system plays a central role in migraine, a condition in need of new treatments. The neuropeptide, calcitonin gene-related peptide (CGRP), is proposed as causative in migraine and is the subject of intensive drug discovery efforts. This...

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Walker CS, Eftekhari S, Bower RL, et al. A second trigeminal CGRP receptor: function and expression of the AMY1 receptor. Ann Clin Transl Neurol. 2015;2(6):595-608doi: 10.1002/acn3.197.
Walker, C. S., Eftekhari, S., Bower, R. L., Wilderman, A., Insel, P. A., Edvinsson, L., Waldvogel, H. J., Jamaluddin, M. A., Russo, A. F., & Hay, D. L. (2015). A second trigeminal CGRP receptor: function and expression of the AMY1 receptor. Annals of clinical and translational neurology, 2(6), 595-608. https://doi.org/10.1002/acn3.197
Walker, Christopher S, et al. "A second trigeminal CGRP receptor: function and expression of the AMY1 receptor." Annals of clinical and translational neurology vol. 2,6 (2015): 595-608. doi: https://doi.org/10.1002/acn3.197
Walker CS, Eftekhari S, Bower RL, Wilderman A, Insel PA, Edvinsson L, Waldvogel HJ, Jamaluddin MA, Russo AF, Hay DL. A second trigeminal CGRP receptor: function and expression of the AMY1 receptor. Ann Clin Transl Neurol. 2015 Jun;2(6):595-608. doi: 10.1002/acn3.197. Epub 2015 Apr 01. PMID: 26125036; PMCID: PMC4479521.
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HIF-1α Mediates Isoflurane-Induced Vascular Protection in Subarachnoid Hemorrhage.

Annals of clinical and translational neurology

Milner E, Johnson AW, Nelson JW, Harries MD, Gidday JM, Han BH, Zipfel GJ.
PMID: 25909079
Ann Clin Transl Neurol. 2015 Apr;2(4):325-37. doi: 10.1002/acn3.170. Epub 2015 Feb 21.

OBJECTIVE: Outcome after aneurysmal subarachnoid hemorrhage (SAH) depends critically on delayed cerebral ischemia (DCI) - a process driven primarily by vascular events including cerebral vasospasm, microvessel thrombosis, and microvascular dysfunction. This study sought to determine the impact of postconditioning...

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Milner E, Johnson AW, Nelson JW, et al. HIF-1α Mediates Isoflurane-Induced Vascular Protection in Subarachnoid Hemorrhage. Ann Clin Transl Neurol. 2015;2(4):325-37doi: 10.1002/acn3.170.
Milner, E., Johnson, A. W., Nelson, J. W., Harries, M. D., Gidday, J. M., Han, B. H., & Zipfel, G. J. (2015). HIF-1α Mediates Isoflurane-Induced Vascular Protection in Subarachnoid Hemorrhage. Annals of clinical and translational neurology, 2(4), 325-37. https://doi.org/10.1002/acn3.170
Milner, Eric, et al. "HIF-1α Mediates Isoflurane-Induced Vascular Protection in Subarachnoid Hemorrhage." Annals of clinical and translational neurology vol. 2,4 (2015): 325-37. doi: https://doi.org/10.1002/acn3.170
Milner E, Johnson AW, Nelson JW, Harries MD, Gidday JM, Han BH, Zipfel GJ. HIF-1α Mediates Isoflurane-Induced Vascular Protection in Subarachnoid Hemorrhage. Ann Clin Transl Neurol. 2015 Apr;2(4):325-37. doi: 10.1002/acn3.170. Epub 2015 Feb 21. PMID: 25909079; PMCID: PMC4402079.
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Progressive decline of glucocerebrosidase in aging and Parkinson's disease.

Annals of clinical and translational neurology

Rocha EM, Smith GA, Park E, Cao H, Brown E, Hallett P, Isacson O.
PMID: 25909088
Ann Clin Transl Neurol. 2015 Apr;2(4):433-8. doi: 10.1002/acn3.177. Epub 2015 Feb 06.

The principal risk factor for developing most adult onset neurodegenerative diseases is aging, with incidence rising significantly after age 50. Despite research efforts, the causes of Parkinson's disease (PD) remain unknown. As neurons age, they show signs of diminished...

