Good news in the beginning of 2025! Our assistant researchers Dr. Yue Cai and Dr. Guoyu Lan published their new works on Alzheimer's & Dementia. More information please refer to:

 https://alz-journals.onlinelibrary.wiley.com/doi/pdfdirect/10.1002/alz.14400  and

 https://alz-journals.onlinelibrary.wiley.com/doi/pdfdirect/10.1002/alz.14550.

Abstract  

INTRODUCTION: Alzheimer’s disease (AD) patients with higher educational attain ment(EA)oftenexhibitbettercognitivefunction.However,therelationshipamongEA status, AD pathology, structural brain reserve, and cognitive decline requires further investigation. METHODS: We compared cognitive performance across different amyloid beta (Aβ) positron emission tomography (A ±) statuses and EA levels (High EA/Low EA). We examined the effects of Aβ plaques, tau tangles, and gray matter volume (GMV) on the relationship between EA and domain-specific cognitive decline. 

RESULTS: A+/High-EA individuals exhibited slower cognitive decline in global cognition and language domains than A+/Low-EA individuals. This cognitive benefit was independently and synergistically explained by reduced AD pathology, including lower Aβ and tau burdens, as well as preserved GMV. Additionally, High-EAindividuals experienced a median delay of 1.9 years in the onset of significant brain atrophy among A+ individuals. 

DISCUSSION: These findings highlight the independent and synergistic contributions of EA-associated AD pathology and GMV alterations to longitudinal cognitive decline.

Abstract 

INTRODUCTION: Novel fluid biomarkers for tracking neurodegeneration specific to Alzheimer’s disease (AD)aregreatlyneeded. 

METHODS: Using two independent well-characterized cohorts (n = 881 in total), we investigated the group differences in plasma N-terminal tau (NT1-tau) fragmentsacross different AD stages and their association with cross-sectional and longitudinal amyloid beta(Aβ) plaques, tautangles, brainatrophy, and cognitive decline. 

RESULTS: Plasma NT1-tau significantly increased in symptomatic AD and displayed positive associations with Aβ PET (positron emission tomography) and tau PET. Higher baseline NT1-tau levels predicted greater tau PET, with 2- to 10-year intervals and faster longitudinal Aβ PET increases, AD-typical neurodegeneration, and cognitive decline. Plasma NT1-tau showed negative correlations with baseline regional brain volume and thickness, superior to plasma brain-derived tau (BD-tau) and neurofilament light (NfL) in Aβ-positive participants. 

DISCUSSION: This study suggests that plasma NT1-tau is an Aβ-dependent biomarker and outperforms BD-tau and NfL in detecting cross-sectional neurodegeneration in the AD continuum.