development and degeneration - week 11 Flashcards

Question

neural degneration loss of synaptic connections

Answer 1

axons degenerate less white matter - because no point in maintaining non functional connections therefore smaller brain

Answer 2

apoptosis necrosis

Answer 3

genetic environmental or combination

Answer 4

lack of o2 cant generate enough energy neurons die strokes transient ischemic attacks

Answer 5

excitotoxic lesions in rodents glutamate hypothesis in epilepsy

Answer 6

disease with no identifiable cause/ / occurring at irregular intervals or only in a few places; scattered or isolated.

Answer 7

protien aggregations cause apoptosis not beneficial

Answer 8

mutation in a single gene 'simpler than other neurodegernative disorders mutation in huntington gene inital degradation in basal ganglia

Answer 9

site of loss

Answer 10

depends on circumstances eg. how long brain is starved of o2

Answer 11

varies in nervous system peripheral cells can regenerate limited / absent in CNS - spinal injury - brain injury / degeneration

Answer 12

axon regrowth not possible following injury axons deteriorate the ones that dont deteriorate become dysfunctional due to their loss of insulating myelin cellular debris and bleeding results in a fluid filled cavity/cyst filling space where neurons and axons used to be glial cells proliferate abnormally - forming clusters of glial scars together cysts and scars create a barrier to axons - so prevent regrowth

Answer 13

complexity of connections connections in adulthood not the same as developing brain,, comapred to the stable connects in PNS - synaptic plasticity over many years - therefore functional recovery difficult as no way to reconnect and restore all the function - where PNS based on simple connections and basic anatomy potenially possible in spinal cord

Answer 14

reconnecting neurons only helps so much neurons whose cell bodies have died cannot reconnect

Answer 15

adult neurogenesis in some areas of brain (adult) neurons continue to proliferate eg. dentate gyrus of hippocampus

Answer 16

from animal studies new neurons are functional - eg. in hippocampus they differentaiate they migrate they form connections they are myelinated but if able to stimulate neurogenesis or introduce stem cells - will correct / usefull connection be made? - might rebuild better capactity for relearning and behavioural recovery - unlikely to recover lost memory or skills

Answer 17

where in the nervous system the damage is

Answer 18

tremor rigid muscles brodykinsea hypokinsea initally unilateral v. early symptoms in facial expressions

Answer 19

cognitive and emotional effects 2ndary as triggered by a loss in motor function but not just a consequence of being aware of movement problems, can characterise a general slowing of brain function explained as a general loss of brain function sleep deficits depression related to pathological processes that cause it

Answer 20

thought not to be a single condition but several underlying

Answer 21

no identifiable cause most common combination of lifestyle factors and old age

Answer 22

slightly different from normal PD can be caused by anti-psycotic medication drug would need to have strong affect on the dopaminergic system --> particularly blocking action of dopamine features differ - tremor, slow movement but dont progress into more severe symptoms - clearly triggered by medication most patients recover in months/weeks/days after stopping drug

Answer 23

less than 5% of cases inherited mutation s increase likelihood early onset disease (under 40) only for a small minority genetic links

Answer 24

factors can increase risk presticides, heavy metal infection (influenza) alcohol / caffine?

Answer 25

all patient exhibit loss region of midbrain this nucleus is a component of the basal ganglia - a group a interconnected structures found in various parts of brain - mediates a viarity of functions (including contrubuting to motor control) - neruons of SNpc appear darker because they contain the pigment melanin ---> byproduct of synthesis of neurotransmitter dopamine ---> dopamine is a catecholamine neurotransmitter

Answer 26

gradual accumalation of cellular inclusions lnown as lewy bodies ---> composed of aggregates of a no. of protiens (incl. alpha-synuclein)

Answer 27

progressive accumulation of lewy bodies throughout the brain and loss of dopaminergic neurons ultimately results in the signs and symptoms that form basis of an initial pre mortem diagnosis of PD

Answer 28

evidence suggests behavioural changes not seen until 80% lf nigral dopamine is lost

Answer 29

by labelling the dopamine transporters normally found on healthy presynaptic terminals of dopaminergic neurons can assess if indivduals show the cardinal signs of PD also has signs of degneration of nigral neuron terminals

Answer 30

other monoamines - altered seretonin and noradrenaline some studies suggest cholinergic transmission via basal nucleus of meynert may be affected (particulary later stages) suggested that non-motor symptoms caused by non-dopaminergic changes

Answer 31

basal nucleus of meynet cholinergic transmission

Answer 32

aim of replacing / increasing dopamine but dopamine isnt rapidly metabolised and doesnt cross blood brain barrier

