Tau Proteins in the Temporal and Frontal Cortices in Patients With Vascular Dementia. Issue 2 (February 2015)

• Record Type: Journal Article
• Authors: Mukaetova-Ladinska, Elizabeta B.; Abdel-All, Zeinab; Mugica, Estibaliz Santiago; Li, Mosi; Craggs, Lucy J. L.; Oakley, Arthur E.; Honer, William G.; Kalaria, Raj N.
• Is Part Of: Journal of neuropathology and experimental neurology. Volume 74:Issue 2(2015:Feb.)
• Publication Date: 2015-02
• Subjects: Aging -- Alzheimer disease -- Ischemia -- Microvascular -- Stroke -- Tau -- Vascular dementia; Neurology -- Diseases -- Periodicals; Neurology -- Diseases -- Physiopathology -- Periodicals; 616.8047
• DOI: 10.1097/NEN.0000000000000157
• Languages: English
• ISSNs: 0022-3069

Abstract

Abstract : Abstract: We previously reported that, in the brains of older patients with vascular dementia (VaD), there is a distinctive accumulation of detergent-extractable soluble amyloid-β, with a predominance of Aβ42 species. It is unclear, however, if tau proteins also accumulate in the brains of older VaD subjects. Using antibody-specific immunoassays, we assessed concentrations of total tau (t-tau) and phosphorylated tau protein, measured at 3 phosphorylated sites (i.e. Thr181, Ser202/Thr205, and Ser262), as well as synaptophysin in the temporal and frontal cortices of 18 VaD, 16 Alzheimer disease (AD), and 16 normal age-matched control subjects. There was selective loss of t-tau protein in VaD compared with controls and AD subjects (p < 0.021 and p < 0.001, respectively). In contrast, phosphorylated tau levels were similar to controls in VaD in both regions, but they were increased in the temporal lobes of patients with AD (p < 0.01 and p < 0.0001 for Ser202/Thr205 and Ser262 phosphorylated sites, respectively). The reduced t-tau in the VaD group was unrelated to any low-level neurofibrillary or amyloid pathology or age at death. These findings suggest that breaches of microvascular or microstructural tissue integrity subsequent to ischemic injury in older age may modify tau protein metabolism or phosphorylation and have effects on the burden of neurofibrillary pathology characteristic of AD. Abstract : Supplemental digital content is available in the text.