L12 Cognitive ageing and role nutrition
27 important questions on L12 Cognitive ageing and role nutrition
What can you tell about the ageing brain on structural level? [name 5 min.]
- Gray matter volume decline - thinner cortex
- Decrease in neuronal size
- Decrease in number of synapses ± synaptic density
- White matter changes
- Loss of myelin sheets
- Loss of glial cells
- Altered neurotransmitter production + receptor changes
- Reduction in weight of 2-3% each deca
de
- More progressive reduction around ages =50-60
- 11% reduction at age 90 ± 150g loss
What can you tell about the ageing brain on Molecular-protein-neuropathological level?
- Immune dysregulation & epigenetic changes
- DNA damage & lysosomal dysfunction
- Abnormal protein assemblies
What can you tell about the ageing brain on Cellular level ["Sirtuins" = NAD+ - dependent deacetylases]?
- Class of signaling proteins involved in metabolic regulation
- Sensors of amounts of energy, day light, stress ± cellular distress
- Promote cell survival and health
- Play a critical part in ageing/longevity =± neurodegeneration
- Higher grades + faster learning
- Never study anything twice
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What can you tell about the ageing brain on neuro-immunological level?
- Abundant histological changes --> related to neuron, glial cell types (increased microglia activity), neuronal processes (synapses, myelin)
- Chronic low-grade neuroinflammation
What can you tell about the ageing brain on clinical level
- Cognitive decline =± 'cognitive aging'
- Crystallized intelligence
- learned-knowledge
- Fluid intelligence
- Novel - processing
- Five cognitive domains
- Processing speed
- Attention/concentration
- Memory
- Language
- Visuospatial abilities
- Behavioral changes
- e.g.
depression/sleep
When are you talking about successful cognitive ageing
crossroad: physiological, successful, or, pathological brain ageing
What happens in the normal ageing brain and in the severe AD brain in the regions
- Entorhinal cortex
- Temporal cortex
- Hippocampus
Entorhinal cortex
- normal ageing
- no neuronal loss, few NFT
- severe AD
- 90% neuronal loss, extensive NFT
Temporal cortex
- normal ageing
- no neuronal loss, few NFT
- severe AD
- neuronal loss, extensive NFT
Hippocampus
- normal ageing
- neuronal loss only in dentate gyrus, subiculum
- severe AD
- Neuronal loss in CA1, extensive NFT
Which two types of MCI [Mild Cognitive Impairment] (pathological brain ageing) are there?
- Largely intact executive functions & activities of daily living (ADL)
- Predominantly affects memory
Non-amnestic
- Affecting thinking skills other than memory
- Decline in language, executive functions, visuospatial abilities
What is the intermediate state of Mild cognitive impairment (MCI)
- Annual conversion rate to Alzheimer's disease (AD) = 10-15%
- Reversion to normal cognitive state = 20-25%
Dementia knows three syndromes:
- Irreversible
- Alzheimer's disease (AD), frontotemporal dementia (FTD), Parkinson's disease dementia (PDD), dementia with Lewy bodies (DLB), Huntington's disease (HD), Creutzfeldt-Jakob disease (CJD) etc
- Potentially reversible
- Dementia-like deficits due to other CNS disorder AIDS dementia complex, Korsakoff (alcohol abuse), normal pressure hydrocephalus, meningitis, brain tumors, CVA (vascular dementia), head trauma (hematomas)
- Completely reversible - no neurodegeneration
- Depression, endocrine/metabolic disorders (hypothyroidism), malnutrition/vitamin deficiencies (e.g. folic acid or vitB12), toxicological/substance-related (sleep medication, anxiolytics, sedatives)
What is proteinopathies [primary dementia syndromes]
subtype = based on topographical spread + protein subtype
What is the function of Tau - MAPT (microtubuli associated tau protein)
- Stabilization microtubili
- *Hyperphosphorylation
- At position threonine 181 (P)
- Paired helical filaments
- Tangles
Amyloid and Alzheimer's disease
- APP: amyloid precursor protein
- Sy
napse formation
- Iron export
- Antimicrobial activity
- Neural plasticity
- 'Amyloid cascade hypothesis'
- Combines effect of beta-/gamma-secretase
- Insoluble amyloid fibrils
- Plaques
What are the genetic risk factors for AD
- PSEN1/2 + APP
- ApoE (APOE)
- apolipoprotein-E
- Link with CVD
- Part of plaques
- ...
- ...
- .
- .
- .
- .
- .
