icon-    folder.gif   Conference Reports for NATAP  
  20th Conference on Retroviruses and
Opportunistic Infections
Atlanta, GA March 3 - 6, 2013
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CROI 2013 Adult Neurology Presentation and Abstracts
  Written for NATAP by
Kevin R. Robertson, Ph.D.1, Charles Upton2
contributions by Jules Levin
1Professor, Director of Neuropsychology
Director, AIDS Neurological Center
Neurology, School of Medicine
University of North Carolina at Chapel Hill
2Research Assistant, AIDS Neurological Center
Neurology Department, School of Medicine
University of North Carolina at Chapel Hill
Oral Abstracts
Neurocognitive Disorders: New Developments and Therapies

Serena Spudich (abstract 18) presented findings from a compartmentalization study with a Thai cohort of very acute infection subjects. Both plasma and CSF viral populations had low genetic diversity. The sequences and time-to-most-recent-common-ancestor were also similar in both populations for each subject. These results suggest that in the very early stages of infection, there is free traffic of virus to the CNS with no genetic bottleneck and minimal selection pressure. Compartmentalization, the establishment of a separate, genetically distinct viral population in the CNS, appears to occur later in the course of infection. Occurrence of compartmentalization likely plays a role in the development of HIV-Associated Neurocognitive Disorders (HAND), and determining the typical timeline of compartmentalization is important for HAND treatment and further efforts toward eradication of HIV.
Ronald Ellis (abstract 20) described a randomized control trial of the effects of CNS-targeted ART, or NeuroHAART, on HAND symptomology. The study was ended prematurely, and incomplete results did not indicate any significant effect of NeuroHAART on HAND.
Cecilia Shikuma and colleagues investigated the effects of mitochondrial dysfunction and oxidative stress. Mitochondrial Complex I, a protein involved in cellular metabolic processes, functions abnormally in conditions of oxidative stress, a molecular imbalance associated with a wide variety of diseases, including HIV. Abnormal functioning of mitochondrial Complex I was associated with poorer neurocognitive functioning and regional brain atrophy. Shikuma posits that the inflammatory response associated with HIV leads to Complex I related mitochondrial dysfunction, which in turn contributes to worsening inflammation, creating a harmful feedback loop. While mitochondrial dysfunction is a systemic problem in HIV infection, the brain is particularly vulnerable to its negative effects.
Jennifer Campbell (abstract 22) and colleagues investigated a potential direction for treatment. Tysabri, a drug administered to multiple sclerosis and Crohn's disease patients, blocks leukocyte and macrophage traffic. In order to investigate the effects of Tysabri on retrovirus infection, one group of SIV-infected Rhesus macaques were initiated on treatment concurrently with infection, and one group 28 weeks post infection. For subjects whose treatment was initiated later in the course of infection, the virus-associated decrease of NAA, a marker of normal neuronal function, stabilized upon treatment initiation. In those initiated concurrently with infection, incidence of infected cells in brain and gut tissue was significantly below normal infection levels. While these results are compelling, the application of this treatment to human populations remains unclear.
Christina Sturdevant (abstract 23) and colleagues investigated CNS compartmentalization in young children (three years old and younger). Nearly half of their sample displayed equilibrated genetic populations and showed no evidence of genetic compartmentalization. However, 28% of subjects showed genetic evidence of CNS compartmentalization, and 26% appeared to be in an intermediate stage with some evidence of CNS specific evolution but no overt compartmentalization. Older subjects had significantly higher rates of compartmentalization, suggesting that compartmentalization generally occurs later than primary infection.
Compartmentalized subjects also possessed higher CSF viral loads in comparison to their plasma levels, further indicating CSF specific replication. A small number of subjects showed evidence of very early sequestration and possessed viral populations that diverged before the subjects were conceived, indicating that they were infected with more than one genetically distinct virus. Sturdevant and colleagues suggest a model in which CNS colonization occurs early in the course of infection, with compartmentalization gradually progressing over the following years; very early sequestration is possible if infants are infected with more than one parent virus.
