ArticleNeuropathology and applied neurobiology2009
Does Alzheimer's disease begin in the brainstem?
Article in Neuropathology and applied neurobiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
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Who cites it
105 citing papers in PubMed, 208 citations in OpenAlex.
- Amyloid beta plaque pathology induces chemosensory deficits and increases apnoeas in the 5XFAD mouse model of Alzheimer's disease.The Journal of physiology · 2026Article
- PET Imaging of the Human Brain with Microvolumetric Spatial Resolution.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025Article
- Biochemical characterization of Tau protein changes and amyloid dynamics in a novel non-transgenic rat model of tauopathy.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Automated MRI Segmentation of Brainstem Nuclei Critical to Consciousness.Human brain mapping · 2025Observational
- Reductions in brainstem volume as a key macrostructural indicator in at-risk populations for Alzheimer's disease.Alzheimer's research & therapy · 2025Article
- Subcortical tau deposition and plasma glial fibrillary acidic protein as predictors of cognitive decline in mild cognitive impairment and Alzheimer's disease.European journal of nuclear medicine and molecular imaging · 2025Article
- Locus coeruleus tau validates and informs high-resolution MRI in aging and at earliest Alzheimer's pathology stages.Acta neuropathologica communications · 2025Article
- Tau pathology in the dorsal raphe may be a prodromal indicator of Alzheimer's disease.Molecular psychiatry · 2025Article
- InGSA: integrating generalized self-attention in CNN for Alzheimer's disease classification.Frontiers in artificial intelligence · 2025Article
- Spatial differences in gene expression across the dorsal raphe nucleus in a model of early Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2025Article
- From Fundamentals to Innovation in Alzheimer's Disease: Molecular Findings and Revolutionary Therapies.International journal of molecular sciences · 2024Review
- Article
- Pathogenesis of Depression in Alzheimer's Disease.Neurochemical research · 2024Review
- Respiratory Dysfunction in Alzheimer's Disease-Consequence or Underlying Cause? Applying Animal Models to the Study of Respiratory Malfunctions.International journal of molecular sciences · 2024Review
- Predicting conversion from mild cognitive impairment to Alzheimer's disease: a multimodal approach.Brain communications · 2024Article
- Cognition Mediates the Association Between Cerebrospinal Fluid Biomarkers of Amyloid and P-Tau and Neuropsychiatric Symptoms.Journal of Alzheimer's disease : JAD · 2024Article
- Unique Pathology in the Locus Coeruleus of Individuals with Down Syndrome.Journal of Alzheimer's disease : JAD · 2024Article
- Oligomeric, phosphorylated, and truncated tau and spliceosome pathology within the entorhinal-hippocampal connectome across stages of Alzheimer's disease.The Journal of comparative neurology · 2023Article
- The Effect of the Human Brainstem Myelination on Gait Speed in Normative Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
- Higher performance for women than men in MRI-based Alzheimer's disease detection.Alzheimer's research & therapy · 2023Article
45 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Although substantial evidence indicates that the progression of pathological changes of the neuronal cytoskeleton is crucial in determining the severity of dementia in Alzheimer's disease (AD), the exact causes and evolution of these changes, the initial site at which they begin, and the neuronal susceptibility levels for their development are poorly understood. The current clinical criteria for diagnosis of AD are focused mostly on cognitive deficits produced by dysfunction of hippocampal and high-order neocortical areas, whereas noncognitive, behavioural and psychological symptoms of dementia such as disturbances in mood, emotion, appetite, and wake-sleep cycle, confusion, agitation and depression have been less considered. The early occurrence of these symptoms suggests brainstem involvement, and more specifically of the serotonergic nuclei. In spite of the fact that the Braak and Braak staging system and National Institutes of Aging - Reagan Institute (NIA-RI) criteria do not include their evaluation, several recent reports drew attention to the possibility of selective and early involvement of raphe nuclei, particularly the dorsal raphe nucleus (DRN), in the pathogenesis of AD. Based on these findings of differential susceptibility and anatomical connectivity, a novel pathogenetic scheme of AD progression was proposed. Although the precise mechanisms of neurofibrillary degeneration still await elucidation, we speculated that cumulative oxidative damage may be the main cause of DRN alterations, as the age is the main risk factor for sporadic AD. Within such a framework, beta-amyloid production is considered only as one of the factors (although a significant one in familial cases) that promotes molecular series of events underlying AD-related neuropathological changes.
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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.