Ageing MS and Parkinsons Flashcards
(41 cards)
Define Alzheimers?
Misfolding of Amyloid beta/Tau proteins. Hippocamal neurons are lost.
Describe the 3 types of alzheimers
Hot/Inflammed: M1 + reduced SIRT1. M1-M2 (using nrf2). NFkb increases M1.
Cold Atrophic - reduced BDNF (neuroprotective protein)
Cortical/toxic - linked to environmental toxins - chronic inflamm +brain atrophy.
What is nrf2?
a transcription factor supporting shift from M1 to M2 (microglia - resident immune cells of the brain).
It senses cellular stress to increase glutathione enzymes/ SODs/Catalase/ Phase2 detox enzymes
Risk factors for Alzheimers
Dysbiosis - via microbiota brain-gut axis - comms to TLR on brain microglia
Oxytoxin: enriched social interactions - through vagus nerve can supress microglia-related inflammation
Oral dysbiosis: P Gingivalis - increased risk of Alzhimers
Aluminium/lead/mercury
Obesity - T2DM stress on body/brain. Pheripheral/neurological inflammation
Diets and natural approach to Alzheimers?
MIND (mediterranean + DASH) - mildly ketogenic 12/3.
Medditerranean diet
Coconut oil (MCT rich) -easily absorbed. increase blood ketone + cognitive/brain energy.
Yoga
vagus nerve stimulation
Dietary choline (aceytlcholine for mood/memory/learning)
Supplements and doses for Alzheimers
Vit C (mg)
Lactobaccilus Acidiphillus (1-4bn)
CoQ10/B Complex/Vit E
Citicholine (250mg)
Curcumin (500)
Vit D (2000iu)
Omega 3 (750mg)
Reservetrol (100) - protect from misfolded Amyloid
Multiple Sclerosis - what is it?
Inflammation of immune cells infiltrate BBB and attack myelin Sheath. Oligodendrocytes reduce (which produce myelin sheath) and neurodegeneration ensues.
T cell mediated - TH17 (away from T-Regs)
Types of MS?
Relapse/remitting
primary/progressive
Secondary/progressive
CIS (once)
Risk factors for MS
low vit D/K/B12
EBV
Childhood trauma
Mitochondrial dysfunction
Smoke
AI
Toxins
Obesity (BBB permeability - CNS inflammation) Leptin increases TH17. Increased M1 microglias (M2 boosts myelin sheath/oligodendrocytes)
Thymic involution increases autoreactive T cells.
Parasympathetic vs sympathetic state - Autoreactive T cells/myelination
Diets for MS
Swank diet (low saturated fat/fruit and veg/ no read meat or pork for 1 year/limited fish and poultry.
Wahls protocol: DGLV/sulphur rich/colourful/Omega 3/grassfed/seaweed
Supplements for MS
Vit D/K
Quercetin (500mg)
Alpha Lipoic (300)
Citicholine (250)
Omega 3 (750mg)
B12 (1g)
Methyl folate (500mcg)
Describe Parkinsons Disease
Gradula loss of dopamine producing neurons.
Affects substantia Nigra
Misfolded protein Alpha Synuclein - oxidative stress - lewy bodies (aggregate around dopamione neurons) - mito loss/neuron loss, OX stress.
Initial symptoms of PD
Constipation and loss of smell
Causes/risk factors of PD
Recreational Drugs (esp Amphetamines)
Brain injury/trauma
Mitochondrial dysfunction (Oxidative stress and inflammation)
Toxicity
stress/depression
pesticides/herbicides (Rotenone, paraquat)
Aluminium toxicity. Mangenese/iron/mercury toxicity
Ways to diagnose PD
DatScan (Tremors v PD)
PET scan (Brain irregularities)
How does L-dopa act in the treatment of Parkinson’s disease (PD)?
L-dopa can cross the blood-brain barrier and is converted into dopamine within the central nervous system, serving as a precursor to dopamine.
What is the role of serotonin neurons in L-dopa medication?
Serotonin-producing neurons convert L-dopa to dopamine using the enzyme amino acid decarboxylase. However, L-dopa can damage serotonin neurons, leading to potential negative psychological effects.
How does the decarboxylase inhibitor in L-dopa medication function?
Prevents the conversion of L-dopa into dopamine outside the brain, ensuring a higher level of dopamine reaches the brain.
Why is it recommended to take Vitamin B6 away from L-dopa medication?
It may interfere with the function of decarboxylase inhibitors.
From where is L-dopa derived, and how can patients benefit from it?
Amino acid tyrosine.
Some patients benefit from eating protein-containing meals after their medication, facilitating easier L-dopa passage into the brain.
What is the Catecholaldehyde Theory of PD?
The theory involves the degradation of dopamine in a neuron’s cytosol to form the toxic compound DOPAL, primarily through the action of the enzyme monoamine oxidase B (MAO B). L-Dopa medication can significantly increase DOPAL levels.
How does DOPAL interact with alpha-synuclein in the context of PD?
DOPAL interacts with alpha-synuclein, promoting misfolding and the formation of toxic Lewy bodies. Misfolded alpha-synuclein accelerates the formation of toxic DOPAL.
What are suggested neuroprotection strategies in PD treatment?
Slowing down monoamine oxidase B (MAO B) and promoting the detoxification of DOPAL to its metabolite, DOPAC, for protecting dopaminergic neurons.
Other things that can be done for PD patients
Hyerbaric oxygen
Avoid EMFs from mobile phones and microwaves
Chelation of Aluminium
Alpha Lipoc acid can chelate iron deposits from brain