Early Alzheimer-type lesions in cognitively normal subjects
| Autor: | Patrick R. Hof, Constantin Bouras, Eniko Veronika Kovari, Aikaterini Xekardaki, Stergios Tsartsalis |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
Adult
Male 0301 basic medicine Aging Pathology medicine.medical_specialty Tau protein tau Proteins Article Cohort Studies Healthy Aging 03 medical and health sciences ddc:616.89 Cognition 0302 clinical medicine Alzheimer Disease Cortex (anatomy) mental disorders medicine Humans Senile plaques Brodmann area 9 Aged Aged 80 and over Temporal cortex Amyloid beta-Peptides biology General Neuroscience Brain Neurofibrillary Tangles Neurofibrillary tangle Brodmann area 20 Middle Aged medicine.disease Entorhinal cortex 030104 developmental biology medicine.anatomical_structure Tauopathies Nerve Degeneration biology.protein Female Neurology (clinical) Geriatrics and Gerontology Psychology Neuroscience 030217 neurology & neurosurgery Developmental Biology |
| Zdroj: | Neurobiology of Aging, Vol. 62 (2018) pp. 34-44 |
| ISSN: | 0197-4580 |
| Popis: | Amyloid deposits and tau-immunoreactive neurofibrillary tangles, together with neuronal and synaptic loss, are the neuropathological hallmarks of Alzheimer's disease (AD). Both proteins are present in the normal brain during aging. However, the temporal sequence of their involvement in the onset of AD pathology remains controversial. To define whether amyloid β protein deposits or tau protein lesions appear first during normal brain aging, we performed an immunohistological study on serial sections from 105 autopsy brains (age range: 40-104 years) from patients free of clinical signs of cognitive decline, using anti-tau (AT8) and anti-amyloid (4G8) antibodies in the hippocampus, entorhinal cortex, inferior temporal cortex (Brodmann area 20), prefrontal cortex (Brodmann area 9), occipital cortex (Brodmann areas 17 and 18), and in the brainstem. All cases older than 48 years displayed at least a few neurofibrillary tangles, which appeared more frequently in the entorhinal than in the transentorhinal cortex. Tau pathology in these areas preceded tau inclusions in the brainstem. Furthermore, the first site of the apparition of tau pathology is inconsistent, being the entorhinal cortex in most cases, and in fewer cases, the transentorhinal region. There was no case presenting with amyloid deposition in the absence of neurofibrillary tangles, lending evidence to the fact that neurofibrillary tangles appear earlier than amyloid plaques during normal brain aging. However, the role of amyloid in promoting tau deposition cannot be excluded in some cases but may not represent the sole mechanism of disease induction and progression. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect