Alzheimers

Mere som dette

downs syndrome mind map

af Sophie lutz

SOAP Notes in MSD and orthopedic injury.

af Jalal Nasir

CompSys

af stephen chen

VIRGINIA WOLF

af Daniele Modica

Q1 Alzheimers

e) What are the possible drawbacks or limitations of the barcode test and are there any ethical considerations of doing such a test?

Other drawbacks

Still only 90% probabilty

Does not have to break out

As shows Schizophrenia evenif identical twin has it there is onlya 50% chance

So there is an environmentalside to it

Ethical considerations

Would employers make you test

Would insurances make you test

Leading to a self fulfilling prophecy?

What if the diagnosis is wrong as in breast cancer

Subtopic

Cruel: Its not curable so it's bad news of a slow and certain and cruel death

d) Why does the article state that diagnosis is only about 50 to 85% accurate? How can it be positively confirmed?

Currently no diagnosticmethod that can detectAlzheimerswith 100% probabilty

Using a varity of diagnosticmethods

Brain Scans(can only be usedto exclude other conditions)

CT

Pet scan

MRI

fMRI

Cognitive Tests

i.e. Memory Tests

Behavioural assessment

Skilled Doctors

Postive Confirmation: Can only be diagnosedpost-mortem via autopsy

Histological Methods

i.e. microscopy

at best: 15% remain undiagnosedbecause they are diagnosed as otherdiseases i.e. depression (impaired memory etc.)

Difficulty: Other disesaes / dementias show Alzheimer-Like Symptoms

Schizophrenia

Stroke

Lesion in the Hippocampus

c) What are the likely causes of Alzheimer’s disease?

Likely genetic plus environmental factorsare interacting in some cases

factors that increase risk

other aren't

Genes: inheriting a certain allele of a protein apolipo protein e

Age is highest risk factor

behaviour factors are under our control (healty life style)

clinical depression

smoking

arthereosklerosis

hypertension

diabetes

elevated cholesterol and obesity

head injury (boxers)

Reminds me of schizophrenia anways ...

Amyloid hypothesis(Genetic Problem)

Likely a genetic disease leadingto abnormal/Mutant proteins

However only 50% of monocygotic twinsdevelope schizophrenia

However only < 10 percent of the occurrance can be acounted for gene defects

Cholinergic Hypothesis(Lack of Neurotransmtters)

Reduced synthesis of the neurotramsmiiteracetylcholine

b) Describe the brain changes in Alzheimer’s disease shown in brain imaging studiesand explain how these might account for the clinical symptoms, in particular those related to cognition.

how do the changesaccoutn for clinical symptoms?

Cell Loss leads to loss of structuresor connectiviyin specific areas

Raphe Nuclei

Regulation of mood(serotonergic projections to the cortex)

depression

Lymbic structures

Amygdala

the appreciation of theemotional significancof sth. in a normal way is lost

fear

mood changes

abnormal social behaviour

Hippocampus (old cortex) and Entorhinal cortex (neocorte)

learning and memory- short term memoryin particular

are among thefirst areas to degenerate

-->loss of short term memory

Neocortex

loss in highest order assotiation areas

primar areas remain intact(propriocepton; smell, taste touch, vision, hearing)

Prefrontal cortex

ability to plan andreason is lost

-->hence confusion

Brain Changes

Loss ofwhole structures

Loss of connectivity because of the loss of dentrites and synapses

Loss of neurons

Abnormal chnange in extracellular space

NeurofibrilaryTangles

abnormal depositions (filament) in Neurons

Intracellular: Abnormal changesin Neurons

Plaques

Abnormal extracellular depositsof (normal) Beta-Amyloid Protein surrounded by abnormal neuronal processes and glial cellswho try to get rid of it

a) What is Alzheimer’s disease (AD) and what are its clinical symptoms?

Cinical symptoms

Late stage

Gradual loss of physiological (bodily)functions

Leading to death

Mean time from diagnosis to death= 7 years

Heamorrhage in the brain

because of depostion ofamyloid in blood vessels which makes them rupture

loss of cog funct

Language break down

Memory Loss

Loss of sense of self:individuals forget who they are

Loss of episodic memoryin Hippocampus

Long term memory loss

late stage because ltm is widely distributed

Middle stage

Emotional problems

Mood swings

irritability

agression

significant Losss of cog. function

loss of higher ordre cog func. like inabilty to understand jokes

significant memoryloss

Early stage

Depression

Decreased initiative(loss of interest in hobbiesor personal hygiene)

Faulty judgement

Deficits in attention

Loss of Short TermMemory (Can't rememberrecently learned things)

What is it?

No cure!

can not be positively diagnozed until autopsy

Genetic Mutation at differnt Genes but they only account for less than 1% of the occurrence (Importantly shown in patients - swedish) with early onset)

Animal model: An animal model using mice with a mutation in the gene coding for APP can show this

show tangles and plaques

show Impairment

Impairments in spatial tasks

shows age dependet (at 10 month) impairment in learning

... result of boht a) and b) is a toxic form of of Amyloid called beta amyloid

released in extracellular space forming aggregates called plaques which are toxic

b) Mutations involved in the processing of APP (enzymes)so that APP ins inappropriately cleaved

a) Gene that codes for amyloid precursor protein (APP) can have a numver of mutations

for the rest: cause unknown!

late onset >65

Early onset <65

High risk factor is age

45% of People over 85

3. Brain autopsies show accumulation of toxic tangles and plaques

Intracellular Tangles (Hyperphosphorylated tau protein)

Extracellular Plaques (Beta Amyloid Protein)

2. Involving Memory loss and loss of higher cognitve functions

no loss of primary areas

1. Neurodegenerative Disease(or neurological disease)

A specific type of progressive dementia (there are other dementias)

Characterized by neuron loss in specific areas

Significan neurons loss in the CNS - neurons are dying