Dataset Information

The Interplay Between Beta-Amyloid 1-42 (Aβ_1-42)-Induced Hippocampal Inflammatory Response, p-tau, Vascular Pathology, and Their Synergistic Contributions to Neuronal Death and Behavioral Deficits.

ABSTRACT: Alzheimer's disease (AD), the most common chronic neurodegenerative disorder, has complex neuropathology. The principal neuropathological hallmarks of the disease are the deposition of extracellular β-amyloid (Aβ) plaques and neurofibrillary tangles (NFTs) comprised of hyperphosphorylated tau (p-tau) protein. These changes occur with neuroinflammation, a compromised blood-brain barrier (BBB) integrity, and neuronal synaptic dysfunction, all of which ultimately lead to neuronal cell loss and cognitive deficits in AD. Aβ_1-42 was stereotaxically administered bilaterally into the CA1 region of the hippocampi of 18-month-old male C57BL/6 mice. This study aimed to characterize, utilizing immunohistochemistry and behavioral testing, the spatial and temporal effects of Aβ_1-42

SUBMITTER: Calvo-Flores Guzman B

PROVIDER: S-EPMC7667153 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

ACCESS DATA

Dataset Information

The Interplay Between Beta-Amyloid 1-42 (Aβ_1-42)-Induced Hippocampal Inflammatory Response, p-tau, Vascular Pathology, and Their Synergistic Contributions to Neuronal Death and Behavioral Deficits.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

The Interplay Between Beta-Amyloid 1-42 (Aβ1-42)-Induced Hippocampal Inflammatory Response, p-tau, Vascular Pathology, and Their Synergistic Contributions to Neuronal Death and Behavioral Deficits.

OmicsDI is part of the ELIXIR infrastructure

Tweets

The Interplay Between Beta-Amyloid 1-42 (Aβ_1-42)-Induced Hippocampal Inflammatory Response, p-tau, Vascular Pathology, and Their Synergistic Contributions to Neuronal Death and Behavioral Deficits.