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PD: primarily caused by loss of? men vs. women?

gradual loss of DA producing neurons in SN pars compacta and striatum. men get it at a higher rate, 2:1


PD: prevalence? # people affected?

2nd most prevalent ND disease. over 1 million US, 130 000 Cads.


7 major functions of DA

control/regulation of bevhaiour. mental health. voluntary movement. reward seeking behaviour. memory. ability to learn. secretion of prolactin from ant pit.


3 DA pathways

nigrostriatal. mesolimbic/mesocortical. tuberinfundibular.


most neurons that produce DA originate in? name of brain part?

ventral midbrain: substantia nigra and ventral tegmental area. midbrain = mesencephalon


where to SN neurons project to? two parts of SN?

project to striatum to regulate motor control. pars compacta + pars reticulata.


pars compacta vs. pars reticulata

compacta: input to basal ganglia circuit, main DA conduit to striatum. reticulata: major ouput from BG, mostly GABA neurons and go to extrinsic structures


DA neurons: what enzymes? also expresses high lllevels of? expresses what transporter?

tyrosine hydroxylase and l-aromatic amino acid decarboxylase to make DA. neuromelanin. dopamine active transporter


neuromenalin: does what?

makes DA neurons appear blackened. by product of dopamine metabolism by MAO. might be protective against oxidative stress; decreased neuromelanin = increased neurotoxicity


development of DA neurons: what signal?

SHH sonic hedge hog; induces ventral cells


2 major forms of DP?

familial = genetic aberrations + mutations. idiopathic = combo of genetic suscpebility + enviornment factors


risk factors for PD

familiar genetic risk factors. exogenous neurotoxins. insecticides, herbicides, infections, cranial trauma, stress, age


6 major genes for familial PD

SNCA for a synuclein. Prkn = parkin. LRRK 2. PINK1. UCHL 1. DJ 1


DA neurotoxicity associated with what features?

lewy body formation. abnormalities in protein degradation. protein trafficking. mitochondrial malfunction. microtubule assembly. embryonic development. inflmammation


autosomal dominant: what 3 proteins?

a-synuclein. LRRK2. UCHL1 --> gain of function


autosomal recessive: what mutations?

Parkin, PINK1, DJ1 --> loss of function


a synuclein: expressed where? localized? associated with?

highly expressed throughout NS, esp in presynp terminals. significant localized with vesicles associated with vesicular transport; can be found associated with membrane lipids


LRRK2: aka? important for? also involved in?

Dardarin. important signalling molecule. also involved with other NDDs like AD>


LRRK2: lcoalized? involved in what processes? mutations and PD?

cytoplasm, membraneous organelles, mitochondria, plasma membrane. endosomal recycling, signalling pathways. pts with LRRK2 mutations = milder, more treatable.


UCHL 1: abundance? found where?

highly abundant total brain protein. found mostly in neurons and neuroendocrine cells.


UCHL 1: what function?

involved in recyling of ubiquitin: de-ubiquinating enzyme, and so protects protein from degradation


overexpress UCHL1 = what?

accumulation of a-synuclein