What is the clinical progression of Alzheimer's disease
- Slow beginning, gradual progression
- Late-onset (LOAD; >65y) vs. Early onset (EOAD; 40-50y)
- Symptoms
- Cognitive dysfuntion
- Difficulties remembering
- Language - disorientation
- Various BPSD - timeline
- (I)ADL
What are the clinical symptoms of Alzheimer's disease (AD)
- Amnesia: memory loss
- Aphasia: language loss
- Apraxia: loss of learned movements
- Agnosia: loss of recognising things
- ADL: activities of daily living
- (I)ADL: instrumental ADL
- BPSD: depression -> agitation/paranoia -> apathy
What kind of therapies are there for AD?
- Aducanumab
- removes plaques
- Binds to epitope of BAP
- FDA: approval pending
- Phase 4?
- Fecal microbiota transplant (phase 1)
- Omega-3 PUFA (phase 2)
- Ginko Biloba (phase 3)
- Non-amyloid > amyloid-based drugs
Vascular dementia (VAD) =
- Secondary dementia syndrome
- Ischemic or hemorrhagic infarct
- Cerebral amyloid angiopathy (CAA)
- amyloid in blood vessels
- mixed variant common: AD + CVD = MXD (mixed)
- Insidious onset <-> AD
- TIA = transient ischemic infarcts -> microbleeds
- Variety of symptoms = localised vs. Full blown
- Leucoencephalopathy = white matter lesioning
- Risk factors: BP, smoking, diabetes, cholesterol
Dementia with Lewy bodies (DLB) =
- Relatively fluctuating course of events
- Parkinsonism (but first: cognitive symptomatology!)
- triade of motor symptoms (rigidity, bradykinasia, tremor)
- Fluctuating memory complaints (<-> AD)
- Visual hallucinations, psychosis, depression
- RBD (REM-sleep behavior disorder)
- "Peripheral symptomatology" (e.g. Constipation, hypotension)
- 90% of DLB patients have AD pathology in their brains
- Protein: alfa-synuclein ± Lewy bodies/neurites
- Destruction of substantia nigra + locus coeruleus
- Genes involved: LRRK2, SCNA, Parkin, PINK1, ...
Frontotemporal dementia (FTD) =
- Very heterogeneous disorder
- Abrupt onset
- Frontal/temporal lesions
- Variants: behavior (bvFTD)
- Variants: language (PPA (primary progressive aphasia))
- Mostly behavior fist >> cognition
- Restlessness, decorum loss, dietary changes
- Early onset (as early as 30-40y)
- 70% = determined by genetic mutations
- Proteins: tau, TDP43, FUS
What are risk factors for dementia
- Less education
- Hearing loss
- Traumatic brain injury
- Hypertension
- Alcohol
- Obesity
- Smoking
- Depression
- Social isolation
- Physical inactivity
- Air pollution
- Diabetes
60% = non-modifiable [age, genetics]
40% = modifiable [<education, alcohol, obesity, smoking etc]
What are the basic brain functions of fats/lipids and proteins and amino acids?
- Brain = fatty organ
- Good fats/key players: omega-3 & omega-6, essential fatty acids
- Creation and maintenance of cell membranes
- Bad fats: long-term consumption of saturated and trans fats harmful
Proteins and amino acids
- Building blocks
- Precursors of neurotransmitters (e.g. Dopamine, serotonin, norepinephrine)
- Competition: varied diet important
What can you tell about the brain and energy (carbohydrates)?
- brain weight of average adult human = 1.4 kg
- 2% of total body weight
- using 20% of our total energy consumption
- ±2/3 to fuel electrical impulses that neurons use to communicate with one another
- ±1/3 cell health maintenance
- Normal physiological conditions: glucose primarily utilised for energy (ATP generation)
The use of glucose versus ketones, what are the characteristics of ketones
- If glucose sparse, e.g. Prolonged fasting: ketone bodies used
- Glucose and ketones can both pass the BBB
- For ketones depending on levels in blood
- Dietary approaches may facilitate significant changes in the brain's metabolism
Which pathways towards cognitive decline are sensitive to nutrition?
- Cerebral energy deficit
- Tau and amyloid aggregation
- Epigenetics
- Synaptic dysfunction
- Neurovascular dysfunction
- Inflammation
What are potential protective nutrients
- B vitamins: B6, B12, folate (or combination)
- Antioxidants: carotenoids, vitamin C, E, Selenium, copper, flavonoids
- Vitamin D
- Macronutrients
What are the effects of MIND diet on Cognitive Performance and Brain Structure in Healthy Obese Women?
- Small (n=37) and short (3 months) RCT
- Working memory verbal recognition memory and attention improved more compared with control group
- Brain MRI: increase in surface area of inferior frontal gyrus in the MIND diet group
- First large (n=600) and long (3 years) RCT ongoing in US
- + MIND diet integrated in first multi domain interventions
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