scholarly journals Structural covariance of superficial white matter in mild Alzheimer's disease compared to normal aging

2014 ◽  
Vol 4 (5) ◽  
pp. 721-737 ◽  
Author(s):  
Cristian Carmeli ◽  
Eleonora Fornari ◽  
Mahdi Jalili ◽  
Reto Meuli ◽  
Maria G. Knyazeva
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Normal Aging ◽  
Structural Covariance

Possible Retrogenesis Observed with Fiber Tracking: An Anteroposterior Pattern of White Matter Disintegrity in Normal Aging and Alzheimer's Disease

2011 ◽  
Vol 26 (1) ◽  
pp. 47-58 ◽  
Author(s):  
Junling Gao ◽  
Raymond Tak-Fai Cheung ◽  
Tatia M.C. Lee ◽  
Leung-Wing Chu ◽  
Ying-Shing Chan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Fiber Tracking ◽  
Normal Aging

scholarly journals Ventricular expansion, white matter hyperintensities, and global cognition in Alzheimer’s disease and normal aging

2020 ◽  
Author(s):  
Sabrina Adamo ◽  
Joel Ramirez ◽  
Melissa F. Holmes ◽  
Fuqiang Gao ◽  
Ljubica Zotovic ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
White Matter Hyperintensities ◽  
Small Vessel Disease ◽  
Normal Aging ◽  
Small Vessel ◽  
Cognitive Test ◽  
Vessel Disease ◽  
Link Type

ABSTRACTBackgroundThe progression of Alzheimer’s Disease (AD) may be tracked by measuring the growth of the ventricular cerebrospinal fluid (vCSF) over time. AD is commonly comorbid with markers of cerebral small vessel disease (SVD), viewed on MRI as white matter hyperintensities (WMH). Larger WMH volumes are correlated with poorer cognitive test scores. Additionally, periventricular WMHs have a proposed relationship to the vCSF.PurposeThis study will examine ventricular expansion and its associations between periventricular/deep WMH and cognition in AD and normal aging.MethodsBaseline and 1-year follow-up data were collected from AD (n=117) and cognitively normal control (NCs; n=49) participants taking part in the Sunnybrook Dementia Study. MRI (1.5T) and scores from both the Mini-Mental State Examination (MMSE) and the Dementia Rating Scale (DRS) were assessed at each time point. Volumetric data was generated using a semi-automated pipeline and each individual’s vCSF and WMHs were transformed to an intermediate space to determine volumetric growth. Regressions were used to determine relationships between vCSF growth measures, SVD burden, and cognition, accounting for demographics and individual interscan intervals.ResultsThe AD group displayed 14.6% annual ventricular growth as opposed to NC who had only 11.8% annual growth. AD showed significant growth in vCSF (p < 0.001), a trend toward greater pWMH growth (p = 0.06) and no difference in dWMH growth volumes compared to NC. vCSF growth was positively associated with pWMH (β = 0.32, p < 0.001) but not dWMH growth in AD while in NC it was associated with both pWMH (β = 0.48, p < 0.001) and dWMH growth (β = 0.35, p = 0.02). In AD, vCSF growth was associated with the both the MMSE (β = -0.30, p < 0.001) and the DRS (β = -0.31, p < 0.001) in separate models.ConclusionsThe findings from this study suggest that in just under 1.5 years, the significantly rapid ventricular expansion observed in AD may be closely related to periventricular small vessel disease. As vCSF growth rates are an important biomarker of AD neurodegeneration that corresponds with cognitive decline, future research should further explore atrophy associated with periventricular vasculopathy.Trial RegistrationClinicalTrials.gov, NCT01800214. Registered on 27 February 2013.

scholarly journals Neuroinflammation and Myelin Status in Alzheimer’s Disease, Parkinson’s Disease, and Normal Aging Brains: A Small Sample Study

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Fei Han ◽  
Richard J. Perrin ◽  
Qing Wang ◽  
Yong Wang ◽  
Joel S. Perlmutter ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
White Matter ◽  
Brain Tissue ◽  
Amyloid Beta ◽  
Calcium Binding ◽  
Normal Aging ◽  
Small Sample

Microglia and astrocytes play important roles in mediating the immune processes and nutritional support in the central nervous system (CNS). Neuroinflammation has been indicated in the progression of neurodegenerative diseases Alzheimer’s disease (AD) and Parkinson’s disease (PD). Chronic neuroinflammation with sustained activation of microglia and astrocytes may affect white matter tracts and disrupt communication between neurons. Recent studies indicate astrogliosis may inhibit remyelination in demyelinating disorders such as multiple sclerosis. In this study, we investigated the relationship between neuroinflammation and myelin status in postmortem human brain tissue (n = 15 including 6 AD, 5 PD, and 4 age-matched, neurologically normal controls (NC)). We conducted systematic and quantitative immunohistochemistry for glial fibrillary acidic protein (GFAP), ionized calcium-binding adaptor molecule 1 (Iba1), amyloid beta, and highly phosphorylated tau (tauopathy). White matter intactness was evaluated by myelin and axon staining in adjacent brain tissue sections. Eight of 15 cases (4 AD, 3 PD, and 1 NC) showed increased immunoreactivity for microglia and astrocytes in the white matter that connects striatum and cortex. Quantitative analysis of these 8 cases showed a significant negative correlation between GFAP (but not Iba-1) and myelin (but not axon) staining in white matter (r2 = 0.78, p<0.005). Tau, but not amyloid beta plaques, is significantly higher in AD vs. PD and NC. Tau burden increases with age in AD cases. These observations indicate that astrocytosis in white matter is associated with loss of myelin in AD, PD, and normal aging and that tau is a potent biomarker for AD.

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