Evidence map›Paper›PMID 16260393›Full record

ReviewNeurotoxicity research2005

Adjunctive therapies for HIV-1 associated neurologic disease.

S W Perry, J P Norman, H A Gelbard

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurotoxicity research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.5field-weighted citation impact, top 43% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Potential roles of microglial cell progranulin in HIV-associated CNS pathologies and neurocognitive impairment.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Neuroprotective activities of CEP-1347 in models of neuroAIDS.Journal of immunology (Baltimore, Md. : 1950) · 2010
    Article
  13. Article
  14. Feline immunodeficiency virus neuropathogenesis: from cats to calcium.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2007
    Review
  15. Review
  16. Neuroimmunity and the blood-brain barrier: molecular regulation of leukocyte transmigration and viral entry into the nervous system with a focus on neuroAIDS.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2006
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

S W PerryCenter for Aging and Developmental Biology, Kornberg Medical Research Institute, Rochester, NY 14642, USA.
J P Norman
H A Gelbard
University of Rochester Medical Center · US

Funding

Targeted Neuro Protection of HIV-1 Associated Neurologic DiseaseP01MH064570 · NIMH · UNIVERSITY OF ROCHESTER · PI GELBARD, HARRIS A · 2001 to 2014
$19.4M
Role of EAAT2 and AEG-1 in Astrocyte Dysfunction and NeurodegenerationP01NS031492 · NINDS · ST. LUKE'S-ROOSEVELT INST FOR HLTH SCIS · PI GELBARD, HARRIS A · 1993 to 2007
$10.9M
ROLE OF PAF IN HIV-1 NEUROPATHOGENESISR01MH056838 · NIMH · UNIVERSITY OF ROCHESTER · PI GELBARD, HARRIS A · 1996 to 2014
$5.2M
Training in HIV Replication and PathogenesisT32AI049815 · NIAID · UNIVERSITY OF ROCHESTER · PI WEDEKIND, JOSEPH E · 2001 to 2020
$3.5M
In Vitro Cell Models of NeuroAIDSR21MH071176 · NIMH · UNIVERSITY OF ROCHESTER · PI GELBARD, HARRIS A · 2004 to 2005
$473k
NCEH CDC HHS EHS07026NIAID NIH HHS AI49815NIMH NIH HHS MH071176NIMH NIH HHS MH56838NIMH NIH HHS MH64570NINDS NIH HHS NS31492
6 · The paper itself

Abstract

In the past decade we have seen a milder phenotype and decreased incidence of HIV-1 associated dementia (HAD), largely due to the widespread use of combination chemotherapy to reduce viral burden. However, the prevalence of neurologic disease in people living with HIV-1 has actually increased, raising significant concerns that new therapeutic strategies, directed at restoring neuronal and glial homeostasis and signaling in the central nervous system (CNS), as opposed to directly interfering with the life cycle of HIV-1, must be developed. In this review, we focus briefly on previous Phase 1 clinical trials for adjunctive (i.e., chemotherapeutic agents that do not have a primary antiretroviral mechanism of action) therapy in patients with HAD, followed by an overview of key molecular events in the neuropathogenesis of HAD, and then discuss in more detail our rationale for investigating the effects of therapeutic agents that restore impaired mitochondrial bioenergetics in the CNS. Specifically, we focus on agents that either work in part through K-ATP channels, present in both mitochondria and plasma membranes, and agents that work to weakly uncouple the respiratory capacity of the electron transport chain in mitochondria from ATP production. We propose these agents may be complementary to currently available antiretroviral agents and may significantly improve the capacity of CNS infected with HIV-1 to meet increased bioenergetic demands involved in normal synaptic communication.

Indexed as

HIV-1AIDS Dementia ComplexAnimalsAntiretroviral Therapy, Highly ActiveEnergy MetabolismHumansNeuroprotective AgentsNeuroprotective Agents

Identifiers

PMID16260393
OpenAlexW2003858743

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.