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24 Cards in this Set

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What is the pathology of AD?
1) senile plaques qith amiloid beta
2)neurofibrally tangles with hyperphosphorylated tau
3) neuronal loss in hypocampuss and selective cortical and subcortical area
4) white matter lessions
Describe beta amyloid production.
Amyloid precursor protein is processed by Y secretase ( not alfa and beta) thus generating small peptides which will form later amyloid plaques. ( aggregation)
What is AD?
* gradual progressive memory impairment with disorder of aquired skills. Interference daily life.

Impaired recognition objects. Impairment of spatial orientation. mostly over 65 years.
What is dissconnection syndrome?
Lose of white matter.

Dissconnection visual, auditive, sensory cortex with motor cortex.>>>
1) Loss aquired skills:dress underneth underware
2)Brushing tees : naming toothbrush but not knowing its function.
3) constructional apraxia: clock drawing
loss of ability to recognize sounds.
2)
What is the clinical phenotype of AD?
early gradual episodic memory impairment.
What is huge overlap in AD pathology?
36% AD patients - no plaques
33% of non AD patients >>> moderate to severe plaques formation
What are the AD risc factors?
age, hypertension, cholesterol , homocyteine, APOE4 allel, atrial fibrillation, diabetes type 2, smoking.
How do vascular factors influence AD?
Hypertension, atrial fibrillation, atherosclerosis. Are related to white matter pathology
What is the core diagnostic criterial for AD?
Presence of early and significant memory imparment.

1)Presence of medial temporasl lobe atrophy: volume loss of hyppocampi, entorhinal cortex, amyglada evidence on MRI.
2) Specific pattern of functional neroimaging with PET reduced glucose metabolism in belateral, temporal , perietal regions. Visualized amyloid beta
3)Abnormal cerebrospinal fluid biomaker , low amyloid concentration, increased total tau concentration.
4) proven autosomal dominant mutation within the immediate family.
CT,MRI,PET, what you see on each of it during AD?
CT: Atrophy , space occuping lesions
MRI: Atrophy , space occuping , white matter hyperintensity.
PET: Glucose metabolism , amyloid plaques and tau tangles.
What do you see on SPECT, functional MRI, DTI, MRS?
SPECT: blood flow
functional MRI: blood flow , functional connectivity
DTI: neuronal connectivity, white matter integrity.
MRS: metabolite concentration
Which research on tretments there is?
immunisation against amyloid
blood thinning aspitine
inflamatory inhibitors
blood, stathine.
What are the vascular preventatives for AD?
prevention vascular desease, no beneficial effect on AD pathology(statins, aspirins)

stroke prevention, no beneficial effect ( aspirin)

prevention of cardiovascular desease - beneficial effect in patients with mild AD. ( fish oil)
Which diet molecular compounds influence ischemic heart desease?
EPA,DHA acids
What is the effect of LCPUFA combination diet?
effect on cognition, cerebral metabolism, blood volume in APP/PS1 AH mice.
What is the effect of combination diet Fortasyn on behaviour?
explorative, less anxious

spatial memory is improved

Fortasyn increases CBF in APP/PS1 mice.

DHA increases CBF, cholesterol decreases CBF.
Which markers there are for neurodegeneration?
N acetyl aspartate NAA: neuronal marker neuronal integrity

Myo-inositol: glial marker associated with inflammation.
What is the effect of DHA on pathology?
DHA decreases amyloid deposition in plaques and bloodvessels walls.

Cholesterol increases plaques in hyppocampus.
How do excercice influence AD?
induces changes in frontal and temporal lobes, improves short term memory.
What effect has combined diet+DHA effect?
positive effect on BDNF synaptic plasticity and cognition
Which vulnerable neurons there are?
long myelinated axons traveling relative long distances, between CNS regions and peripheral area.
What are the reasong for vulnerability of these neurons with aging?
Need a lot of energy , dependent on axonal transport ( anterograde, retrograde) for nutrition

have large cell surface for exposure of toxic agents.

cytoskeleton of large neurons is vulnerable for dysfunction , due to aggregation and dyslocation axonal neurofilaments and formation of microtubulus associated protein tau.
What are the stroke symptoms?
paresis, leg, especially trouble walking.

trouble speaking , trouble seeing, eye movement disorders , coma, trouble with speaking, swallowing.
Which treatment for stroke there are?
Definition: A surgical procedure performed to repair an aneurysm that stems from the wall of a blood vessel inside of the brain. The technique involves the surgical placement of a clip across the aneurysm "neck," which prevents it from growing and/or bleeding further. Aneurysm clipping is an alternative to endovascular aneurysm "coiling."