Summary neural networks- neuroplasticity and aging
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Course
Neural networks
Institution
Katholieke Universiteit Leuven (KU Leuven)
Summary of the neuroplasticity and aging lesson given by prof. K. alaerts of the neuroscientific aspects course. It is a summary of the powerpoint slides and additional items noted during the lesson. The slides were in English and my own notes are always in Dutch as much as possible. It is therefor...
Neural networks: neuroplasticity & aging
AGEING – A BIOLOGICAL PERSPECTIVE
Nine metabolic "hallmarks" of ageing
- 1. genomic instability (mutations in nuclear DNA)
- 2. telomere shortening
- 3. epigenetic alterations (e.g. DNA methylation patterns)
- 4. loss of proteostasis (protein folding and proteolysis)
- 5. deregulated nutrient sensing
- 6. mitochondrial dysfunction
- 7. cellular senescence (accumulation of no longer dividing cells)
- 8. stem cell exhaustion
- 9. altered intercellular communication
Mutations
- In nuclear DNA/ mitochondria (important for energy production)
Accumulation of ‘junk’
- Inside cells/ outside cells
- Problems with ‘cleaning’ the cells
Cells
- Cellular loss – too few new cells
- Cellular senescence – too many old cells (cells fail to die)
Extracellular cross-links
- Loss of elasticity in tissues
The processes that characterize neurodegenerative diseases (e.g. Alzheimer’s) take place in most old
brains !
- Bij normal agingook vorm hiervan
However! some people might have compensatory mechanisms that enable them to cope better with these
processes and to maintain normal cognition
- Compensating mech: bij normale aging meer aanwezig
=> Tempting to view neurodegeneration as accelerated ageing…
- we see the same in an old brain but with less abnormalities as in a neurodegenerating brain
normal aging= good strategies to cope with/regenerate/restore
AGEING AT THE BRAIN SYSTEM LEVEL
ANATOMICAL CHANGES
The brain shrinks with age => volume loss
- in both gray matter and white matter
Gray matter loss may start earlier, but progress more gradually
o Niet heel snel
White matter loss may start later, but progress more rapidly
1. GRAY MATTER AND WHITE MATTER VOLUME LOSS
Most pronounced in frontal lobe, followed by temporal lobe
Primary sensory areas and occipital lobes seem relatively spared by the shrinking process relevant to
normal aging
Greater age-related reductions in FA in frontal regions, compared to posterior regions
- ~ anterior-posterior gradient of age-related FA reductions
FA is a sensitive marker of aging that may precede atrophy in many regions of the brain
- ∆in ana.integrity might proceed the volume loss veradering
Example study – FA of corpus callosum
- Higher FA => better
- mostly in prefrontal lobes, posterior regions are similar in older and younger people
- FA meeste fedaald bij oudere
Vnl. Super regeions frontal corpus calosum tov post
Post= vrij intact
3. CONCLUSION ANATOMICAL CHANGES (snelle samenvatti ng )
GM & WM volumes loss
- GM= grey matter
- WM= white matter
Loss of white matter integrity (FA)
- Mostly in frontal lobes!
INTRINSIC FUNCTIONAL CHANGES
1. RESTING-STATE FMRI
Measurement of intrinsic functional connectivity
- Overall, connectivity and network integrity appear to decrease in healthy aging
- Decrease is accelerated in Alzheimer’s disease
- specific systems hit hardest, such as the default mode network (DMN)
2. DEFAULT MODE NETWORK
One of the most robustly identified and extensively investigated resting state networks
Includes regions in the
- Posterior cingulate/precuneus
- medial prefrontal cortex
- lateral parietal cortex
In general, DMN activity increases during rest, but decreases during attention demanding tasks
Linked to ‘mind-wandering’
- Self-referential thoughts
- Thinking about other
- Remembering the past and thinking about the future
3. EXAMPLE STUDY
Nala Melis Pagina 2
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