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Variations in several biomarkers, including proteins found in cerebrospinal fluid (CSF), might appear 6 to 18 years before a person develops Alzheimer disease, according to a prospective cohort study that included more than 600 participants in China with no family history of the condition.
Studio preliminare Ifom e Int, promettente strategia combinata
New England Journal of Medicine, Volume 390, Issue 12, March 2024.
Autore/Fonte: International Journal of Molecular Sciences
Autore/Fonte: Cleveland Clinic
Solo l’1% delle ricerche sono dedicate a condizioni specifiche di genere. Intervista alla neuroscienziata Antonella Santuccione Chadha: «Donne enorme bacino di pazienti sottodiagnosticato»
New England Journal of Medicine, Volume 390, Issue 10, March 2024.
Rivedere la normativa Ue per accrescere conoscenza prodotto
New England Journal of Medicine, Volume 390, Issue 9, Page 866-867, February 2024.
A commercially available blood test that measures levels of a tau protein known as phosphorylated tau 217, or p-tau217, was able to identify people whose brains showed signs of Alzheimer disease pathology, according to data from an observational study. The research involved about 800 participants with and without cognitive impairment.
New England Journal of Medicine, Volume 390, Issue 8, Page 712-722, February 2024.
New England Journal of Medicine, Volume 390, Issue 8, Page 761-763, February 2024.
Ridurranno del 70% gli esami inutili
Autore/Fonte: American Academy of Neurology
Stroke, Volume 55, Issue Suppl_1, Page ATP312-ATP312, February 1, 2024. Traumatic brain injury (TBI) afflicts 70 million people worldwide annually and is the 3rd overall risk factor for developing Alzheimer’s disease (AD), behind genetics and aging. In patients with AD, a history of TBI is associated with a 3-4 year earlier onset of cognitive impairment. TBI and AD share many pathologies, including blood brain barrier dysfunction, neuroinflammation, and protein aggregation. Yet, the underlying mechanism of this relationship is not understood, and there are no treatments that protect patients from accelerated AD after TBI. We recently reported that tau, a microtubule binding protein essential for neuronal health, is acetylated after TBI. Acetylation impairs tau binding to microtubules, leading to its mis-localization into the cell soma and pathological aggregation. Acetylated tau is also elevated early in AD, and acetylated tau was significantly more elevated in the brains of human AD subjects with a history of TBI, compared to AD alone and healthy controls. Therefore, we hypothesize that TBI-induced tau acetylation drives the acceleration of AD. To study this phenomenon, we developed a mouse model of TBI that accelerates AD-like pathology and cognitive impairment in 5xFAD mice, and amyloid-driven AD model. Our unique model of multimodal TBI produces a complex and reproducible brain injury with neurodegeneration and neurobehavioral impairment, beginning with acute axonal degeneration and persisting chronically with blood-brain barrier degradation and nerve cell death. This model of TBI also produces the same systemic metabolic alterations that are reported in TBI patients. TBI causes learning deficits in young 5xFAD mice that are not seen in either sham-injured 5xFAD mice or in wild type littermates subjected to TBI. TBI also accelerates amyloid deposition in 5xFAD mice. We hypothesize that TBI will also worsen blood brain barrier function in 5xFAD mice. Importantly, 5xFAD mice show greater elevation of acetylated tau after TBI, compared to WT mice. Preliminary data suggests that treatment with the FDA-approved non-steroidal inflammatory drug diflunisal, which inhibits the enzyme that acetylates tau, reduces acetylated tau and rescues behavior deficits after TBI in 5xFAD mice.
Un nuovo studio dell’Università Tor Vergata ne dimostra il ruolo benefico
