The critical axonopathy- producing effect of acrylamide (ACR) is hypothesized to be an interruption of fast vesicular transport resulting in a deficiency of distal axonal proteins. This study used the accumulation of growth associated protein- 43 (GAP-43) in neurite tips of cultured hippocampal neurons as a model to examine the effect of an ACR block of fast transport on the eventual protein concentration within the distal axon. Twenty-four hour incubation with ACR produced a dose-dependent reduction with 0.5mM and 1.0mM concentrations in the percent of neurites with a terminal GAP-43 accumulation. No change in cell size (area), cell body GAP-43 fluorescence, distal neurite fluorescence, absolute tip fluorescence or neurite length were observed. Another known inhibitor of transport, colchicine (COL) also caused a significant decrease in the percent of neurites with a GAP-43 accumulation; propionamide (PA), a non-neurotoxic analogue of ACR, had no effect on protein accumulation. These findings support the hypothesis that the disruption of fast transport by ACR can lead to depletion of vital proteins in the distal axon.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Research on the protective effect of Rhizoma of Anemarrhena asphodeloides on TMT induced AD mice model based on network pharmacology combined with in vitro and in vivo experimental validation.
J Pharmacol Sci
February 2025
Department of Pharmacy, Anhui University of Chinese Medicine, Hefei, 230012, China; Anhui Province Key Laboratory of Traditional Chinese Medicine Decoction Pieces of New Manufacturing Technology, Hefei, 236000, China. Electronic address:
Background: Alzheimer's disease (AD) is a neurodegenerative disease, and neuroprotection is an important approach to improving AD outcomes. Rhizoma of Anemarrhena asphodeloides (RAA) is a commonly used Traditional Chinese Medicine (TCM) with demonstrated neuroprotective effects, but its anti-AD mechanism requires further exploration.
Aim Of The Study: To elucidate the neuroprotective mechanism of RAA on TMT-induced AD mice.
Altered brain connectivity in mild cognitive impairment is linked to elevated tau and phosphorylated tau, but not to GAP-43 and Amyloid-β measurements: a resting-state fMRI study.
Mol Brain
August 2024
School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mild Cognitive Impairment (MCI) is a neurological condition characterized by a noticeable decline in cognitive abilities that falls between normal aging and dementia. Along with some biomarkers like GAP-43, Aβ, tau, and P-tau, brain activity and connectivity are ascribed to MCI; however, the link between brain connectivity changes and such biomarkers in MCI is still being investigated. This study explores the relationship between biomarkers like GAP-43, Aβ, tau, and P-tau, and brain connectivity.
View Article and Find Full Text PDFErgosterol promotes neurite outgrowth, inhibits amyloid-beta synthesis, and extends longevity: In vitro neuroblastoma and in vivo Caenorhabditis elegans evidence.
Life Sci
May 2024
Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok 10330, Thailand; Natural Products for Neuroprotection and Anti-ageing Research Unit, Chulalongkorn University, Bangkok 10330, Thailand. Electronic address:
Aims: Alzheimer's disease (AD), the most common neurodegenerative disorder associated with aging, is characterized by amyloid-β (Aβ) plaques in the hippocampus. Ergosterol, a mushroom sterol, exhibits neuroprotective activities; however, the underlying mechanisms of ergosterol in promoting neurite outgrowth and preventing Aβ-associated aging have never been investigated. We aim to determine the beneficial activities of ergosterol in neuronal cells and Caenorhabditis elegans (C.
View Article and Find Full Text PDFElevated CSF GAP-43 is associated with accelerated tau accumulation and spread in Alzheimer's disease.
Nat Commun
January 2024
University of Gothenburg, The Sahlgrenska Academy, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Mölndal and Gothenburg, Sweden.
Article Synopsis
- - In Alzheimer's disease, amyloid-beta (Aβ) causes tau pathology to spread through the brain, and abnormal synaptic activity contributes to this process.
- - The study examined 93 patients and found that higher levels of the presynaptic protein GAP-43, which indicates synaptic changes, were linked to quicker tau accumulation related to Aβ.
- - The results suggest that targeting synapses could be a potential strategy for preventing the spread of tau pathology in Alzheimer's, highlighting the connection between synaptic changes and tau spread.
Restoring Synaptic Function: How Intranasal Delivery of 3D-Cultured hUSSC Exosomes Improve Learning and Memory Deficits in Alzheimer's Disease.
Mol Neurobiol
June 2024
Department of Hematology and Cell Therapy, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Article Synopsis
- Memory issues are often the initial indicators of Alzheimer's Disease (AD), leading to research on the therapeutic potential of stem cells and their exosomes to enhance cognitive function.
- A study using exosomes from 3D-cultured human Unrestricted Somatic Stem Cells (hUSSCs) found that intranasal delivery reduced amyloid-beta (Aβ) levels and improved spatial memory in a rat model of AD.
- The results highlighted an increase in neuroplasticity-related proteins in the hippocampus, suggesting exosome therapy may enhance memory and learning by promoting neural adaptability.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!