Idil Kore (abstract 19) and colleagues investigated neurocognitive performance in subjects in the early acute stages of infection and monitored the progress of performance after initiation of ART. Two different treatment regimens were tested, a standard HAART regiment of tenofovir, emtricitabine, and efavirenz, as well as a 'MegaHAART' regiment of the three previous drugs as well as raltegravir, an integrase inhibitor, and maraviroc, a CCR5 inhibitor. Kore and colleagues found that poorer neurocognitive baseline performance was correlated to longer time since infection and higher CSF HIV RNA levels. The latter effect was moderated by CD4 count. Subjects' neurocognitive performance improved over the six months of the study after HAART initiation, but only more than that of uninfected controls on the Color Trails 1 test, a simple test of processing speed. No difference was observed between the HAART and MegaHAART regiment groups.
Poster Sessions
Central Nervous System Penetration, ART Intensification, and Cerebrospinal Fluid Escape

The progression of HIV infection from the bloodstream into the central nervous system (CNS) is important in the development of HAND, thus penetration into the CNS by ART agents could be important in treating neurological symptoms. Levels of drugs in cerebrospinal fluid (CSF) and biomarkersare thought to be important in tracking HIV infection in the CNS. Several abstracts focused on these measures.
HAND rates in the context of ART were reported by two different studies. Letendre and colleagues found that patients on ART experienced long term decline of HIV RNA levels in the CSF but not in plasma (#401). Interaction analyses also potentially suggested (p=0.06) poorer neurocognitive performance in subjects whose plasma and CSF RNA levels remained detectable over the course of the study. An observational study of a Canadian sample showed steady rates of neurocognitive impairment in individuals on ART. Additionally, 13% experienced a categorical decline in NP functioning (#404).
In a longitudinal study investigating CSF viral escape (CVE), Perez Valero and colleagues found that CVE is rare and is associated with low-level plasma viremia and high CSF WBC count (#402). CSF viral escape (defined here as CSF HIV RNA >50 cop/mL while plasma HIV RNA <50 cop/mL) is a condition that occurs despite successful systemic ART and has been proposed to be associated with impaired neurocognitive performance. Neurocognitive evolution of subjects presenting CSF viral escape during the follow up was not demonstrated to be different from that of subjects without CVE in this study.
Three studies investigated the effects of CNS-targeted ART on neurocognitive functioning. Ndhlovu and colleagues found that intensifying ART with Maraviroc led to improvement in neurocognitive performance, particularly in impaired subjects, as well as decreasing immune inflammation (#403) Fabbiani found that CPE correlated more closely with improved neurocognitive performance when corrected for drug susceptibility (#405). Results regarding the treatment effectiveness of CNS-targeted regimens have been mixed, but this suggests that combining this targeting with consideration of potential viral resistance may make for more predictable benefits. Another study by Perez-Valero found that protease inhibitor monotherapy was not associated with higher rates of neurocognitive impairment, CVE, or inflammatory or brain injury biomarkers (#406).
ART, Neurocognitive Outcomes, and New CNS-targeted Therapies
Several abstracts compared neurocognitive benefits of different ART strategies. These included comparisons of neurocognitive outcomes with current ART regimens as well as explorations of potential new avenues for targeting CNS damage with ART.
Neurocognitive outcomes of different ART regimens were compared in two studies. An analysis of the CHARTER cohort found that patients using EFV had lower neurocognitive functioning than those using LPV/r, however a potentially important moderator of neurotoxicity is concurrent HCV infection (#407). The ASSURE study found no difference in cognitive outcomes for patients whose ART regimens were simplified from TDF/FTC + ATV/r to (ABC/3TC) +ATV (#410).
