Neurogranin, a CSF Biomarker for Synaptic Loss, is Found to Predict Progression from MCI to Alzheimer’s Disease

Levels of neurogranin, a cerebrospinal fluid (CSF) biomarker for synaptic loss, were elevated in patients with Alzheimer’s disease (AD) compared with cognitively normal individuals. Neurogranin levels also predicted progression from mild cognitive impairment (MCI) to AD dementia, researchers reported here on Monday at the Alzheimer’s Association International Conference (AAIC).

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A new study published in JAMA Psychiatry suggests that clinical depression is associated with a 30% increase in brain inflammation.

This finding provides the most compelling evidence to date of brain inflammation, and more specifically microglial activation, in MDE. The correlation between higher ACC TSPO VT and the severity of MDE is consistent with the concept that neuroinflammation in specific regions may contribute to sickness behaviors that overlap with the symptoms of MDE.

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The FDA accepted Namzaric‘s New Drug Application (NDA) as a fixed-dose combination of memantine hydrochloride extended-release and donepezil hydrochloride tabilized on memantine hydrochloride and donepezil hydrochloride

“Namzaric combines, in one capsule, two complementary therapeutic agents which are often co-prescribed as approximately 70% of Namenda XR patients are also on AChEI therapy.  Both Namenda XR and donepezil have proven efficacy and safety, for the treatment of moderate/severe Alzheimer’s disease.”

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Dr. Neil Buckholtz of the NIA discusses ADNI in a summary of the recent presentations at the AAIC in Copenhagen and other Alzheimer’s research news.

From early morning to late evening, at symposium and plenary sessions, during poster sessions and coffee breaks, at add-on meetings and consortium sessions, some 4,300 investigators from 75 different countries shared recent findings and explored ways to overcome the challenges of finding ways to treat or prevent this complex disease.

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A team of researchers from Columbia University Medical Center (CUMC), Weill Cornell Medical College, and Brandeis University has devised a wholly new approach to the treatment of Alzheimer’s disease involving the so-called retromer protein complex.

Retromer plays a vital role in neurons, steering amyloid precursor protein (APP) away from a region of the cell where APP is cleaved, creating the potentially toxic byproduct amyloid-beta, which is thought to contribute to the development of Alzheimer’s.

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