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1. Normative data for subcortical regional volumes over the lifetime of the adult human brain. Neuroimage. 2016 Aug 15;137:9-20.
3. Does vigabatrin treatment for infantile spasms cause visual field defects? An international multicentre study. Dev Med Child Neurol. 2015 Jan;57(1):60-7.
5. Evidence of motor-control difficulties in children with attention deficit hyperactivity disorder, explored through a hierarchical motor-systems perspective. J Clin Exp Neuropsychol. 2016;38(2):183-96.
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9. Complementary assessments of executive function in preterm and full-term preschoolers. Child Neuropsychol. 2015;21(3):331-53.
11. Two Chronic Stress Models Based on Movement Restriction in Rats Respond Selectively to Antidepressant Drugs: Aldolase C As a Potential Biomarker. Int J Neuropsychopharmacol. 2015 Mar 26;18(10):pyv038.
14. The role of the acidic domain of α-synuclein in amyloid fibril formation: a molecular dynamics study. J Biomol Struct Dyn. 2016;34(2):376-83.
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20. Development and preliminary validation of an Observation List for detecting mental disorders and social Problems in the elderly in primary and home care (OLP). Int J Geriatr Psychiatry. 2016 Jul;31(7):755-64.
22. The study of in vivo quantification of aluminum (Al) in human bone with a compact DD generator-based neutron activation analysis (NAA) system. Physiol Meas. 2016 May;37(5):649-60.
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27. Dramatic Response After Lamotrigine in a Patient With Epileptic Encephalopathy and a De NovoCACNA1A Variant. Pediatr Neurol. 2016 Jul;60:79-82.
2. Changes in the BDNF-immunopositive cell population of neocortical layers I and II/III after focal cerebral ischemia in rats. Brain Res. 2015 Apr 24;1605:76-82.
4. Altered top-down cognitive control and auditory processing in tinnitus: evidences from auditory and visual spatial stroop. Restor Neurol Neurosci. 2015 Jan; 33(1):67-80.
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1. Improvement of cold injury-induced mouse brain edema by endothelin ETB antagonists is accompanied by decreases in matrixmetalloproteinase 9 and vascular endothelial growth factor-A. Eur J Neurosci. 2015 Sep;42(6):2356-70.
3. Isoallopregnanolone antagonize allopregnanolone-induced effects on saccadic eye velocity and self-reported sedation in humans. Psychoneuroendocrinology. 2015 Feb;52:22-31.
5. Dysfunction in ribosomal gene expression in the hypothalamus and hippocampus following chronic social defeat stress in male mice as revealed by RNA-Seq. Neural Plast. 2016;2016:3289187.
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2. Patterned, but not tonic, optogenetic stimulation in motor thalamus improves reaching in acute drug-induced Parkinsonian rats. J Neurosci. 2015 Jan 21;35(3):1211-6.
4. Aberrant Monoaminergic System in Thyroid Hormone Receptor-β Deficient Mice as a Model of Attention-Deficit/Hyperactivity Disorder. Int J Neuropsychopharmacol. 2015 Jan 22;18(7):pyv004.
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8. Molecular architecture of the stria vascularis membrane transport system, which is essential for physiological functions of the mammalian cochlea. Eur J Neurosci. 2015 Aug;42(3):1984-2002.
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BREAKING NEWS: Editors’ Picks
- A new study suggests Alzheimer’s disease may come from the brain infections. Science Translational Medicine, 2016 May.
The new study could change the way we think about the disease, and develop new drugs for treatment.
- New Alzheimer’s disease causing proline substitutions. The EMBO Journal, Nov 3, 2015
The failure to develop efficient Alzheimer’s therapy might come from the pooling, in clinical experiments, of patients who suffer from distinct disorders that eventually lead to Alzheimer’s symptoms. Therefore it is essential to carefully characterize and classify the mechanisms that underlie Alzheimer’s disease, in order to allow for the development of novel therapies.
- Modulating brain’s stress circuitry might prevent alzheimer’s disease. Alzheimer’s & Dementia, Nov 16, 2015.
long-term treatment using a small molecule drug that reduces activity of the brain’s stress circuitry significantly reduces Alzheimer’s disease (AD) neuropathology and prevents onset of cognitive impairment in a mouse model of the neurodegenerative condition.
- Alzheimer protein’s structure may explain its toxicity. Nature Structural & Molecular Biology, 2015 May.
Knowing the physical structure of the 42 amino acid-long form of amyloid beta in the fibers is key to understanding how it folds up improperly and aggregates into toxic plaques.
- New link between diabetes and Alzheimer. Journal of Clinical Investigation, 2015 May
A unique connection between diabetes and Alzheimer’s disease has been uncovered, providing further evidence that a disease that robs people of their memories may be affected by elevated blood sugar.
- Major pathway (SARM1) identified in nerve cell death offers hope for therapies. Science, 2015 April
New research highlights how nerves start to die, a discovery that unveils novel targets for developing drugs to slow or halt peripheral neuropathies and devastating neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease.
- ‘Tangles’ trigger early-stage Alzheimer’s abnormalities in neocortical networks. Neuron, 2015 March.
The study’s dramatic results are due, in part, to the scientists’ decision to focus on a seldom-studied brain cell pathology known as “tangles”.
- Even mild traumatic brain injury may cause brain damage. Neurology, 2014 July.
Those with injuries had brain damage in brain white matter consisting of disruption to nerve axons. This finding is especially important, as 90 percent of all traumatic brain injuries are mild to moderate.
- Autophagy mediates the formation of amyloid beta plaques. Cell Reports, 2013 October.
The study sheds light on the metabolism of amyloid beta, and its role in neurodegeneration and memory loss. It might be a potential drug target for the treatment of the disease.
- XIAP Regulates Caspase Activity in Degenerating Axons. Cell Reports, 2013 August.
Excessive nerve cell pruning leads to disease. Scientists have made important discoveries about a cellular process that occurs during normal brain development and may play an important role in neurodegenerative diseases. The study’s findings point to new pathways and targets for novel therapies for Alzheimer’s.
- Prion-like proteins drive several diseases of aging. Nature, 2013 September
A new emerging concept that many of the brain diseases associated with aging, such as Alzheimer’s and Parkinson’s, are caused by specific proteins that misfold and aggregate into harmful seeds. These seeds behave very much like the pathogenic agents known as prions, which cause mad cow disease.