PREVENTION
Ten percent of persons older than 65,
50% of those older than 85 years have AD
Early pathological changes
- depositation of beta amyloid (A B 42)
- related tau accumulation
APP generates beta amyloid rangin from 39 to 42 aminoacid peptide
Later pathological changes
- AB 42 and TAU aggregates progress to plaques e tangles widespread in the brain
- synaptic dysfunction
- neuronal loss
- degeneration of some regions due to neurotransmitter deficit: degeneration on basal forebrain is associated with decrements in acetylcholine-mediated neuronal activity involved in memory
AD risk factor
- Genetic
- clinical
- environmental
- vascular (diabetes mellitus, hypertension, dyslipidemia, smoking)
prophilaxes
- primary: avoidance of age-related decline
- secondary: prevention or slowing progression MCI to dementia
- tertiary: treatment of dementia
- AB and tau aggregation inhibitors
- antioxidants
- anti-inflammatory compounds
- cognitive enhancers or facilitators
- neuroprotective agents
- pleiotropic interventions
Vitamins e Minerals
B1 vitamin (Thiamine) exist in
- grain cereals
- orhan meats
- milk
- vegetables
Low thiamine diet causes
- impaired cognitive performance
- brain damage
- blood-brain barrier dysfunction
- intracellular edema
High thiamine - improvement in ADAS (AD scale)
- scores in MMSE
- Low is not asociated to AD
B2 vitamin (ribofralin) is in the same products as B1
- improve cognitive performance
- better MMSE
- low B2 is not associated to AD
B6 vitamin (pyridoxine) e B12 (cobalamin) come from meat, poultry, seafood, eggs, cereals
Low B6
- worst motor skills
high dose improve LTM - Low associated with AD
Low B12 associated to faster rate of cognitive decline, especially in APOEe4 carries.
It causes a reversible cause of dementia
Folates (B9)
- green leafe vegetables: spinach, parsley, romaine lettuce,
- asparagus, cauliflower, broccoli, beets
- legumes
Folate supplemention
- improves cognitive scores in aged patients with cognitive impairment
- improve cognition in O
- in mices APOE-deficient, idecrement in the amount of oxidative = mices getting well
- high folate dietary protects against cognitive decline
Folate deficience
- In CA3 20% fewer neurons
B12, B6, Folate are antioxydant e antiinflammatory. they interact in the metabolism of homocysteine
It's neurotoxic and it's a risk factor for vascular desease and dementia
Vitamin C e E
- powerful antioxidant
- better cognitive performance with vitamin C
- high C e E higher MMSE scores
- Low lower MMSE scores
Chromium
It's a trace mineral used in insulin receptor signal. It amplify insulin signal
Chromium supplementation increases activation in thalamus e frontal cortex
Polyphenolic compounds -Flavonoids
- wine related myricetin
- curcumin
- nordihydroguaiaretic acid (NDGA)
- rosmarinic acid (RA)
antioxidative, antiviral, anticarcinogenic
strong anti AB aggregation
Berries:
- against oxidative e inflammatory processes
- improve cognitive performance, increase neurogenesis in dentate
Curcumin:
- antioxidant
- inhibit ab oligomers and fibrils
Omega-3
- polyunsatured fatty acid
- in marine algae, fatty fish, fish oil
- pleiotropic mechanism
- antiinflammatory activity, neuroprotection, neurogenesis, antioxidant, metabolic enhancer
- prevention on cognitive decline in APOEe4 patients
Diet
Mediterranean diet associated with better cognition
Other supplements
Garlic
- reduce cardiovascular risk factors and their impact on developing AD
- antioxidant
- reduce homocysteine
Ginko Biloba
- antiinflammatory e antioxidant
- improvement in cognitive scales
Alcohol
- low moderate consume decrease risk of dementia
Caffeine
- peak in plasma after 45-120 min, halflife 2.5-4.5 h
- facilitate learning in passively tasks
- boost cognitive performance among fatigued individuals
Cardiovascular risk profile
Strongly associated with cognitive decline e dementia
Advantage of being modifiable
risk factor: hypertension, diabetes, dyslipidemia, smoking
vascular desease associated with cerebral hypoperfusion, oxidative stress, neurodegeneration, cognitive decline
AD pure is less than 20%. AD with cardiovascular desease is more common
hypertension e hypercholesterolemia
- higher level of systolic pressure in midlife = higher risk for dementia
- also lower level associated with dementia
- same for coholesterol
diabetes and insulin resistance
- insuline facilitates cognition
- deficit in insuline = increased deposition of AB and tau
- patient with diabetes have lower hippocampal and prefrontal volume
smoking
- higher exposure to nicotine lower risk of dementia
- elderly smokers increased risk of dementia
Protective factors
- physical exercise
- cognitive engagement
- social engagement
highly complex mental activity is a protective factor with a dose-dependent effect
Active trial study
cognitive trained subjects have improved cognitive abilities specific to the abilities trained
In MCI is better a multimodal training
It's difficult to isolate depression from dementia:
- patients with dementia have a higher prevalence of depression
- depression can be a prodromal sign of dementia
- depression as a risk factor
Pharmacological strategies
Hormones
- slow degeneration in women, but reverse after menopause
- memory problem in menopause
- estrogenes influence verbal fluency, verbal memory, spatial skills, fine motor skills
- there are no studies in which estrogen e progesterone are protective against dementia
- this treatment improve the risk (double risk)
Piracetam
- protection against cognitive decline in various clinical settins (trauma, cerebrovascular insufficiency, mci)
Acetylcholinesterase inhibitors
- acetylcholine disfunction is responsible for memory dysfunction in AD e MCI
- neurodegeneration in AD hit the basak forebrain taht produce acetylcholine
- block or inhibit the enzime that degrade acetylcholine
- recommended for AD e vascular dementia
Memantine
- for moderate e severe dementia with AchE inhibitors
Immune therapy
veccines with antibodies against AB reduce deposition and increase clearance of AB deposition