Ageing and Cognition Flashcards
Explore the similarities and differences between Spellman’s Crystallized and Fluid cognition model. (4) marks
1904 Spellman split the term cognition into:
Crystallised and Fluid cognition
Crystallized Intelligence is based on prior learning and actions that have become familiar + comfortable via (years) of repetition
Reading a book requires PRIOR knowledge of language, vocab, words+ grammar structure (action that has become familiar)
Therefore, they became crystallised (solid connections)
On the other hand, Fluid intelligence is the Capacity to reason e.g. finishing a puzzle. We would think about shape of the puzzle piece + potential Fit with the rest of the puzzle (Capacity to reason)
Area associated with language processing is Broca’s area (frontal gyrus)
Maintained/INCREASES W/ AGE (0.002-0.003 standard deviation every decade after 60~years
CONTRASTINGLY, can learn new things
DECREASED W/ AGE (0.002-0.003 standard deviation after 30 ~ years
Through their differences in nature, the concepts do come together
Explain the relationship between a brain reserve and Independence (4 Marks)
What is brain reserve (1) Ability to cope with continuous damage while function adequately/fulfil brain duties
Brain reserve can be moderate, low, high (1) depending on cognitive training (e.g. advanced academia)
What is Independence (1) Ability to look after yourself without the need of others/carers/assistant
People with a higher brain reserve are cognitively independent for longer (can cater to their own needs without assistance.) In contrast, those with lower brain reserve will consequently lead to earlier dependency (1) explained the relationship between brain reserve and independence both
Describe the role of Insulin signalling on longevity (healthy ageing) (6 Marks)
Insulin to Insulin Receptor (IR) = (2)
Tyrosine phosphorylation of insulin receptor substrate (IRS).
= activates phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) consist of regulatory p85 and catalytic p110 subunits.
PI3K converts phosphatidylinositol (3,4)-bisphosphate (PIP2) into phosphatidylinositol (3,4,5)-trisphosphate (PIP3), which recruits Akt-kinase to cell membrane= triggers array of secondary cascade including forehead box (FOX) transcription factors regulate many functions, such as cell survival and we are the product of our cells
PIP3 activates phosphoinositide-dependent protein kinase 1 (PDK1) = phosphorylates threonine 308 site in Akt1= partial activation.
For full activation of Akt = serine 473 phosphorylation by mammalian target for rapamycin complex 2 (mTORC2) is needed.
PI3K-Akt pathway regulates several cellular functions via downstream factors; Akt substrate 160 kDa (AS160) controls insulin dependently on glucose transporter 4 (GLUT4) translocation to the cell membrane and glucose uptake into the cell, mTORC1 regulates autophagy, protein synthesis, and cell growth, glycogen synthase kinase 3 (GSK3) affects glycogen synthesis, axon growth, and tau phosphorylation, and forkhead box (FOX) transcription factors regulate many functions, such as cell survival.
In microglia, cell surface receptor TREM2 signaling regulates the phagocytosis, motility, autophagy, survival, and proliferation. TREM2 is activated by several ligands including phospholipids, lipoproteins, and oligomeric Aβ leading to interaction with activating adaptor protein DAP12.
This in turn, leads to activation of PI3K-Akt pathway.
Explore the function of ROS induced age-associated cognitive decline (10 marks)
Normal ageing of mitochondria leads to Modest reactive Oxygen species m(ROS)- (1) correctly identifying the role of m(ROS) in regular ageing (ONLY if linked with normal ageing + compared t)
With age, mitochondria accumulate more damage (constant damage + repair= Homodynamic space, more damage than repair as we age),
Failure to maintain ROS at modest levels leads to a severe accumulation of ROS which are toxic to the cell and induce mitochondrial damage. This is commonly observed in older people, even if they don’t appear to have profound physiological symptoms.
This indicates that the accumulation of mROS is more of a general hallmark of ageing as opposed to relating to a specific cause or disorder of a prominent signs of age induced pathologies
On the other hand, Severe ROS (sROS) levels are often hallmarks of many neurodegenerative e.g. Alzheimer’s disease, Lou Gehrig’s disease etc.) and accelerates the natural ageing process
sROS place the mitochondrion under sustained cellular stress the mitochondria can’t effectively deal with= sustain for long causing them to break down
Disruption of oxidative phosphorylation (ox-phos) due to mitochondrial break result in the ability to synthesise ATP, the fuel that drives the biochemical reactions that control life.
Especially in brain that is 2% of bodyweight but needs 20% of total glucose output areas affected include the hippocampus, where we store memories as well form the connections to make new ones.
Due to loss of neurons supplying this region (due to NO ATP) = region begins to shrink and areas where memories were stored degenerates/areas used to make new memories gone
