Volume 1, Issue 1, p1-30
Articles published in this issue are Open Access and licensed under Creative Commons Attribution License (CC BY NC) where the readers can reuse, download, distribute the article in whole or part by mentioning proper credits to the authors.
To explore the pathological mechanism and clinical treatment of cerebellar infarction through the clinical imaging changes of cerebellar infarction.J Exp Neurol, 2020, Volume 1, Issue 1, p1-9 | DOI: 10.33696/Neurol.1.001
People suffering with neurological diseases are at risk of committing suicide. A case-control study found increased risk of attempted suicide in patients with nine chronic neurological diseases J Exp Neurol, 2020, Volume 1, Issue 1, p10-12 | DOI: 10.33696/Neurol.1.002
Case Summary - We published a case report of a 22-year-old woman who presented to our university hospital with encephalopathy and left hemiparesis of a few weeks duration.J Exp Neurol, 2020, Volume 1, Issue 1, p13-16 | DOI: 10.33696/Neurol.1.003
What is the Time Necessary to be Able to Place Transpedicular Screws According to the Chosen Technique?
Transpedicular screw placement techniques are technically plaintiffs have relied on navigation intraoperative which is limited by its high cost, limited use of a fluoroscope with the radiological overexposure of the personnel of health and patient offers limited help when placing screws, and vertebral anatomical modifications especially in patients with degenerative pathology result an index of placement-related complications suboptimal of the screws [1,2].J Exp Neurol, 2020, Volume 1, Issue 1, p26-30 | DOI: 10.33696/Neurol.1.005
Commentary on "Dysfunction of the Magnocellular Stream in Alzheimer Disease Evaluated by Pattern Electroretinograms and Visual Evoked Potentials"
Alzheimer’s disease (AD) represents the most common cause of dementia. Even if AD is commonly viewed as a disorder primarily of memory, there are several other additional domains, including visual function.J Exp Neurol, 2020, Volume 1, Issue 1, p17-25 | DOI: 10.33696/Neurol.1.004
Alzheimer’s disease (AD) is an age-related neurodegenerative disorder  and the most common cause of human dementia, accounting for approximately 60%?80% of cases. It is estimated that more than 30 million AD patients, and the number likely to increase to over 100 million by 2050 because of the increase of the elderly population .
AD is a neurodegenerative disease characterized by progressive cognitive impairment, behavioral changes, memory loss and executive dysfunction, all of which present serious threats to the health of older people.
The number of people with Alzheimer’s disease (AD) is on the rise, yet there is no effective pharmacological treatment that can slow or reverse the disease’s progress
Glucose Metabolism is a Better Marker for Predicting Clinical Alzheimer’s Disease than Amyloid or Tau
Alzheimer’s disease (AD) research has long been dominated with communications regarding the amyloid hypothesis and targeting amyloid clearance through pharmacological therapies from the brain .
Human Gray and White Matter Metabolomics to Differentiate APOE and Stage Dependent Changes in Alzheimer’s Disease
Alzheimer’s disease (AD) is a leading cause of death and morbidity in the United States . The hallmarks of AD are β-amyloid (Aβ) and tau. However, studies have indicated that metabolic dysfunction may play a more pivotal role in the progression of AD . Glucose hypometabolism and mitochondrial dysfunction are well-known features of AD .
Alzheimer’s Disease (AD) is the most common form of dementia. Patients diagnosed with AD experience disordered cognition and memory, as well as changes in behaviour and personality. The vast majority of AD is diagnosed in patients aged over 65 years and classified as late onset (LOAD), with the remaining ~1% of cases termed early onset AD (EOAD).
Before the age of 65, people with mutations in the genes for Presenilin 1 (PSEN1), Presenilin 2 (PSEN2), and the amyloid precursor protein (APP) experience familial Alzheimer’s disease (FAD). The sporadic type of Alzheimer’s disease (AD) is multifactorial and associated with the Apolipoprotein E ε4 allele (APOE ε4), which can up to 12 times increase the risk of getting the condition
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