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Last update 08 May 2025

Lead Poisoning, Nervous System

Last update 08 May 2025

Basic Info

Synonyms

Lead Neurotoxicity Syndrome, Lead Neurotoxicity Syndromes, Lead Poisoning, Nervous System

+ [25]

Introduction

Injury to the nervous system secondary to exposure to lead compounds. Two distinct clinical patterns occur in children (LEAD POISONING, NERVOUS SYSTEM, CHILDHOOD) and adults (LEAD POISONING, NERVOUS SYSTEM, ADULT). In children, lead poisoning typically produces an encephalopathy. In adults, exposure to toxic levels of lead is associated with a peripheral neuropathy.

Drugs associated with Lead Poisoning, Nervous System

TMF

Target-

Mechanism-

Active Org.

Chitkara University

Originator Org.-

Active Indication

Lead Poisoning, Nervous System

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with Lead Poisoning, Nervous System

TCTR20180625003

/ Active, not recruitingNot ApplicableIIT

What is the best sample in detecting chronic lead poisoning: blood, hair or nail?

Start Date29 Jun 2018

Sponsor / Collaborator

King Chulalongkorn Memorial Hospital

[+1]

TCTR20170928001

/ Not yet recruitingNot ApplicableIIT

A comparative study of biophysical property changes between patients with chronic lead toxicity and normal control

Start Date04 Oct 2017

Sponsor / Collaborator-

100 Clinical Results associated with Lead Poisoning, Nervous System

100 Translational Medicine associated with Lead Poisoning, Nervous System

0 Patents (Medical) associated with Lead Poisoning, Nervous System

544

Literatures (Medical) associated with Lead Poisoning, Nervous System

01 Mar 2025·Med

Results from the phase 2/3 DAFFODIL study of trofinetide in girls aged 2–4 years with Rett syndrome

Article

Author: Lieberman, David N ; Fu, Cary ; Berry-Kravis, Elizabeth M ; Percy, Alan K ; Feyma, Timothy ; Barrett, Amy ; Bishop, Kathie M ; Youakim, James M ; Neul, Jeffrey L ; Benke, Timothy A ; Buhrfiend, Colleen ; An, Di ; Marsh, Eric D ; Ananth, Amitha L ; Doshi, Dilesh ; Darwish, Mona ; Ryther, Robin

BACKGROUNDTrofinetide is the first available treatment for Rett syndrome (RTT) and is approved in the United States in adults and pediatric patients aged ≥2 years. The DAFFODIL study was conducted in girls aged 2-4 years with RTT to examine the safety, tolerability, and efficacy of trofinetide and to validate that the recommended dosage, according to body weight, achieved target exposure.METHODSDAFFODIL was a phase 2/3, open-label study of trofinetide consisting of two treatment periods (12 weeks [period A] and ∼21 months [period B]). Pharmacokinetic samples were collected at regular intervals during period A. Assessments included treatment-emergent adverse events (TEAEs) and exploratory efficacy (Clinical Global Impressions-Improvement [CGI-I], CGI-Severity, caregiver GI-I [CaGI-I], and overall quality of life rating of the Impact of Childhood Neurologic Disability Scale [ICND-QoL]). Optional caregiver exit interviews were also conducted.FINDINGSFifteen participants were enrolled. Overall, the most common TEAEs were diarrhea (80.0%) and vomiting (53.3%), which were mild or moderate in severity. Steady-state exposure at clinical doses fell within the target exposure range. RTT symptoms improved throughout the study as measured by the CGI-I, CaGI-I, and change from baseline in the ICND-QoL. In caregiver interviews (n = 7), all caregivers reported they were "very satisfied" or "satisfied" with trofinetide benefits.CONCLUSIONSTrofinetide has acceptable tolerability in girls 2-4 years of age with RTT and provides long-term efficacy. Weight-based dosage achieves target exposure in younger children.FUNDINGThe study was supported by Acadia Pharmaceuticals (San Diego, CA). This study was registered at ClinicalTrials.gov (NCT04988867).

01 Mar 2025·Food and Chemical Toxicology

The effect of resveratrol on lead-induced oxidative damage and apoptosis in HT-22 cells

Article

Author: Wei, Peiqi ; Jiang, Yueming ; Yi, Xiang ; Li, Shaojun ; Huang, Shaoni ; Ou, Shiyan ; Li, HuiShuai ; Li, Zhenning ; Wei, Ruokun ; Aschner, Michael

OBJECTIVEThe purpose of this work was to investigate whether resveratrol affects lead-induced oxidative damage in HT-22 cells, characterizing mechanisms and strategies for preventing and treating lead-induced neurotoxicity.METHODSVarious lead and resveratrol concentrations were applied to HT-22 cells over different time periods. First, we established the lead treatment (12.5, 50 and 200 μmol/L) and resveratrol (40 μmol/L) intervention model for the study. MTT was used to analyze HT-22 cell survival rate. The rates of cell death, mitochondrial membrane potential, lipid peroxidation, and reactive oxygen species (ROS) generation were all measured by flow cytometry. Cellular oxidant (MDA) and antioxidant (SOD, GSH-Px) levels were measured with test kits. Western blotting was used to assess the expression of proteins related to autophagy and apoptosis.RESULTSLead reduced HT-22 cell viability in a concentration/time-dependent manner. In addition, lead (200 μmol/L) decreased the protein expression of BCL2, while increasing PARP and BAX expression and apoptotic rate. Moreover, the lead-exposed group had significantly higher levels of ROS, lipid-ROS, and MDA than the control group. This was accompanied by increased MDA levels and decreased SOD, GSH-Px, and MMP levels in the lead-exposed cells. Furthermore, lead lowered SIRT1 protein expression, while increasing the levels of autophagy-related proteins, including P62, ATG5, Beclin-1 and LC3 Ⅱ/Ⅰ. Resveratrol (40 μmol/L), an agonist of SIRT1, restored the effects of lead (200 μmol/L) to levelsindistinguishable from controls.CONCLUSIONResveratrol inhibited mitochondrial damage and restored the lead-induced block of autophagic flux and oxidative stress by activating SIRT1, thereby alleviating lead-induced damage in HT-22 cells.

01 Mar 2025·Neuroscience

Ameliorative role of bioactive compounds against lead-induced neurotoxicity

Review

Author: Parithathvi, Aluru ; Dsouza, Herman Sunil ; Neha, Venkatesan

Lead (Pb) is an environmental toxin ubiquitously present in the human environment due to anthropogenic activities and industrialization. Lead can enter the human body through various sources and pathways, such as inhalation, ingestion and dermal contact, leading to detrimental health effects. The majority of lead that enters the body is removed by urine or feces; however, under chronic exposure conditions, lead is not efficient, as lead is absorbed and transferred to numerous organs, such as the brain, liver, kidney, muscles, and heart, and it is ultimately stored in mineralizing tissues such as bones and teeth. The central nervous system is the most affected among all the organs and systems affected, as lead is a known neurotoxin. Lead absorption is elevated in the fasting state than in the fed state. Chelation therapy, which is used to treat lead poisoning, has various adverse effects, making this treatment detrimental because it disrupts the levels of other essential elements and redistributes lead to various tissues. One of the main mechanisms by which lead induces toxicity is through the generation of reactive oxygen species. Hence, bioactive compounds that are the source of antioxidants if consumed along with ongoing lead exposure can ameliorate the toxic effects of lead.

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Lead Poisoning, Nervous System

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