Answer 33

can cross blood brain barrier dopamine precursor effectivness diminshes as PD progresses only effective of still dopaminergic neurons left adverse effects

Answer 34

target postsynaptic neurons so can still be effective but eventually PD progressive degeration also leads to post synaptic degeneration - neurons not recieving inputs will die (secondary / transneuronal degeneration)

Answer 35

replacing lost neurons attactive for PD as appears to be confined to distinct anatomical locations the only suitable treatment as drugs dont work long term

Answer 36

introduce into brain right now not standard treatment - unknown long term effects

Answer 37

aim of enhancing the function of remaining dopamine circuits approach revisited after discovery of long term limitations of L-dopa the stimulation delievered affects the neurons of the basal gangllia structure into which the electrode is implanted causing a cascade of changed to the firing characteristics of the structures of the basal ganglia activity if no longer benefitting for l-dopa this is considered

Answer 38

most common form of dementia 5% of pop. 1:6 people over 80

Answer 39

impairment in learning and memory 1st sign of disease - initally poor memory for recent events - more so than age related decline followed by later impairment in attention, exectuative function, language and visual spatial function (including spatial navigation) as progresses patients become worried, depressed or experience personality changes (become angry/violent)

Answer 40

although memory probs considered earliest sign in some cases spatial navigation probs are the 1st early impairment some reseachers suggest it should ne considered a preclinical signs (10-20 years before clinial onset)

Answer 41

sporalic / late onset early onset

Answer 42

no obvious cause most common (more than 90% of all cases) later than 65 genetic predisosition + environmental factors contribute

Answer 43

in addition to age significant head injuries heavy metals , fungicides, hypothermia no single factor emeraged as a key candiate keeping brain active can offset as loss i smore noticable lifestyle risks - inactivity, smoking diet, low educational attainment

Answer 44

1-2% caused by varients less than 10% of all cases 1-2% inherited under 40

Answer 45

is associated with specific gene mutation amyloid percursor protien (APP) 1 of the 2 presenilin genes mutations in these genes thought to result in abnormal accumulation of beta-amyloid formations of amyloid plaques

Answer 46

inital area of degeneration

Answer 47

abnormal accumulation of beta-amyloid and tau protiens - forming amyloid plaques and neurofibrially tangles - aggregates of amyloid plaques form in extra cellular space between neurons - neurofibilarly tangles from inside cell bodies and inside neuntes, axons and dentrates - thought that plaques and tangles increase risk of degeneration direct link not fully understood

Answer 48

inside cell bodies and inside neuntes, axons and dentrates

Answer 49

in extra cellular space between neurons

Answer 50

in temporal lobes - entrotinal cortex and hippocampus (memory) - damages memory parts 1st

Answer 51

level of beta-a accumulation reaches a tipping point then rapid spread of tau happens leading to more widespread neurodegeneration so further cognitive decline

Answer 52

corrolates with coginitve impairment particularly effects chlolinergic and glutamatergic synpases

Answer 53

learning and memory and is the principle correlate of disease progression and cognitive impairment

Answer 54

loss of cholinergic neurons in basal buccal of meyert and other subcortical structures shown to contribute to memory and attention deficits in AD

Answer 55

know that amyloid plaques affect cellular function of neurons including synaptic activity (synaptic loss) but many studies failed to find corrolation between levels of amyloid plaques and cognitive impairment

Answer 56

currently no successful interventions which can prevent pprogression of AD due to complexity of AD unlikely one drug can treat it current approaches focus on helping patients to manage and maintain mental function and slow down memory loss

Answer 57

inital aim of boosting cholinergic transmission (acetylcholine) prolong presence of remaing acetylcholine in synapse acetylcholinestease inhibitors - prevent breakdown of Ach or niotinic agonists ----> continues to stimulate receptors (minics actions) not very effective --> helps to reduce cognitive symptoms - dont change underlying disease progression only help for limited time

Answer 58

smoking seems to incease risk of dementia but some studies suggest that nicotine patches could improve memory in early stages of AD

Answer 59

pathological modification divert Amyloid percurosor protein away from amlyoid antibodies away from amyloid not v. effective is amyloid actually causal for AD ?? treatments targeting pathology aim to reduce the existing deposits or further accumulation of beta amyloid / tau proteins - inclused beta-amyloid directed immotherapy using antibodies targeting these proteins and inhibitors taget APP - lots of side effects

development and degeneration - week 11 Flashcards

(83 cards)