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Rocha EM, Smith GA, Park E, et al. Progressive decline of glucocerebrosidase in aging and Parkinson's disease. Ann Clin Transl Neurol. 2015;2(4):433-8doi: 10.1002/acn3.177.
Rocha, E. M., Smith, G. A., Park, E., Cao, H., Brown, E., Hallett, P., & Isacson, O. (2015). Progressive decline of glucocerebrosidase in aging and Parkinson's disease. Annals of clinical and translational neurology, 2(4), 433-8. https://doi.org/10.1002/acn3.177
Rocha, Emily M, et al. "Progressive decline of glucocerebrosidase in aging and Parkinson's disease." Annals of clinical and translational neurology vol. 2,4 (2015): 433-8. doi: https://doi.org/10.1002/acn3.177
Rocha EM, Smith GA, Park E, Cao H, Brown E, Hallett P, Isacson O. Progressive decline of glucocerebrosidase in aging and Parkinson's disease. Ann Clin Transl Neurol. 2015 Apr;2(4):433-8. doi: 10.1002/acn3.177. Epub 2015 Feb 06. PMID: 25909088; PMCID: PMC4402088.
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Chronic enzyme replacement therapy ameliorates neuropathology in alpha-mannosidosis mice.

Annals of clinical and translational neurology

Damme M, Stroobants S, Lüdemann M, Rothaug M, Lüllmann-Rauch R, Beck HC, Ericsson A, Andersson C, Fogh J, D'Hooge R, Saftig P, Blanz J.
PMID: 26817023
Ann Clin Transl Neurol. 2015 Sep 19;2(11):987-1001. doi: 10.1002/acn3.245. eCollection 2015 Nov.

OBJECTIVE: The lysosomal storage disease alpha-mannosidosis is caused by the deficiency of the lysosomal acid hydrolase alpha-mannosidase (LAMAN) leading to lysosomal accumulation of neutral mannose-linked oligosaccharides throughout the body, including the brain. Clinical findings in alpha-mannosidosis include skeletal malformations,...

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Damme M, Stroobants S, Lüdemann M, et al. Chronic enzyme replacement therapy ameliorates neuropathology in alpha-mannosidosis mice. Ann Clin Transl Neurol. 2015;2(11):987-1001doi: 10.1002/acn3.245.
Damme, M., Stroobants, S., Lüdemann, M., Rothaug, M., Lüllmann-Rauch, R., Beck, H. C., Ericsson, A., Andersson, C., Fogh, J., D'Hooge, R., Saftig, P., & Blanz, J. (2015). Chronic enzyme replacement therapy ameliorates neuropathology in alpha-mannosidosis mice. Annals of clinical and translational neurology, 2(11), 987-1001. https://doi.org/10.1002/acn3.245
Damme, Markus, et al. "Chronic enzyme replacement therapy ameliorates neuropathology in alpha-mannosidosis mice." Annals of clinical and translational neurology vol. 2,11 (2015): 987-1001. doi: https://doi.org/10.1002/acn3.245
Damme M, Stroobants S, Lüdemann M, Rothaug M, Lüllmann-Rauch R, Beck HC, Ericsson A, Andersson C, Fogh J, D'Hooge R, Saftig P, Blanz J. Chronic enzyme replacement therapy ameliorates neuropathology in alpha-mannosidosis mice. Ann Clin Transl Neurol. 2015 Sep 19;2(11):987-1001. doi: 10.1002/acn3.245. eCollection 2015 Nov. PMID: 26817023; PMCID: PMC4693626.
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POLG2 deficiency causes adult-onset syndromic sensory neuropathy, ataxia and parkinsonism.

Annals of clinical and translational neurology

Van Maldergem L, Besse A, De Paepe B, Blakely EL, Appadurai V, Humble MM, Piard J, Craig K, He L, Hella P, Debray FG, Martin JJ, Gaussen M, Laloux P, Stevanin G, Van Coster R, Taylor RW, Copeland WC, Mormont E, Bonnen PE.
PMID: 28078310
Ann Clin Transl Neurol. 2016 Nov 16;4(1):4-14. doi: 10.1002/acn3.361. eCollection 2017 Jan.

