SynthesisFrontiers in pharmacology2022
Molecular mechanisms of programmed cell death in methamphetamine-induced neuronal damage.
Synthesis in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mechanisms and treatments of methamphetamine and HIV-1 co-induced neurotoxicity: a systematic review.Frontiers in immunology · 2024Pooled it
- Molecular Mechanisms of Hippocampal Synaptic Plasticity Disruption Induced by Chronic Methamphetamine Exposure: A Narrative Review.Cellular and molecular neurobiology · 2026Review
- Roles of gut and oral microbiota in methamphetamine-induced multi-organ toxicity.Cell biology and toxicology · 2026Review
- Ferroptosis in Neuropsychiatric and Neurodegenerative Disorders: Shared Mechanisms and Disease-Specific Signatures.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Oxidative and histopathological changes in the hippocampus and prefrontal cortex following light-at-night and methamphetamine exposure.BMC neuroscience · 2026Article
- Gastrodia elata fermentation alleviates methamphetamine-induced neuroinflammation and anxiety- and depression-like behaviors by regulating the PI3K-AKT signaling pathway.Frontiers in medicine · 2026Article
- Neuroprotective Effects of Platelet-Derived Exosomes in a Rat Model of Methamphetamine-Induced Neurotoxicity.Molecular neurobiology · 2025Article
- Adolescent methamphetamine exposure drives neuroinflammation and aberrant neurogenesis linked to anxiety and cognitive impairments in adult mice.Translational psychiatry · 2025Article
- LY-2183240 enhances reward-seeking behavior with inducing neuronal excitation and early apoptosis in mouse.iScience · 2024Article
- Methamphetamine Increases Tubulo-Vesicular Areas While Dissipating Proteins from Vesicles Involved in Cell Clearance.International journal of molecular sciences · 2024Article
- Can Methamphetamine-Induced Cardiotoxicity be Ameliorated by Aerobic Training and Nutrition Bio-shield Superfood Supplementation in Rats After Withdrawal?Cardiovascular toxicology · 2024Article
- Exploring amygdala structural changes and signaling pathways in postmortem brains: consequences of long-term methamphetamine addiction.Anatomy & cell biology · 2024Article
- Methamphetamine: Mechanism of Action and Chinese Herbal Medicine Treatment for Its Addiction.Chinese journal of integrative medicine · 2023Review
- Aggregation-prone A53T mutant of α-synuclein exaggerates methamphetamine neurotoxicity in SH-SY5Y cells: Protective role of cellular cholesterol.Toxicology reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methamphetamine, commonly referred to as METH, is a highly addictive psychostimulant and one of the most commonly misused drugs on the planet. Using METH continuously can increase your risk for drug addiction, along with other health complications like attention deficit disorder, memory loss, and cognitive decline. Neurotoxicity caused by METH is thought to play a significant role in the onset of these neurological complications. The molecular mechanisms responsible for METH-caused neuronal damage are discussed in this review. According to our analysis, METH is closely associated with programmed cell death (PCD) in the process that causes neuronal impairment, such as apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis. In reviewing this article, some insights are gained into how METH addiction is accompanied by cell death and may help to identify potential therapeutic targets for the neurological impairment caused by METH abuse.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.