alteration in cognitive systems

three neural systems essential to cognitive function

1. attentional system; helps us stay alert and focused overtime

2. memory and language system; helps us store and share info

3. affective or emotive; control out feelings, mood and intentions

three alterations in cognitive systems

1. alteration in conciousness

2. alternation in arousal

3. alteration in awareness

data processing deficts

problem understanding and handling sensory info

types of data processing deficits

1. agnosia

2. aphasia

3. acute confusion state (delirum)

4. demetia

5. alzhemiers

agnosia

cant recogonize things, faces, objects even if their senses work fine

aphasia

has trouble talking or understanding language even if brain is not damaged in other ways

acute confusion state (delirum)

• affects a lot of areas in brain

• changes how you think, feel, see things or stay aware

• can be transient (acute) or persistant (chronic)

• can be sudden or gradual onset

• can get better w/ treatment

• older adults in hopsital most at risk

demetia

• gradual loss of many brain functions

• affects thinking, memory, laguage, decision-making

• starts with loss of memory

• starts slowly can be sudden

• progressively gets worse

• alzhemiers disease most common cause

demetia grouped based on CAUSES

• genetics

• tramua

• tumors

• vascular disorders

• infections

causes grouped as

• poteintially reversible

• irreverisble

is alzhemiers reversible?

• no irreversible neurodegenerative cause

clinical manifestations in dementia

• d/t reduced thinking skills, person may show signs of changes of behaviour; agitation, wandering and aggression

alzhemier disease aka alzhemier type dementia (ATD)

• alzhemiers is the main cause of serious memory and behaviour problems in older people

• only way to confirm alzhemiers is after death w/ an autopsy

• can check progession of disease w/history, lab tests, brain images and clinical history

forms of ATD

1. late-onset nonhereditary sporadiac AD (common)

2. early onset familial AD

3. early onset AD (rare)

risk factors for AD

• familial/genetic (early onset)

  • genetic variation

• sporadiac late onset

  • aging (over 65)

  • ApoEgene (chromosome 19)

  • tramuatic brain injury

  • infectious factors

  • estrogen decline during menopause

  • HTN, hyperlipidemia, atherscelorsis

  • obesity

  • insulin resistance

  • sleep deprivation; sleep apnea

  • high fat diet

  • alternation gut-brain microbial axis

oral and gut microbiome and AD

• chronic gum disease (periodontitis) major factor linking gut microbe to AD

  • tend to have more memory decline

how is gum disease linked with AD

• gram-negative bacteria releases toxins tht hurt blood brain barrier (BBB) causes brain inflammation, buildup of proteins linked w/ alzhemiers and other brain damage

• people w/ gum disease swallow lots of bacteria causing inflammation in gut, making it more leaky, causing it to enter bloodstream

• body wide inflammation→ BBB leaks→harmful chemicals and bacteria in brain→ inflammation of brain, cell damage and death

patho of early onset familial AD

• linked to gene mutations on chromosome 21, these mutations causes problems w/ protein called amyloid-beta protein that builds up in brain and causes plaque in brain

patho of late onset AD

linked to gene chromosome 19, makes it harder to remove amyloid beta protein from brain, protein gets broken down in harmful pieces form plaques and tangles in brain

which AD is more common

• late-onset AD, does not usually have specific genetic cause

cellular patho AD

1. abnormal plaques created from amyloid beta proteins build up outside brain cells, tangled proteins called tau buildup inside cells, nerve cells in brain lose a chemical called acetylcholine

2. brain cannot breakdown amyloid precursor protein, causes buildup of toxic pieces of amyloid-beta protein.

3. causes plaque to form, messes up nerve signals and leads to death of brain cells

patho cont.

• as people age, it can cause changes in the body that lead to inflammation

• misfolded proteins; amyloid beta and tau buildup causing immune system to react

  • brain inflammation and stress

  • less oxygen and energy reaching brain

  • change in blood vessel and protective barrier in brain

  • problems w/ how cells produce energy and handle proteins; cause brain cells to die

patho; RESULT

• amyloid-beta protein

  • if the brain is unable to get rid of a protein called amyloid precursor protein, it breaks down into toxic pieces called amyloid beta

  • these then clump together form a plaque mess w/ nerve signals and kill brain cells

• tau protein

  • tau protein usually keeps cell structure intact, but in AD it breaks off and forms tangled clumps

  • tangles block flow of nutrients to brain cells→die

• plaques and tangles build up in brain that controls learning and memory→brain cells die→brain shrinks and as brain cells die, lose acetylcholine→hard time doing tasks

Non-hereditary sporadic form of Alzheimer disease is the most frequent one (T/F)

true

Clearance of amyloid-beta protein is increased in Alzheimer disease (T/F)

false

Cellular pathology for hereditary and non-hereditary form of Alzheimer disease differs (T/F)

False

The accumulation of amyloid precursor protein leads to formation of diffuse neuritic plaques and death of neurons (T/F)

true

clinical manifestations

• AD can start years before symptoms show up

• start of with mild memory and then slowly gets worse overtime→total loss of memory and thinking skills

what stages does AD go through

• forgetting things

• getting upset easily

• feeling lost or confused

• having trouble concentrating, solving problems, making decisons

• issues w/ coordiation (dyspraxia)

• behavioural changes

mild cognitive impairment

• cognitive

  • mild memory loss, mostly for a recent event (episodic memory) and new info (semantic memory)

• functional

  • possibly depression, mild anxiety

early stage

• cognitive

  • measurable short-term memory loss; difficulty planning; disorientation to location

• functional

  • mild IADL problems

middle stage

• cognitive

  • significant forgetfulness; easy to get lost; may dress inappropirately; may hallucinate

• functional

  • IADL-dependant, some ADL problems

late stage

• cognitive

  • little cognitive ability; lang not clear, personality change, does not recognize family members, wanderingm repetitive beahviour

• functional

  • ADL dependant, incontintent, difficult eating

end stage

• cognitive

  • no significant cognitve function; loss of word speech

• functional

  • nonambulatory/bedbound, unable to eat

evaluation of AD

• clinical history

  • mental status examination

  • cerebrospinal fluid analysis

  • brain imaging (CT, MRI, PET) of structure, blood flow, metabolism

  • course of illness

• genetic suspectibility test; screen early onset

  • PSEN 1

  • PSEN 2

  • amyloid b precursor protein

is there a cure?

no cure, just tools to help memory and thinking problems; memory aids and maintain cognitive function or general state of wellbeing (hygiene, nutrition or health)

drug therapy for alzhemiers

• help with ADLS, behaviour, thinking

• slow progession of disease

• start treatment as soon as alzhemiers is diagnosed

NMDA (N-Methyl-D-Aspartate receptor antagonist); Memantine INDICATIONS

• moderate to severe dementia

NMDA- Memantine MOA

• blocks NMDA receptors, stops too much gluctamate from building up

• prevents gluctamate from damaging nerve cells

NMDA- Memantine DESIRED EFFECTS