OBJECTIVE: Mitochondrial dysfunction plays a key role in the pathophysiology of neurodegenerative disorders such as ataxia and Parkinson's disease. We describe an extended Belgian pedigree where seven individuals presented with adult-onset cerebellar ataxia, axonal peripheral ataxic neuropathy, and tremor,...

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Van Maldergem L, Besse A, De Paepe B, et al. POLG2 deficiency causes adult-onset syndromic sensory neuropathy, ataxia and parkinsonism. Ann Clin Transl Neurol. 2016;4(1):4-14doi: 10.1002/acn3.361.
Van Maldergem, L., Besse, A., De Paepe, B., Blakely, E. L., Appadurai, V., Humble, M. M., Piard, J., Craig, K., He, L., Hella, P., Debray, F. G., Martin, J. J., Gaussen, M., Laloux, P., Stevanin, G., Van Coster, R., Taylor, R. W., Copeland, W. C., Mormont, E., & Bonnen, P. E. (2017). POLG2 deficiency causes adult-onset syndromic sensory neuropathy, ataxia and parkinsonism. Annals of clinical and translational neurology, 4(1), 4-14. https://doi.org/10.1002/acn3.361
Van Maldergem, Lionel, et al. "POLG2 deficiency causes adult-onset syndromic sensory neuropathy, ataxia and parkinsonism." Annals of clinical and translational neurology vol. 4,1 (2017): 4-14. doi: https://doi.org/10.1002/acn3.361
Van Maldergem L, Besse A, De Paepe B, Blakely EL, Appadurai V, Humble MM, Piard J, Craig K, He L, Hella P, Debray FG, Martin JJ, Gaussen M, Laloux P, Stevanin G, Van Coster R, Taylor RW, Copeland WC, Mormont E, Bonnen PE. POLG2 deficiency causes adult-onset syndromic sensory neuropathy, ataxia and parkinsonism. Ann Clin Transl Neurol. 2016 Nov 16;4(1):4-14. doi: 10.1002/acn3.361. eCollection 2017 Jan. PMID: 28078310; PMCID: PMC5221457.
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Corrigendum.

Annals of clinical and translational neurology

[No authors listed]
PMID: 28078317
Ann Clin Transl Neurol. 2017 Jan 09;4(1):71. doi: 10.1002/acn3.391. eCollection 2017 Jan.

[This corrects the article DOI: 10.1002/acn3.307.].

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Corrigendum. Ann Clin Transl Neurol. 2017;4(1):71doi: 10.1002/acn3.391.
(2017). Corrigendum. Annals of clinical and translational neurology, 4(1), 71. https://doi.org/10.1002/acn3.391
"Corrigendum." Annals of clinical and translational neurology vol. 4,1 (2017): 71. doi: https://doi.org/10.1002/acn3.391
Corrigendum. Ann Clin Transl Neurol. 2017 Jan 09;4(1):71. doi: 10.1002/acn3.391. eCollection 2017 Jan. PMID: 28078317; PMCID: PMC5221470.
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Visual pathway neurodegeneration winged by mitochondrial dysfunction.

Annals of clinical and translational neurology

Petzold A, Nijland PG, Balk LJ, Amorini AM, Lazzarino G, Wattjes MP, Gasperini C, van der Valk P, Tavazzi B, Lazzarino G, van Horssen J.
PMID: 25750919
Ann Clin Transl Neurol. 2015 Feb;2(2):140-50. doi: 10.1002/acn3.157. Epub 2014 Dec 17.

OBJECTIVES: To test for structural and functional contribution of mitochondrial dysfunction to neurodegeneration in multiple sclerosis (MS). A visual pathway model void of MS lesions was chosen in order to exclude neurodegeneration secondary to lesion related axonotmesis.METHODS: A single-centre...

