Sentences with phrase «deposition of amyloid plaques»

Alzheimer's disease results from the deposition of amyloid plaques in the brain.

Given the lack of definitive AD biomarkers in humans, transgenic animal models of the amyloid pathology continue to be valuable tools to examine molecular changes preceding the deposition of amyloid plaques and associated pathology (i.e. late inflammation, neuritic dystrophy, etc.).

However, it is widely accepted that before the overt deposition of amyloid plaques and neurofibrillary tangles, the accumulation of amyloid - β (Aβ) peptides is one of the first steps in the series of pathogenic changes that lead to neurodegeneration and dementia [5, 6].

Not exact matches

High levels of «good» cholesterol and low levels of «bad» cholesterol are correlated with lower levels of the amyloid plaque deposition in the brain that is a hallmark of Alzheimer's disease, in a pattern that mirrors the relationship between good and bad cholesterol in cardiovascular disease, UC Davis researchers have found.

«This study has allowed us to sort out, in mice, which effects of the different types of APOE were most important to variation in amyloid plaque deposition,» says Eloise Hudry, PhD, of MGH - MIND, lead author of the Science Translational Medicine report.

The main hypothesis on the cause of Alzheimer's involves amyloid deposition, the buildup of plaques in the brain that impair neurological function; most biomedical efforts to tackle the disease have focused on this issue.

This is the proposal that deposition of amyloid - beta, a major protein ingredient of the plaques that accumulate in the brains of Alzheimerâ $ ™ s patients, is a central event in the pathology of the disease.

Dendritic Spine Density, Morphology, and Fibrillar Actin Content Surrounding Amyloid -[beta] Plaques in a Mouse Model of Amyloid -[beta] Deposition.

The early intraneuronal pathology was accompanied by a significant elevation of soluble Aβ42 peptides that paralleled the presence and progression of early cognitive deficits, several months prior to amyloid plaque deposition.

Alzheimer's disease (AD) is characterized by deposition of amyloid - β (Aβ) plaques and neurofibrillary tangles in the brain, accompanied by synaptic dysfunction and neurodegeneration.

This technique allowed the detection of C - terminally truncated peptides, including Aβ38, Aβ39, Aβ40 and Aβ42 species, as early as 3 months of age; a time point which precedes amyloid plaque deposition by several months (4 — 6 months).

These results support the amyloid cascade of tau phosphorylation in AD regarding phosphorylation of tau dependent on beta - amyloid deposition in neuritic plaques, but not of tau in neurofibrillary tangles and threads.

Immunizing transgenic PDAPP mice, which overexpress mutant APP and develop beta - amyloid deposition resembling plaques in Alzheimer's disease (AD), results in a decrease of amyloid burden when compared with non-treated transgenic animals.

BACKGROUND: AD is characterized by cerebral deposition of beta - amyloid plaques with amyloid beta - peptide (Abeta) 42 as the major peptide constituent, along with neurofibrillary tangles and neuronal loss.

High Vitamin C supplementation reduces amyloid plaque deposition (cause of AD), blood brain barrier disruptions and mitochondrial dysfunction in the brains.

Other studies have shown that dogs affected by this syndrome show deposition of amyloid (a protein) in their brains in patterns very similar to the amyloid plaques found in the brains of human Alzheimer's patients.

Other studies have shown that dogs affected by this syndrome show deposition of a protein called amyloid in their brains in patterns similar to the amyloid plaques found in the brains of humans with Alzheimer's disease.