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1.  Multilevel Intramedullary Spinal Neurocysticercosis With Eosinophilic Meningitis 
Archives of neurology  2004;61(5):770-772.
Background
Cysticercal involvement of the spinal cord is a very rare form of neurocysticercosis. Intramedullary cysts are even less common.
Objective
To describe a novel presentation of multilevel intramedullary neurocysticercosis with eosinophilic meningitis.
Design
Case report.
Patient
A 35-year-old man with a history of cerebral neurocysticercosis who presented with both cauda equina and Brown-Sequard syndromes associated with cerebrospinal fluid findings of eosinophilic meningitis.
Results
Magnetic resonance imaging confirmed the multilevel intramedullary cord lesions. The patientwas treated medically with dexamethasone and albendazole and had a good recovery.
Conclusion
Intramedullary neurocysticercosis should be considered as a potentially treatable cause of multilevel spinal lesions with subacute meningitis.
doi:10.1001/archneur.61.5.770
PMCID: PMC3902854  PMID: 15148157
2.  Mechanisms Underlying Recovery of Motor Function After Stroke 
Archives of neurology  2004;61(12):1844-1848.
Stroke is the leading cause of long-term disability worldwide and a condition for which there is no universally accepted treatment. The development of new effective therapeutic strategies relies on a better understanding of the mechanisms underlying recovery of function. Noninvasive techniques to study brain function, including functional magnetic resonance imaging, positron emission tomography, transcranial magnetic stimulation, electroencephalography, and magnetoencephalography, led to recent studies that identified some of these operating mechanisms, resulting in the formulation of novel approaches to motor rehabilitation.
doi:10.1001/archneur.61.12.1844
PMCID: PMC3713312  PMID: 15596603
3.  Cognitive Reserve–Mediated Modulation of Positron Emission Tomographic Activations During Memory Tasks in Alzheimer Disease 
Archives of neurology  2004;61(1):73-78.
Background
Cognitive reserve (CR) is the ability of an individual to cope with advancing brain pathological abnormalities so that he or she remains free of symptoms. Epidemiological data and evidence from positron emission tomography suggest that it may be mediated through education or IQ.
Objective
To investigate CR-mediated differential brain activation in Alzheimer disease (AD) subjects compared with healthy elderly persons.
Participants
Using radioactive water positron emission tomography, we scanned 12 AD patients and 17 healthy elderly persons while performing a serial recognition memory task for nonverbalizable shapes under 2 conditions: low demand, in which one shape was presented in each study trial, and titrated demand, in which the study list length was adjusted so that each subject recognized shapes at approximately 75% accuracy. Positron emission tomographic scan acquisition included the encoding and recognition phases. A CR factor score that summarized years of education, National Adult Reading Test estimated IQ, and Wechsler Adult Intelligence Scale–Revised vocabulary subtest score (explaining 71% of the total variance) was used as an index of CR. Voxel-wise, multiple regression analyses were performed with the “activation” difference (titrated demand–low demand) as the dependent variables and the CR factor score as the independent one. Brain regions where regression slopes differed between the 2 groups were identified.
Results
The slopes were significantly more positive for the AD patients in the left precentral gyrus and in the left hippocampus and significantly more negative in the right fusiform, right middle occipital, left superior occipital, and left middle temporal gyri.
Conclusion
Brain regions where systematic relationships (slopes) between subjects’ education-IQ and brain activation differ as a function of disease status may mediate the differential ability to cope with (ie, delay or modify) clinical manifestations of AD.
doi:10.1001/archneur.61.1.73
PMCID: PMC3028435  PMID: 14732623
4.  Relation of Plasma Lipids to Alzheimer Disease and Vascular Dementia 
Archives of neurology  2004;61(5):705-714.
Background
The relation between plasma lipid levels and Alzheimer disease (AD) and vascular dementia (VaD), and the impact of drugs to lower lipid levels remains unclear.
Objective
To investigate the relation between plasma lipid levels and the risk of AD and VaD and the impact of drugs to lower lipid levels on this relationship.
