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Posterior Cortical Atrophy / Alzheimer Disease, Early Onset / TEP/IRM · Interventional Study
ClinicalTrials.gov · August 20, 2026
Early or partial results. Treat as a signal, not a conclusion.
This is a recruiting, interventional study designed to identify neural mechanisms of resilience in early-onset Alzheimer's disease and posterior cortical atrophy using simultaneous PET/MR imaging. No results are yet available in this registry record. The study aims to explain why some patients with the same neuropathology show focal rather than diffuse cognitive and anatomical impairment.
Interventional, Non Randomized, Parallel, Open label, Diagnostic purpose. Alzheimer Disease, Early Onset, Posterior Cortical Atrophy; age from 40 Years; to 80 Years; accepts healthy volunteers. Intervention: Patients with Alzheimer (<65 years) (AD-Y); Patients with posterior Cortical Atrophy (PCA). Compared with: Control — Active Comparator. n = 45. 2 sites: France.
This is a recruiting, interventional study designed to identify neural mechanisms of resilience in early-onset Alzheimer's disease and posterior cortical atrophy using simultaneous PET/MR imaging. No results are yet available in this registry record. The study aims to explain why some patients with the same neuropathology show focal rather than diffuse cognitive and anatomical impairment.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
If successful, this study may identify neurobiological mechanisms that confer resistance to cognitive decline despite neuropathological burden, potentially informing future therapeutic strategies for Alzheimer's disease. Results are not yet available.
This is a recruiting interventional study with no results posted; it is designed to explore mechanistic hypotheses about neuronal resilience in Alzheimer's disease using PET/MR imaging.
As stated by the source record.
Quoted from the source exactly as published.
If successful, this study may identify neurobiological mechanisms that confer resistance to cognitive decline despite neuropathological burden, potentially informing future therapeutic strategies for Alzheimer's disease. Results are not yet available.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no key findings. That is a gap in the analysis, not a judgement about the study.
Registry record from ClinicalTrials.gov (NCT04150198). This is a study registration, not published results. Lead sponsor: Institut National de la Santé Et de la Recherche Médicale, France. Recruitment status: RECRUITING. Phase: NA. Study type: INTERVENTIONAL. Enrollment: 45 participants (ESTIMATED). Conditions: Alzheimer Disease, Early Onset, Posterior Cortical Atrophy. Interventions: DEVICE: TEP/IRM. Primary outcome measures: highlight of the "resilient" neural networks , up to 3 months; quantify the impairment (ie brain vulnerability) in AD-Y and in PCA , up to 3 months. Brief summary: Patients with Alzheimer's disease and with early onset of symptoms (\<65 years) (AD-Y) have a multi-domain cognitive deficit, whereas memory disorders (typical of the elderly patient's AD) are less often in the foreground. In addition, some MA-J have an atypical phenotype indicating focal brain damage, although they have the same pathological lesions: amyloid deposits and tau protein deposition (DNF). This is the case of posterior cortical atrophy (PCA) characterized by complex visual disturbances and atrophy affecting the more posterior regions of the brain. Based on the clinical profile of PCA patients, a more refined anatomo-clinical classification was proposed, distinguishing a rather "ventral" form and a rather "dorsal" form. The recent arrival of tau-specific PET tracers now makes it possible to evaluate in vivo fibrillary neurodegeneration (FND), which is well correlated with the severity of cognitive disorders. Advances in MRI have shown that each neurodegenerative syndrome targets a large-scale neural network, which in turn shows a vulnerability for a specific biological disease. In the case of AD, the reason for such a difference in cognitive and anatomical impairment between patients with diffuse involvement and others with more focal involvement is not known. One possible explanation is the existence, in focal forms, of neuronal mechanisms that oppose vulnerability. These mechanisms may correspond to the so-called "resilience" phenomenon, defined as resistance to a neuropathological process by the ability to optimize cognitive performance via the efficient recruitment of neural networks. The mechanisms underlying resilience in neurodegeneration are unknown. Their identification is very important for the management and treatment of AD.
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