ReviewJournal of Alzheimer's disease : JAD2014
Can BACE1 inhibition mitigate early axonal pathology in neurological diseases?
Review in Journal of Alzheimer's disease : JAD, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Neuritic Plaques - Gateways to Understanding Alzheimer's Disease.Molecular neurobiology · 2024Review
- Skeletal muscle transcriptional networks linked to type I myofiber grouping in Parkinson's disease.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Early Dendritic Dystrophy in Human Brains With Primary Age-Related Tauopathy.Frontiers in aging neuroscience · 2020Article
- Extracellular Sortilin Proteopathy Relative to β-Amyloid and Tau in Aged and Alzheimer's Disease Human Brains.Frontiers in aging neuroscience · 2020Article
- Lack of human-like extracellular sortilin neuropathology in transgenic Alzheimer's disease model mice and macaques.Alzheimer's research & therapy · 2018Article
- Can brain impermeable BACE1 inhibitors serve as anti-CAA medicine?BMC neurology · 2017Article
- Sortilin Fragments Deposit at Senile Plaques in Human Cerebrum.Frontiers in neuroanatomy · 2017Article
- Defining the earliest pathological changes of Alzheimer's disease.Current Alzheimer research · 2016Review
- Experimental microembolism induces localized neuritic pathology in guinea pig cerebrum.Oncotarget · 2015Article
- Non-neuronal and neuronal BACE1 elevation in association with angiopathic and leptomeningeal β-amyloid deposition in the human brain.BMC neurology · 2015Article
- Inverse correlation between Alzheimer's disease and cancer: implication for a strong impact of regenerative propensity on neurodegeneration?BMC neurology · 2014Article
- Lipolysaccharide-Induced Neuroinflammation Is Associated with Alzheimer-Like Amyloidogenic Axonal Pathology and Dendritic Degeneration in Rats.Advances in Alzheimer's disease · 2014Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
β-Secretase-1 (BACE1) is the rate-limiting enzyme for the genesis of amyloid-β (Aβ) peptides, the main constituents of the amyloid plaques in the brains of Alzheimer's disease (AD) patients. BACE1 is being evaluated as an anti-Aβ target for AD therapy. Recent studies indicate that BACE1 elevation is associated with axonal and presynaptic pathology during plaque development. Evidence also points to a biological role for BACE1 in axonal outgrowth and synapse formation during development. Axonal, including presynaptic, pathology exists in AD as well as many other neurological disorders such as Parkinson's disease, epilepsy, stroke, and trauma. In this review, we discuss pharmaceutical BACE1 inhibition as a therapeutic option for axonal pathogenesis, in addition to amyloid pathology. We first introduce the amyloidogenic processing of amyloid-β protein precursor and describe the normal expression pattern of the amyloidogenic proteins in the brain, with an emphasis on BACE1. We then address BACE1 elevation relative to amyloid plaque development, followed by updating recent understanding of a neurotrophic role of BACE1 in axon and synapse development. We further elaborate the occurrence of axonal pathology in some other neurological conditions. Finally, we propose pharmacological inhibition of excessive BACE1 activity as an option to mitigate early axonal pathology occurring in AD and other neurological disorders.
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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.