Design and Setting
Cross-sectional and prospective community-based cohort studies.
Participants
Random sample of 4316 Medicare recipients, 65 years and older, residing in northern Manhattan, NY.
Main Outcome Measures
Vascular dementia and AD according to standard criteria.
Results
Elevated levels of non–high-density lipoprotein (HDL-C) and low-density lipoprotein cholesterol (LDL-C) and decreased levels of HDL-C were weak risk factors for VaD in either cross-sectional or prospective analyses. Higher levels of total cholesterol were associated with a decreased risk of incident AD after adjustment for demographics, apolipoprotein E genotype, and cardiovascular risk factors. Treatment with drugs to lower lipid levels did not change the disease risk of either disorder.
Conclusions
We found a weak relation between non–HDL-C, LDL-C, and HDL-C levels and the risk of VaD. Lipid levels and the use of agents to lower them do not seem to be associated with the risk of AD.
doi:10.1001/archneur.61.5.705
PMCID: PMC2696387  PMID: 15148148
5.  Gene Vaccination to Bias the Immune Response to Amyloid-β Peptide as Therapy for Alzheimer Disease 
Archives of neurology  2004;61(12):1859-1864.
Background
The amyloid-β (Aβ) peptide has a central role in the neurodegeneration of Alzheimer disease (AD). Immunization of AD transgenic mice with Aβ1–42 (Aβ42) peptide reduces both the spatial memory impairments and AD-like neuropathologic changes in these mice. Therapeutic immunization with Aβ in patients with AD was shown to be effective in reducing Aβ deposition, but studies were discontinued owing to the development of an autoimmune, cell-mediated meningoencephalitis. We hypothesized that gene vaccination could be used to generate an immune response to Aβ42 that produced antibody response but avoided an adverse cell-mediated immune effect.
Objective
To develop an effective genetic immunization approach for treatment and prevention of AD without causing an autoimmune, cell-mediated meningoencephalitis.
Methods
Mice were vaccinated with a plasmid that encodes Aβ42, administered by gene gun. The immune response of the mice to Aβ42 was monitored by measurement of (1) antibody levels by enzyme-linked immunosorbent assay (ELISA) and Western blot and (2) Aβ42-specific T-cell response as measured by interferon-γ enzyme-linked immunospot (ELISPOT) assay.
Results
Gene-gun delivery of the mouse Aβ42 dimer gene induced significant humoral immune responses in BALB/c wild-type mice after 3 vaccinations in 10-day intervals. All 3 mice in the treated group showed significant humoral immune responses. The ELISPOT assay for interferon-γ release with mouse Aβ42 peptide and Aβ9–18 showed no evident cytotoxic T-lymphocyte response. We further tested the responses of wild-type BALB/c mice to the monomer Aβ42 gene vaccine. Western blot evaluation showed both human and mouse Aβ monomer gene vaccine elicited detectable humoral immune responses. We also introduced the human Aβ42 monomer gene vaccine into AD double transgenic mice APPswe/PSEN1(A246E). Mice were vaccinated with plasmids that encode Aβ1–42 and Aβ1–16, or with plasmid without the Aβgene. Treated mice showed significant humoral immune responses as demonstrated by ELISA and by Western blot. These mice also showed no significant cellular immune response as tested by ELISPOT. One of the treated mice was killed at 7 months of age for histological observations, and scattered amyloid plaques were noted in all layers of the cerebral cortex and in the hippocampus in both Aβ42- and control-vaccinated mice. No definite difference was discerned between the experimental and control animals.
Conclusions
Gene-gun–administered genetic immunization with the Aβ42 gene in wild-type BALB/c and AD transgenic mice can effectively elicit humoral immune responses without a significant T-cell–mediated immune response to the Aβ peptide. This immunotherapeutic approach could provide an alternative active immunization method for therapy and prevention of AD.
doi:10.1001/archneur.61.12.1859
PMCID: PMC1482312  PMID: 15596606

Results 1-5 (5)