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Petzold A, Nijland PG, Balk LJ, et al. Visual pathway neurodegeneration winged by mitochondrial dysfunction. Ann Clin Transl Neurol. 2014;2(2):140-50doi: 10.1002/acn3.157.
Petzold, A., Nijland, P. G., Balk, L. J., Amorini, A. M., Lazzarino, G., Wattjes, M. P., Gasperini, C., van der Valk, P., Tavazzi, B., Lazzarino, G., & van Horssen, J. (2015). Visual pathway neurodegeneration winged by mitochondrial dysfunction. Annals of clinical and translational neurology, 2(2), 140-50. https://doi.org/10.1002/acn3.157
Petzold, Axel, et al. "Visual pathway neurodegeneration winged by mitochondrial dysfunction." Annals of clinical and translational neurology vol. 2,2 (2015): 140-50. doi: https://doi.org/10.1002/acn3.157
Petzold A, Nijland PG, Balk LJ, Amorini AM, Lazzarino G, Wattjes MP, Gasperini C, van der Valk P, Tavazzi B, Lazzarino G, van Horssen J. Visual pathway neurodegeneration winged by mitochondrial dysfunction. Ann Clin Transl Neurol. 2015 Feb;2(2):140-50. doi: 10.1002/acn3.157. Epub 2014 Dec 17. PMID: 25750919; PMCID: PMC4338955.
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Baclofen facilitates sleep, neuroplasticity, and recovery after stroke in rats.

Annals of clinical and translational neurology

Hodor A, Palchykova S, Baracchi F, Noain D, Bassetti CL.
PMID: 25493268
Ann Clin Transl Neurol. 2014 Oct;1(10):765-77. doi: 10.1002/acn3.115. Epub 2014 Oct 14.

OBJECTIVE: Sleep disruption in the acute phase after stroke has detrimental effects on recovery in both humans and animals. Conversely, the effect of sleep promotion remains unclear. Baclofen (Bac) is a known non-rapid eye movement (NREM) sleep-promoting drug in...

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Hodor A, Palchykova S, Baracchi F, et al. Baclofen facilitates sleep, neuroplasticity, and recovery after stroke in rats. Ann Clin Transl Neurol. 2014;1(10):765-77doi: 10.1002/acn3.115.
Hodor, A., Palchykova, S., Baracchi, F., Noain, D., & Bassetti, C. L. (2014). Baclofen facilitates sleep, neuroplasticity, and recovery after stroke in rats. Annals of clinical and translational neurology, 1(10), 765-77. https://doi.org/10.1002/acn3.115
Hodor, Aleksandra, et al. "Baclofen facilitates sleep, neuroplasticity, and recovery after stroke in rats." Annals of clinical and translational neurology vol. 1,10 (2014): 765-77. doi: https://doi.org/10.1002/acn3.115
Hodor A, Palchykova S, Baracchi F, Noain D, Bassetti CL. Baclofen facilitates sleep, neuroplasticity, and recovery after stroke in rats. Ann Clin Transl Neurol. 2014 Oct;1(10):765-77. doi: 10.1002/acn3.115. Epub 2014 Oct 14. PMID: 25493268; PMCID: PMC4241804.
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Hyperglycemia- and neuropathy-induced changes in mitochondria within sensory nerves.

Annals of clinical and translational neurology

Hamid HS, Mervak CM, Münch AE, Robell NJ, Hayes JM, Porzio MT, Singleton JR, Smith AG, Feldman EL, Lentz SI.
PMID: 25493271
Ann Clin Transl Neurol. 2014 Oct;1(10):799-812. doi: 10.1002/acn3.119. Epub 2014 Oct 01.

OBJECTIVE: This study focused on altered mitochondrial dynamics as a potential mechanism for diabetic peripheral neuropathy (DPN). We employed both an in vitro sensory neuron model and an in situ analysis of human intraepidermal nerve fibers (IENFs) from cutaneous...

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Hamid HS, Mervak CM, Münch AE, et al. Hyperglycemia- and neuropathy-induced changes in mitochondria within sensory nerves. Ann Clin Transl Neurol. 2014;1(10):799-812doi: 10.1002/acn3.119.
Hamid, H. S., Mervak, C. M., Münch, A. E., Robell, N. J., Hayes, J. M., Porzio, M. T., Singleton, J. R., Smith, A. G., Feldman, E. L., & Lentz, S. I. (2014). Hyperglycemia- and neuropathy-induced changes in mitochondria within sensory nerves. Annals of clinical and translational neurology, 1(10), 799-812. https://doi.org/10.1002/acn3.119
Hamid, Hussein S, et al. "Hyperglycemia- and neuropathy-induced changes in mitochondria within sensory nerves." Annals of clinical and translational neurology vol. 1,10 (2014): 799-812. doi: https://doi.org/10.1002/acn3.119
Hamid HS, Mervak CM, Münch AE, Robell NJ, Hayes JM, Porzio MT, Singleton JR, Smith AG, Feldman EL, Lentz SI. Hyperglycemia- and neuropathy-induced changes in mitochondria within sensory nerves. Ann Clin Transl Neurol. 2014 Oct;1(10):799-812. doi: 10.1002/acn3.119. Epub 2014 Oct 01. PMID: 25493271; PMCID: PMC4241807.
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MRI features of Binswanger's disease predict prognosis and associated pathology.

