The stereotypical pattern of neurofibrillary tangle spreading in the earliest stages of typical Alzheimer's dementia (AD) predicts that medial perirhinal cortex (mPRC) atrophy precedes entorhinal cortex (ERC) atrophy, whereas the status of the parahippocampal cortex (PHC) remains unclear. Atrophy studies have focused on more advanced rather than early AD patients, and usually segment the entire PRC as opposed to the mPRC versus lateral PRC (lPRC). The present study therefore determined the extent of ERC, mPRC, lPRC, and PHC atrophy in very early AD (mean Mini-Mental State Examination score = 26) patients and its presumed prodrome amnestic mild cognitive impairment (mean Mini-Mental State Examination score = 28) compared to demographically matched controls. PHG structures were manually segmented (blinded rater) and cortical thicknesses extracted. ERC and mPRC were similarly atrophied in both patient groups. The lPRC was atrophied in the AD group only. Thus, atrophic changes in very early AD broadly map onto the pattern of neurofibrillary tangle spreading and suggest that mPRC, ERC, and lPRC, but not PHC-associated functional impairments, characterize very early-stage AD.
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http://dx.doi.org/10.1016/j.neurobiolaging.2015.11.001 | DOI Listing |
Alzheimers Dement
December 2024
Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus Gualtar, Braga, Portugal.
Introduction: Alzheimer's disease (AD) co-pathology with Lewy bodies (LB) is frequent and influences clinical manifestations and outcomes. Its significance in primary age-related tauopathy (PART) is unknown. We investigated the influence of LB on cognition and brain atrophy in AD and PART.
View Article and Find Full Text PDFJ Alzheimers Dis
December 2024
Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Background: Amyloid-β (Aβ) and hyperphosphorylated tau are crucial biomarkers in Alzheimer's disease (AD) pathogenesis, interacting synergistically to accelerate disease progression. While Aβ initiates cascades leading to tau hyperphosphorylation and neurofibrillary tangles, PET imaging studies suggest a sequential progression from amyloidosis to tauopathy, closely linked with neurocognitive symptoms.
Objective: To analyze the complex interactions between Aβ and tau in AD using probabilistic graphical models, assessing how regional tau accumulation is influenced by Aβ burden.
Int J Pharm
December 2024
Biochemistry Department, Faculty of Science, Alexandria University, Alexandria 21511, Egypt. Electronic address:
J Alzheimers Dis
November 2024
Stony Brook World Trade Center Health and Wellness Program, Renaissance School of Medicine at Stony Brook University, Stony Brook, NY, USA.
Background: Amyloid-β proteins, a hallmark of Alzheimer's disease, are believed to play an adaptive role in the cerebral immune response.
Objective: Amyloid is believed to play a role in cerebral immune response and could play a similar role in response to air pollution exposures. In the present study, we examined whether WTC exposure duration was associated with cerebral amyloidosis in WTC responders.
Metab Brain Dis
November 2024
Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Alzheimer's disease (AD) is a neurodegenerative disorder that progresses over time and is identified by the development of neurofibrillary tangles and amyloid deposits in the brain. Mounting evidence has revealed that microRNAs (miRNAs) are significantly involved in AD progression, and may be used as promising biomarkers for diagnosis and prognosis. Nevertheless, the existing body of data regarding dysregulated circulating miRNAs in AD and their therapeutic applications are characterized by a lack of consistency.
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