Two studies investigated neurological symptomatology in the cART era. Guttierez and colleagues found that each year of ART is associated with a 58% decrease in risk of depression compared to untreated patients (#413). Chow and colleagues found significantly higher rates of autonomic dysfunction in patients on ART than in HIV- controls (#409). This evidence indicates that autonomic symptomatology in HIV persists in the era of cART.
Autonomic dysfunction can manifest in HIV-infected individuals as dry eyes or mouth, dizziness, fatigue, weakness, diarrhea, blurred vision, changes in sweat rate, fainting, difficulty sleeping and orthostatic hypotension. Although ART has changed the course of HIV by dramatically improving the morbidity and mortality of HIV/AIDS progression, its effects on autonomic dysfunction have not been extensively evaluated. Links between HIV/AIDS and autonomic dysfunction have been previously reported on, particularly in the pre-highly active antiretroviral therapy era. The prevalence of symptoms of clinical autonomic neuropathy in HIV has been variable depending on HIV disease status and treatment, ranging from 0 to 84%.
Definition: Dysfunction of the autonomic nervous system (ANS) is known as dysautonomia. The autonomic nervous system regulates unconscious body functions, including heart rate, blood pressure, temperature regulation, gastrointestinal secretion, and metabolic and endocrine responses to stress such as the "fight or flight" syndrome. As regulating these functions involves various and multiple organ systems, dysfunctions of the autonomic nervous systems encompass various and multiple disorders.
Description: The autonomic nervous system consists of three subsystems: the sympathetic nervous system, the parasympathetic nervous system and the enteric nervous system. The ANS regulates the activities of cardiac muscle, smooth muscle, endocrine glands, and exocrine glands. The ANS functions involuntarily (reflexively) in an automatic manner without conscious control.
In contrast to the somatic nervous system that always acts to excite muscles groups, the autonomic nervous systems can act to excite or inhibit innervated tissue. The autonomic nervous system achieves this control via two divisions: the sympathetic nervous system and the parasympathetic nervous system. The ANS achieves this ability to excite or inhibit activity via a dual innervation of target tissues and organs. Most target organs and tissues are innervated by neural fibers from both the parasympathetic and sympathetic systems. The systems can act to stimulate organs and tissues in opposite ways (antagonistic). For example, parasympathetic stimulation acts to decrease heart rate. In contrast, sympathetic stimulation results in increased heart rate. The systems can also act in concert to stimulate activity. Dysfunctions of the autonomic nervous system are recognized by the symptoms that result from failure of the sympathetic or parasympathetic components of the ANS.
New directions for CNS-targeted treatment were explored in two studies testing potential ART vectors. Garrido et al found evidence to support the use of gold nanoparticles (AuNP) in ART. AuNP can cross the blood brain barrier and enter lymphocytes and may be conjugated to raltegravir molecules to act as a vector for antiviral activity (#408). McFarren and colleagues demonstrated that a radiolabeled antibody can cross the BBB and kill infected monocytes (#412), Thus, targeting infected cells across BBB with a radiolabeled antibody to gp41 is a promising strategy for elimination of HIV-1 in the CNS. A third study investigated the potential for reducing neuronal damage with minocycline. Sacktor and colleagues found evidence of decreased levels of CSF lipid biomarkers for neuronal oxidative stress in cognitively impaired patients treated with minocycline, though levels of protein biomarkers remained stable (#411).
Central Nervous System Viral Evolution and Compartmentalization
Genetic distinction between HIV in the bloodstream and CSF characterizes compartmentalization. Two analyses illuminated the specific genetic characteristics of HIV with respect to the CNS. Tlighman et al found specific residues within the tat gene of the HIV Subtype-C genome associated with neurocognitive impairment (#414). Yuh and colleagues used a deep sequencing technique to analyze genetic variants within plasma and CSF viral populations. This study found evidence that HIV can be genetically different in CSF, and this may be present early and continuously throughout the course of infection, suggesting an independent and autonomous source of HIV in the CNS (#415).
