ReviewFrontiers in neuroanatomy2017
The Neuroanatomy of the Reticular Nucleus Locus Coeruleus in Alzheimer's Disease.
Review in Frontiers in neuroanatomy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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.
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Who cites it
30 citing papers in PubMed, 65 citations in OpenAlex.
- Non-linear associations between sleep duration and plasma p-tau181 in the Framingham Heart Study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Regulation of non-emotional memory through αIBRO neuroscience reports · 2025Review
- Fading Blue: Exploring the Causes of Locus Coeruleus Damage Across the Lifespan.Antioxidants (Basel, Switzerland) · 2025Review
- The locus coeruleus, a blue spot for early diagnosis and prognosis of Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- The Neuroanatomy of Induced Pluripotent Stem Cells: In Vitro Models of Subcortical Nuclei in Neurodegenerative Disorders.Current issues in molecular biology · 2024Review
- Automatic Geometry-based Estimation of the Locus Coeruleus Region on TbioRxiv : the preprint server for biology · 2024Article
- Predicting conversion from mild cognitive impairment to Alzheimer's disease: a multimodal approach.Brain communications · 2024Article
- Automatic geometry-based estimation of the locus coeruleus region on TFrontiers in neuroscience · 2024Article
- Exploring the Role of Locus Coeruleus in Alzheimer's Disease: a Comprehensive Update on MRI Studies and Implications.Current neurology and neuroscience reports · 2023Review
- New perspectives on the basal forebrain cholinergic system in Alzheimer's disease.Neuroscience and biobehavioral reviews · 2023Review
- Review
- Locus Coeruleus Dysfunction and Trigeminal Mesencephalic Nucleus Degeneration: A Cue for Periodontal Infection Mediated Damage in Alzheimer's Disease?International journal of environmental research and public health · 2023Review
- Association of Tooth Loss with Alzheimer's Disease Tau Pathologies Assessed by Positron Emission Tomography.Journal of Alzheimer's disease : JAD · 2023Article
- Recent Advances Towards Diagnosis and Therapeutic Fingerprinting for Alzheimer's Disease.Journal of molecular neuroscience : MN · 2022Review
- Grounding the Attentional Boost Effect in Events and the Efficient Brain.Frontiers in psychology · 2022Review
- Article
- Norepinephrine Protects against Methamphetamine Toxicity through β2-Adrenergic Receptors Promoting LC3 Compartmentalization.International journal of molecular sciences · 2021Article
- The connections of Locus Coeruleus with hypothalamus: potential involvement in Alzheimer's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2021Review
- The mechanistic link between selective vulnerability of the locus coeruleus and neurodegeneration in Alzheimer's disease.Acta neuropathologica · 2021Review
- Shear-Induced Amyloid Aggregation in the Brain: V. Are Alzheimer's and Other Amyloid Diseases Initiated in the Lower Brain and Brainstem by Cerebrospinal Fluid Flow Stresses?Journal of Alzheimer's disease : JAD · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's Disease (AD) features the accumulation of β-amyloid and Tau aggregates, which deposit as extracellular plaques and intracellular neurofibrillary tangles (NFTs), respectively. Neuronal Tau aggregates may appear early in life, in the absence of clinical symptoms. This occurs in the brainstem reticular formation and mostly within Locus Coeruleus (LC), which is consistently affected during AD. LC is the main source of forebrain norepinephrine (NE) and it modulates a variety of functions including sleep-waking cycle, alertness, synaptic plasticity, and memory. The iso-dendritic nature of LC neurons allows their axons to spread NE throughout the whole forebrain. Likewise, a prion-like hypothesis suggests that Tau aggregates may travel along LC axons to reach out cortical neurons. Despite this timing is compatible with cross-sectional studies, there is no actual evidence for a causal relationship between these events. In the present mini-review, we dedicate special emphasis to those various mechanisms that may link degeneration of LC neurons to the onset of AD pathology. This includes the hypothesis that a damage to LC neurons contributes to the onset of dementia due to a loss of neuroprotective effects or, even the chance that, LC degenerates independently from cortical pathology. At the same time, since LC neurons are lost in a variety of neuropsychiatric disorders we considered which molecular mechanism may render these brainstem neurons so vulnerable.
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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.