Annals of clinical and translational neurology

Akiguchi I, Budka H, Shirakashi Y, Woehrer A, Watanabe T, Shiino A, Yamamoto Y, Kawamoto Y, Krampla W, Jungwirth S, Fischer P.
PMID: 25493272
Ann Clin Transl Neurol. 2014 Oct;1(10):813-21. doi: 10.1002/acn3.123. Epub 2014 Oct 06.

OBJECTIVE: To identify the prevalence of MRI features of Binswanger's disease (BD), specifically MRI with diffuse white matter lesions and scattered multiple lacunes (BD-MRI), and to describe neurological features and pathological outcomes of a community-based cohort study.METHODS: Of 697...

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Akiguchi I, Budka H, Shirakashi Y, et al. MRI features of Binswanger's disease predict prognosis and associated pathology. Ann Clin Transl Neurol. 2014;1(10):813-21doi: 10.1002/acn3.123.
Akiguchi, I., Budka, H., Shirakashi, Y., Woehrer, A., Watanabe, T., Shiino, A., Yamamoto, Y., Kawamoto, Y., Krampla, W., Jungwirth, S., & Fischer, P. (2014). MRI features of Binswanger's disease predict prognosis and associated pathology. Annals of clinical and translational neurology, 1(10), 813-21. https://doi.org/10.1002/acn3.123
Akiguchi, Ichiro, et al. "MRI features of Binswanger's disease predict prognosis and associated pathology." Annals of clinical and translational neurology vol. 1,10 (2014): 813-21. doi: https://doi.org/10.1002/acn3.123
Akiguchi I, Budka H, Shirakashi Y, Woehrer A, Watanabe T, Shiino A, Yamamoto Y, Kawamoto Y, Krampla W, Jungwirth S, Fischer P. MRI features of Binswanger's disease predict prognosis and associated pathology. Ann Clin Transl Neurol. 2014 Oct;1(10):813-21. doi: 10.1002/acn3.123. Epub 2014 Oct 06. PMID: 25493272; PMCID: PMC4241808.
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Dopaminergic therapy affects learning and impulsivity in Parkinson's disease.

Annals of clinical and translational neurology

Hiebert NM, Seergobin KN, Vo A, Ganjavi H, MacDonald PA.
PMID: 25493274
Ann Clin Transl Neurol. 2014 Oct;1(10):833-43. doi: 10.1002/acn3.128. Epub 2014 Oct 12.

OBJECTIVE: The aim was to examine the effect of dopaminergic medication on stimulus-response learning versus performing decisions based on learning.METHOD: To see the effect of dopaminergic therapy on stimulus-response learning and response selection, participants with Parkinson's disease (PD) were...

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Hiebert NM, Seergobin KN, Vo A, et al. Dopaminergic therapy affects learning and impulsivity in Parkinson's disease. Ann Clin Transl Neurol. 2014;1(10):833-43doi: 10.1002/acn3.128.
Hiebert, N. M., Seergobin, K. N., Vo, A., Ganjavi, H., & MacDonald, P. A. (2014). Dopaminergic therapy affects learning and impulsivity in Parkinson's disease. Annals of clinical and translational neurology, 1(10), 833-43. https://doi.org/10.1002/acn3.128
Hiebert, Nole M, et al. "Dopaminergic therapy affects learning and impulsivity in Parkinson's disease." Annals of clinical and translational neurology vol. 1,10 (2014): 833-43. doi: https://doi.org/10.1002/acn3.128
Hiebert NM, Seergobin KN, Vo A, Ganjavi H, MacDonald PA. Dopaminergic therapy affects learning and impulsivity in Parkinson's disease. Ann Clin Transl Neurol. 2014 Oct;1(10):833-43. doi: 10.1002/acn3.128. Epub 2014 Oct 12. PMID: 25493274; PMCID: PMC4241810.
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