Two animal systems studies, both in Simian Immunodefficiency Virus (SIV), a monkey analogue of HIV, provided further insight into the course of HIV CNS infection. In a study conducted with SIV-infected macaques with encephalitis, Zhuang et al found CNS viral compartmentalization analogous to that found in HIV-infected humans (#418). Strickland et al attempted to characterize the viral evolution in SIV-infected macaques, finding that viral migration to the brain takes place at a number of different sites and that loss of CD8 immune function results in higher rates of viral evolution (#417).
In another animal study using mice with humanized immune systems, Gorantla found that infection with clade C HIV was associated with higher levels of immune activation and T-cell replication than clade B infection (#416).
Neuropathogenesis Mechanisms
HIV-related processes that cause nervous system damage were investigated in several abstracts. CNS disease in HIV is a combination of many different mechanisms both directly and indirectly caused by HIV. Immune responses to HIV were the focus of most neuropathogenesis abstracts.
Inflammation related factors were a specific focus of studies regarding potential neuropathogenesis mechanisms. Heme Oxygenase-1 (HO-1), an agent that limits inflammation was found to be expressed at greater levels but present at lower protein levels by Ambegaokar and Gill, respectively (#420, #421). This suggests that a potential anti-inflammatory response is being stifled at the protein level, possibly by proteosome activity. An inflammatory response protein, CCL2, appears to change K channel activity in microglia, resulting in neurotoxicity, as reported by Xu and colleagues (#425).
Various other immune responses to infection were cited as potential causes of neurotoxicity, including cathepsin B, a protein differentially expressed by HIV+ macrophages (Cantres Rosario, #419). Additionally, cathepsin B production appears to be dysregulated by cocaine abuse, an added neurocognitive concern for HIV+ addicts - suggesting that the drug potentiates the development of HIV-induced chronic inflammation. (Zenon, #429) Dysregulated unfolding protein response, differential expression of Micro RNA, and upregulation of a7-nAChR, a receptor that interacts with gp120, were all cited as potential neuropathogenesis mechanisms by Cross, Espinoza, and Capo-Velez (#422, #423, #427). A potential avenue for treatment was suggested by Buchanan and colleagues in the protective effect of SAMHD, a host restriction factor in astrocytes (#424).
Broadening the application of an important experimental system, Bradshaw and Mangus characterized specific elements of neuronal and spinal cord damage in SIV-infected macaques. (#426, #428) SIV induces neuroinflammatory changes in the lumbar spinal cord (#426). Pediatric HIV infection remains a global health crisis with a worldwide infection rate of 2.5 million. Children are much more susceptible to HIV-1 neurological impairments than adults, which is exacerbated by co-infections. Using design-based stereology, this study reported a 40% reduction in the pyramidal neuron population of the CA1, CA2, and CA3 fields of the hippocampus (p <0.05) in SIV-infected infants. The authors concluded that loss of hippocampal neurons and neurogenic capacity may contribute to the rapid neurocognitive decline associated with pediatric HIV infection. These data suggest that pediatric SIV infection, which leads to significant neuronal loss in the hippocampus within 3 months, closely models a subset of pediatric HIV infections with rapid progression.
Central Nervous System Inflammation and Biomarkers of HIV-associated Neurocognitive Disorder
Biomarkers are measureable biological indicators of various disease states. Keating observed elevated CSF levels of inflammatory biomarkers throughout the progression of infection, which were only partially controlled by ART (#432). Singh found significantly elevated levels of platelet-monocyte complexes in brain tissue samples from HIV+ humans as well as CD40L treated mice (#431).
