ArticleAlzheimer's research & therapy2021
In vivo human molecular neuroimaging of dopaminergic vulnerability along the Alzheimer's disease phases.
Article in Alzheimer's research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 63 citations in OpenAlex.
- Targeting the dopaminergic midbrain in Alzheimer's disease: Therapeutic potential of focusing on specific neural circuits rather than single molecular pathways.Neural regeneration research · 2026Article
- Dopaminergic nigrostriatal vulnerability in Parkinson's Disease with diabetes: evidence from severity-matched cohorts.European journal of nuclear medicine and molecular imaging · 2026Article
- Correspondence of Basal Forebrain Resting-State Functional Connectivity and Cerebral Glucose Metabolism Alterations With Neurotransmitter Maps in Alzheimer's Disease.CNS neuroscience & therapeutics · 2026Article
- Photostimulation of locus coeruleus CA1 catecholaminergic terminals reversed Spatial memory impairment in an alzheimer's disease mouse model.Psychopharmacology · 2026Article
- Alzheimer's Pathology Enhances Excitatory Synaptic Input and Integration in VTA Dopamine Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Age-related dopaminergic integrity in the SNpc and VTA: morphometric and volumetric findings in marmoset (Frontiers in neuroanatomy · 2026Article
- Dopamine D3 receptor blockade restores hippocampal synaptic plasticity and rescues memory deficits in Alzheimer's disease mouse models.Frontiers in aging neuroscience · 2026Article
- Cholinergic network disruptions on cognitive function across the spectrum of cognitive impairment in Parkinson's disease.Journal of neurology · 2025Article
- The impact of polygenic risk for alzheimer's disease on neurotransmitter-related grey matter atrophy in the alzheimer continuum.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Midbrain degeneration triggers astrocyte reactivity and tau pathology in experimental Alzheimer's Disease.Molecular neurodegeneration · 2025Article
- Optogenetic stimulation of midbrain dopaminergic neurons rescues hippocampal synaptic plasticity deficits in a mouse model of Alzheimer's disease.Translational psychiatry · 2025Article
- PKC-dependent enhancement of glutamate input to VTA dopamine neurons in 3xTg-AD mice.bioRxiv : the preprint server for biology · 2025Article
- Disarming COX-1 to disrupt Alzheimer's inflammatory trajectory: preclinical insights and translational promise.Translational neurodegeneration · 2025Article
- Reconsidering dopaminergic modulation in Alzheimer's disease: A case for levodopa/carbidopa as a disease-modifying agent.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Association between the use of levodopa/carbidopa, Alzheimer's disease biomarkers, and cognitive decline among participants in the National Alzheimer's Coordinating Center Uniform Data Set.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Repetitive prefrontal tDCS activates VTA dopaminergic neurons, resulting in attenuation of Alzheimer's Disease-like deficits in Tg2576 mice.Alzheimer's research & therapy · 2025Article
- CSF biomarkers are differentially linked to brain areas high and low in noradrenaline, dopamine and serotonin across the Alzheimer's disease spectrum.Brain communications · 2025Article
- Molecular connectivity studies in neurotransmission: a scoping review.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- Changes in neurotransmitter-related functional connectivity along the Alzheimer's disease continuum.Brain communications · 2025Article
- Insular monoaminergic deficits in prodromal α-synucleinopathies.Annals of clinical and translational neurology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPreclinical and pathology evidence suggests an involvement of brain dopamine (DA) circuitry in Alzheimer's disease (AD). We in vivo investigated if, when, and in which target regions [123I]FP-CIT-SPECT regional binding and molecular connectivity are damaged along the AD course.
methodsWe retrospectively selected 16 amyloid-positive subjects with mild cognitive impairment due to AD (AD-MCI), 22 amyloid-positive patients with probable AD dementia (AD-D), and 74 healthy controls, all with available [123I]FP-CIT-SPECT imaging. We tested whether nigrostriatal vs. mesocorticolimbic dopaminergic targets present binding potential loss, via MANCOVA, and alterations in molecular connectivity, via partial correlation analysis. Results were deemed significant at p < 0.05, after Bonferroni correction for multiple comparisons.
resultsWe found significant reductions of [123I]FP-CIT binding in both AD-MCI and AD-D compared to controls. Binding reductions were prominent in the major targets of the ventrotegmental-mesocorticolimbic pathway, namely the ventral striatum and the hippocampus, in both clinical groups, and in the cingulate gyrus, in patients with dementia only. Within the nigrostriatal projections, only the dorsal caudate nucleus showed reduced [123I]FP-CIT binding, in both groups. Molecular connectivity assessment revealed a widespread loss of inter-connections among subcortical and cortical targets of the mesocorticolimbic network only (poor overlap with the control group as expressed by a Dice coefficient ≤ 0.25) and no alterations of the nigrostriatal network (high overlap with controls, Dice coefficient = 1).
conclusionLocal- and system-level alterations of the mesocorticolimbic dopaminergic circuitry characterize AD, already in prodromal disease phases. These results might foster new therapeutic strategies for AD. The clinical correlates of these findings deserve to be carefully considered within the emergence of both neuropsychiatric symptoms and cognitive deficits.
Indexed as
Identifiers
What OpenQuestion holds
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.