Summary
Summary Overview of Neuronal and Hormonal Regulation disorders
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This is a file with a summary of all disorders, diseases, etc. that are discussed in the Neuronal and Hormonal Regulation course.
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NEURONALE EN HORMONALE REGULATIE – OVERZICHTAANDOENINGEN
NEURONALE AANDOENINGEN
MULTIPELE SCLEROSE
- Impaired nerve signal conduction due to inflammation of
myelin sheath
- Visual disturbances
- Loss of sensation
- Difficulties with walking
- Fatigue
MYASTHENIA GRAVIS
- Autoimmune disease
- Impaired transmission at NMJ
- Muscle weakness, especially of eyelids and
eye movement, facial expression,
swallowing, chewing and speech
- Treatment with neostigmine
UMN / LMN SYNDROME
- LMN syndrome: paralysis, muscular atrophy, absence of deep tendon reflex
o LMN: Lower (spinal cord) motor neurons
- UMN syndrome: spasticity and rigidity, no disuse atrophy, increased deep tendon reflex
o UMN: Upper (cortical) motor neurons
- Poliomyelitis: viral infection of LMNs
APRAXIA
- Inability to properly execute learned movements
- Inability to execute voluntary movements despite being able to demonstrate normal muscle function
- Problem in motor and premotor areas
AMYOTROPHIC LATERAL SCLEROSIS
- Atrophy of UMNs and LMNs
- Death of motor neurons in cortex and spinal cord
- Rapidly progressive and fatal
- ALS and oxidative stress
o Some genetic forms of ALS are caused by mutation
SOD1 gene
o Most ALS cases are sporadic, have no clear genetic
cause
, o Mitochondria produce energy (ATP) using oxygen and electrons derived from glucose
Oxygen radicals are produced as side products during oxidative phosphorylation
Oxygen radicals cause damage to DNA, proteins and lipids
Oxygen radical cause mitochondrial dysfunction
Oxidative stress is important neurotoxic event in many NDs
WALLENBERG SYNDROME
- Lateral medullary syndrome
- Blockage of branch of cerebral artery
- Loss of pain or temperature sensation
- Loss of taste
- Facial muscle paralysis
BELLS PALSY
- Cranial mononeuropathy VII caused by nerve inflammation or tumor
- Facial drooping, facial paralysis
- Difficulties with eating, drinking and closing eyes
WEBER SYNDROME
- Paralysis of cranial never III
- Drooping of eyelids
- Double sight
- Loss of accommodation
- Dilatation of pupil
AUTISM
- Inability to express emotion and affection, dysfunction of amygdala
KLUVER-BUCY SYNDROME
- …
URBACH-WITHE DISEASE
- Inability to express fear, damage/calcification of
amygdala
ALZHEIMER
- Loss of memory, neurotic plaques
in hippocampus
, - Defects in memory, cognition, affection, attention and motivation
- Formation of neurotic plaques and deposition of beta-amyloid peptide; cortical shrinkage
- Loss of cholinergic pathways from basal forebrain and septum to hippocampus and cortex
- Causes serious cognitive impairment
- Progression is uneven in different individuals: stress can accelerate progression
- Most AD patients also have PD and suffer from depression
- Neuropathology
o Atrophy of (sub)cortical
brain regions
o Enlargement of cerebral
ventricles and brain sulci
o 30-40% reduction in brain
weight
o Neurotic plaques:
extracellular lesions containing insoluble form of peptide beta-amyloid
o Neurofibrillary tangles: cytoplasmic bundles of hyper-phosphorylated tau proteins
Tau is normal component of cytoskeleton, but when hyper phosphorylated it forms
insoluble bundles. These structures are also present in other NDs (tauopathies)
- Which neurons die in AD?
o Cholinergic neurons in septum and nucleus basalis of Meyndert (NBM): impairment of
memory consolidation
o Glutamergic pyramidal cells in cortex: probably accounts for most of cognitive deficits
o Noradrenergic and serotonergic neurons
o Neurodegenaretion may start in olfactory bulb
- Etiology
o Most AD cases are idiopatic, possibly with genetic predisposition: apolipoprotein E (apoE) 4
is risk factor for developing AD, seems to enhance aggregation of myloid-- in neuritic
plaques
o Familial AD cases may start early (early-onset AD) and are caused by mutations in three
genes: amyloid precursor protein (APP), presenilin 1 and 2
APP is precursor protein for beta-amyloid
Presenilins are part of -secretase complex
o Why is beta-amyloid toxic?
Normal role of AB is poorly understood, AB binds Cu++ and may act as antioxidant
Overproduction of AB is necessary condition for AD (??)
When AB binds Cu++ it produces H2O2 and causes oxidative stress (??)
Small AB aggregates cause damage to axons and synapses
AB-derived diffusible ligands (ADDLs)
may specifically impair synaptic
function (inhibit LTP) and cause
neuronal apoptosis
- Protein aggregation in ND: is it good or bad?
o Intermediate protein aggregates are toxic (oxidative
stress): inhibition of their formation may improve ND
symptoms
o Formation of final protein aggregates (plaques, tangles,
Lewy bodies, etc.) may protect from toxicity: inhibition
of their formation may cause accumulation of
intermediate aggregates and enhance ND symptoms
- Pharmacological treatment
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