A reliable biomarker for HAND would be highly valuable as an efficient way to inform treatment. Two biomarkers, IFN-a, a cytokine, and HIV DNA from CD14+ cells were found to correlate with HAND by Anderson and Valcour (#437, #435). Levels of several HAND biomarkers were found to be gender differentiated pre- and post-ART initiation in a study by Slike of a Thai sample with chronic HIV infection (#430). Bandera found patients with low CD4 counts despite to have poorer neurocognitive functioning as well as higher levels of monocyte/macrophage proteins that indicated a pro-inflammatory response. Calcagno characterized CSF biomarkers in patients with very low CD4 counts but intact neurocognitive functioning (#438). Tran and colleagues suggest that protein interaction between HIV and AD CSF biomarkers plays a role in compounding neurodegenerative effects (#433).
Ferguson and colleagues investigated a potential treatment avenue in an SIV/macaque model (#434). Vaccine blunted viremia led to lower neuropathology, though the applicability of this system to humans is questionable because of the limitations of treatment initiation timing. However, these results suggest that initiating neuropathology-targeted treatment in early disease stages warrants further investigation.
Aging and Neurocognitive Function in HIV Infection
The interaction between HIV and aging is an increasingly important topic. Several abstracts characterized CNS infection in older HIV patients and investigated the relationship between HIV, neurocognitive impairment, and age related comorbidities.
Peterson and colleagues evaluated several biomarkers for their use in predicting different levels of HAND. CSF NFL levels were elevated in HAD patients as well as asymptomatic patients with low CD4 count. Additional biomarkers were also abnormally high in HAD patients, suggesting that HAD is accompanied by a broader array of neuronal injury (#441). Krut observed CSF NFL levels in treated and untreated neurocognitively asymptomatic patients as well as healthy controls. While NFL levels increased with age in all three groups, this effect was accelerated in untreated patients, though somewhat closer to normal in treated patients (#443). In an fMRI study, Thomas found that modularity, a measure of sub-network discreteness, underwent accelerated age-related decline in HIV+ patients. Further findings suggest that this effect may be due to increased immune activation (#445).
Other studies investigated the relationship between HIV, aging, and neurocognitive outcomes. Goodkin found an interaction between age and HIV-disease stage among older adults in episodic memory and motor function (#439). Cysique found that HIV patients are at significantly higher risk for Alzheimer's Disease than similarly aged uninfected patients. However, risk is likely to vary significantly within the HIV+ population based on factors such as duration of infection and past immunocompromise (#442). Smith found cognitive impairment to be associated with increased risk of frailty among HIV+ men (#444).
The CHARTER group found a significant relationship between Veterans Aging Cohort Study (VACS) Index score, a combination measure of HIV and comorbidity severity, and HIV-associated neurocognitive disorders (#440).
NeuroAIDS Clinical Studies
Many clinical studies presented findings in a wide range of NeuroAIDS topics. Three clinical studies focused on specific HIV-infected groups. Lee sought to neurologically describe HIV controllers (untreated patients with relatively low viral load). This group was found to be metabolically distinct from other experimental groups and to perform more poorly on neuropsychological evaluation, and paradoxically, poorer even that untreated viremic patients. Metabolite differences suggest mild neuronal injury and higher inflammation among controllers, possibly also explaining the neurocognitive deficits (#446). The CIPHER study found minimal NP difference between HIV+ MSM and general male population, though education and drug use were not controlled (#453). Gelman found that brain levels of HIV RNA and DNA are correlated with poorer neuropsychological performance HIV+ patients with HIV encephalitis or microglial nodule encephalitis (#447).
