ArticleCNS & neurological disorders drug targets2014
Therapeutic perspectives of drugs targeting Toll-like receptors based on immune physiopathology theory of Alzheimer's disease.
Article in CNS & neurological disorders drug targets, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Identification and immunological characterization of genes associated with ferroptosis in Alzheimer's disease and experimental demonstration.Molecular medicine reports · 2024Article
- Antiviral responses versus virus-induced cellular shutoff: a game of thrones between influenza A virus NS1 and SARS-CoV-2 Nsp1.Frontiers in cellular and infection microbiology · 2024Review
- Discovery and validation of Ferroptosis-related molecular patterns and immune characteristics in Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- Coronavirus Nsp1: Immune Response Suppression and Protein Expression Inhibition.Frontiers in microbiology · 2021Review
- Hippocampal Cholinergic Neurostimulating Peptide as a Possible Modulating Factor against Glutamatergic Neuronal Disability by Amyloid Oligomers.Cell transplantation · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease associated with the development of dementia. It has been established that the pathological hallmarks of neurofibrillary tau protein tangles and senile β-amyloid protein plaques lead to degeneration of neurons via inflammatory pathways. The progressive death of neurons, primarily cholinergic, results in a gradual and fatal decline of cognitive abilities and memory. By targeting these pathological hallmarks and their associated pathways, AD drug therapy can potentially attenuate the disease state. In this review article, we focus on newly proposed and experimental AD drug treatment. We discuss three characteristic areas of AD treatment: prevention of neurotoxic β-amyloid protein plaque formation, stability of neuronal tau proteins, and increase in neuronal growth and function. The primary drug therapy methods and patents discussed include the use of neurotrophic factors and targeting of the amyloid precursor protein cleavage pathway as prevention of β-amyloid formation and tau aggregation.
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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 OpenQuestion graph.