1 / 29

The ageing brain

The ageing brain. Volume reduction: begins around 50 with a loss of brain weight of around 2-3% per decade Changes in nerve cell numbers and size - various studies with various results ( 10-25%), although some structures seem resistent

bheller
Télécharger la présentation

The ageing brain

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. The ageing brain • Volume reduction: begins around 50 with a loss of brain weight of around 2-3% per decade • Changes in nerve cell numbers and size - various studies with various results ( 10-25%), although some structures seem resistent - dendritic and synaptic changes may be compensated by sprouting

  2. Microscopy of the aging brain • Increase in lipofuscin • Senile plaques • Neurofibrillary tangles • Granulovacuolar degeneration • Hirano bodies • Leukoaraiosis • Amyloid (congophilic) angiopathy

  3. Neurodegenerations • Damage to lysosomes, nuclear DNA, mitochondria leads to release of caspases, initiating apoptosis. • In many if not most neurodegenerations this damage is started by abnormal protein-protein interactions leading to protein storage. • Examples: • Ubiquinopathies • Tauopathies • Synucleinopathies • Prion diseases

  4. Ubiquinopathies: Alzheimer’s disease Pre-senile and senile forms Onset before or after 65 years of age Progression slow (often > 1 decade) Pathological changes are similar to aging, but more severe

  5. Senile plaque Heterogeneous structure Amyloid core surrounded by a clear zone Crown of filamentous or granular material made up of neuronal projections filled with argyrophilic filaments and debris Macrophages and astrocytes

  6. Tauopathies • Pick’s disease • Progressive Supranuclear Palsy • Cortico basal degeneration • etc

  7. Pick’s disease • Dementia with relative rapid progression with frontal symptoms (aggressive behavior often, or problems with initiation of tasks), onset from 50 years of age, frequently hereditary. • Gross findings are characterized by a lobar atrophy affecting the frontal lobe and the anterior temporal lobe (mostly the anterior 1/3 of the superior temporal gyrus) • Histology:Pick’s cells (swollen neurons ), Pick’s bodies ( argyrophilic intracytoplasmic inclusions), neuronal loss and gliosis

  8. Progressive supranuclear palsy • Dementia combined with vertical gaze paralysis, and Parkinsonism • Abnormal tau accumulation in neurons and glial cells, neuronal loss and gliosis • Characteristic topography:In the midbrain and striatum (Substantia nigra, red nucleus, colliculi, globus pallidus, subthalamic nucleus, periaqueductal grey matter, dorsal and medial raphe, locus coeruleus)

  9. Synucleinopathies • Parkinson’s disease • Dementia with Lewy bodies • etc

  10. M. Parkinson • Onset 30-80 • Rest tremor mostly starting with hands (like counting money) • Stooped posture, walking with small steps • Depigmentation of Substantia nigra and Locus coeruleus • Lewy bodies and loss of pigmented neurons • Loss of dopaminergic innervation to the striatum

  11. Parkinson’s disease

  12. Lewy bodies

  13. Synuclein

  14. Dementia with Lewy bodies

More Related