The diagnostic effectiveness of different neuropsychological assessment tools was investigated in several comparison studies. Chalermchai found that the addition of Trailmaking A bolsters the International HIV Dementia Scale for use in diagnosing the milder forms of HAND (#451). Similarly, Antinori found the IHDS in combination with other easy to administer tests to be more accurate in HAND screening than these tests in isolation or self-report forms, which had low sensitivity (#455). A community cohort study by Bloch and colleagues found a HAND rate of 18-30% as assessed with a full neuropsychological battery. CogState, a computerized clinical screening tool, yielded a similar rate but with lower sensitivity (#450). Lu and colleagues found that the HIV Dementia Scale can detect decline even over a period of four months(#461a). Systemic outcomes that impact the CNS were investigated in relation to HAND in several other clinical studies. Grima found high-grade liver steatosis, a marker for visceral obesity, to be correlated with neurocognitive impairment (#452). Lake found that some adipocytokine levels correlated with NP performance, though many did not. Adipostiy itself did not predict NP performance. Longitudinal data is forthcoming (#459). Kalayjian and colleagues found that proteinuria was significantly correlated with neurocognitive impairment, indicating that vascular dysfunction plays a role in HAND (#460). De Luca found that cardiovascular risk factors and immunological parameters such as CD4 count predicted decline on specific neurocognitive tasks in a two-year longitudinal study (#448).
Multiple longitudinal studies addressed rates of neurocognitive impairment over time. Arendt conducted a longitudinal study to further study the progression of HAND. Progression from milder Frascati stages to more severe stages was observed and predicted by age and duration of infection, suggesting that HIV+ patients would benefit from regular NP evaluation (#454). The Neuradapt study found that within its sample the proportion of patients with HAND increased over time. Neuropsychological deficits at baseline were at greater risk for NP decline, while those with high penetration regimens were at lower risk (#449). Early results from a longitudinal study by Haynes et al support an interaction between HIV and aging in cognitive decline (#456). More results including an imaging component will follow. One intervention, however, suggested some hope for cognitive recovery. Livelli and colleagues showed that cognitive rehabilitation can lead to NP improvement in MND and ANI patients (#458). A genetic analysis of the CHARTER study sample found that a loss of function mutation in the Complement Factor H (CFH) gene, a protein involved in inflammatory response, was associated with neurocognitive impairment and imaging abnormalities (#461b) No polymorphisms were found to correlate with PN in ddI/dd4 treated patients in a genome-wide study (#457)
Neuroimaging Studies
Neuroimaging is an important diagnostic and research tool. Using a number of different techniques, several studies investigated the effects of HIV on different brain structures, cell types, and neurochemistry.
A comprehensive structural imaging study with the Chicago Early HIV infection cohort revealed several changes in the brain during the very early stages of seroconversion, including reduced gray matter volume, 3rd ventrical expansion, swelling of the brain stem, reduced white matter integrity in the corpus callosum, and atrophy in the caudate (#463). In another substructure analysis, Ortega et al observed no volumetric differences when imaging the brains of patients infected with clade B and clade C HIV (#464). Dash and colleagues successfully used microstructural bioimaging to monitor CNS pathology in HIV infected humanized mice (#469), proving the feasibility of this technique in an important experimental system.
Several imaging studies specifically addressed changes in white matter in different HIV contexts. White matter in the brain is under particular stress during HIV infection, and white matter disease is thought to be linked directly to HAND symptomatology. An assessment by Fennema-Notestine from the CHARTER study linked both past immunosuppression and neurocognitive impairment with low neuronal integrity and white matter abnormality (#468). Wright and colleagues found that WM integrity in chronic HIV infection patients off of cART was more disrupted than that in primary infection patients or healthy controls, suggesting that white matter damage happens after primary infection (#466). Both studies suggest that WM changes are related to brain inflammation and NP impairment and indicate that early initiation of cART may help control neuronal damage. Another study by Heaps suggests that co-infection with HCV has a compounding negative effect on white matter volume, but no evidence was found to suggest that white matter integrity experiences a similarly compounded effect (#467).
Two studies used imaging to assess cerebral metabolite levels during the course of HIV infection. Winston observed variable changes in levels of cerebral metabolites in patients initiating cART. Such changes may suggest the beginnings of neurotoxicity and highlight the need for long term follow-up (#462). Grill observed that altered CSF tryptophan in PHI patients correlated with CNS inflammation as assessed by increased CSF WBC but not as assessed by altered levels of cerebral metabolites (#465).
CROI/NATAP - Neurological, Cognitive Function - Aging/Frailty MACS
  • Symptoms of Autonomic Dysfunction in HIV-Infected Patients Receiving Stable ART: "The biggest difference was seen within the male sexual dysfunction domain with 47% of the HIV group experiencing symptoms, compared to 11% of the control group experiencing symptoms" - (05/27/13)
  • Very Early Viral Infection of the Central Nervous System without Evidence of Compartmentalization During Acute HIV-1 Infection - (05/27/13)
  • VLA-4 (Tysabri) Treatment Blocks Virus Traffic to the Gut and Brain Early, and Stabilizes CNS Injury Late in Infection - (05/27/13)
  • A Longitudinal Study of the Effects of Ageing and HIV-1 Infection on Cognitive Performance - (04/02/13)
  • Long-Term Efavirenz Use is Associated with Worse Neurocognitive Functioning - (03/07/13)
  • Long-Term Efavirenz Linked to Worse Neurocognitive Function in US CHARTER Group - written by Mark Mascolini - (03/05/13)
  • Longitudinal Association of HIV-associated neurocognitive disorder (HAND) with Frailty in HIV+ Men - (03/08/13)
  • Older Age and Neurocognitive Function in the Multi-Center AIDS Cohort Study - (03/14/13)
  • Low-Level HIV RNA Declines Over Time in CSF but not in Plasma, "HIV between 2-50 c/ml .....worse cognitive functioning" - (04/01/13)
  • Neuropsychological Performance in Acute HIV - (03/20/13)
  • Similar Cognition Outcomes After 24 Weeks for Tenofovir/FTC + Atazanavir/r (ATV/r)-Experienced HIV+ Subjects or Those Simplifying to Abacavir/3TC+ATV - (03/06/13)
  • Follow-up of HIV-Associated Neurocognitive Disorders in the cART Era: the Neuradapt Study - (04/02/13)
  • Prevalence of Chronic Kidney Disease Among HIV-infected Adults in Care in the United States Medical Monitoring Project, 2009 - (04/01/13)
  • Neuroimaging Correlates of Prior Immunosuppression and Cognitive Status in HIV - (04/10/13)
  • A Randomized, Controlled Trial of a CNS-Targeted Antiretroviral Therapy (ART) Strategy for HIV-Associated Neurocognitive Disorders - (03/29/13)
  • Gold Nanoparticles to Improve Drug Delivery to the Central Nervous System - (04/10/13)
  • Proteinuria is Associated with Neurocognitive Impairment in HIV Infected Subjects Enrolled in the AIDS Clinical Trials Group (ACTG) Longitudinal Cohort Study (ALLRT) - (03/28/13)
  • High Grade Liver Steatosis and Cognitive Impairment in HIV+ patients - (04/09/13)
  • Cognitive Rehabilitation Protocol in HIV/AIDS outpatients with ANI and MND: results and clinical applicability - (04/09/13)
  • Associations Between Regional Fat Deposition and Neurocognitive Function in the Multicenter AIDS Cohort Study - (04/09/13)
  • Detectable HIV DNA is Associated with Reduced Cerebellar and Subcortical Gray Matter Volumes - (04/08/13)
  • Maraviroc Intensification in Virally Suppressed HIV Infected Subjects Leads to Improvement in Neurocognitive Test Performance and Declines in Immune Activation - (04/07/13)
  • Changing CSF Concentrations of Neurofilament Light Chain, Tau and Amyloid Proteins, Characterize Evolving CNS Injury in HIV-1 Infection - (04/01/13)
  • Reduced Region-Specific Corpus Callosum Volumes Correlate with Low Nadir CD4 an Decreased Cognition in HIV-Infected Carriers of the ApoE4 Allele - (04/01/13)