Fundamentals Of Human Neuropsychology. Kolb. - Alzheimer's

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Dementia:

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broad term encompassing disorders that involve cognitive decline (without mind)
Very debilitating

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Forms of dementia

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Many different forms exist
** Insult to the brain:
* Neurodegeneration:

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Dementia insult to the brain

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traumatic brain injury (chronic traumatic encephalopathy), stroke (vascular dementia), infection (meningitis, AIDS, syphilis)

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nuerodegenration

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* Korsakoff’s Syndrome (vitamin B deficiency, seen in alcoholics),
* Huntington’s Disease,
* Dementia with Lewy Bodies (related to Parkinson’s Disease),
* Frontotemporal Dementia,
* Alzheimer’s Disease (most common form of dementia)
* internal/metabolic cause

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Alzheimer's Features

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* Most common form of dementia
* Late Onset > 70 years
(sporadic Alzheimer’s)
* “Early onset” <65 years  tends to be more severe and progress more quickly, has a larger genetic component then late onset
* 2x as common in women as in men
* Alzheimer’s numbers are on the rise, expected to more then double by 2050  burden on our healthcare system
* Aging population increases incidence, obesity, stroke, HD also increase which increase risk for Alzheimer’s

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Alzheimer's Symptoms (7)

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Cognitive Deficits:
* Severe memory loss (both reterograde and anterograde amnesia)
* Language Impairments (become anomic  cannot think of names, empty speech)
* Visuospatial impairments (difficulties navigating space)
Behavioural Deficits:
* Anosognosia: not aware of own impairment, seen as * disorder progresses
* Confusion
* Wandering
* Aggression
* Psychosis
 -> due to chemical imbalance in the brain
Sleep Disturbances

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stages of alzheimer's disease

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* mild cognitive impairment
* Mild Alzheimer’s Disease
* Moderate Alzheimer’s Disease
* Severe Alzheimer’s Disease

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Mild Cognitive Impairment

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* Transitionary stage: transitioning from someone who has normal decline w/ aging to Alzheimer’s disease
* Difficult to diagnose
 difficult to tell you who has declined more, overlap w/ symptoms b/w other forms of dementia
Not everyone progresses to AD

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Mild Alzheimer’s Disease

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people begin to seek out healthcare
* Memory loss for recent events
 anterograde amnesia
* Getting lost, misplacing things

* Difficulties performing tasks, problem solving, decision making
* Conversation becomes difficult

* Can become withdrawn or aggressive

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Moderate Alzheimer’s Disease

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begin to have trouble w/ daily life
* Problems continue to intensify, people begin to need help with activities of daily living (difficult for caregivers)
* Memory loss worsens, includes autobiographical memory
(retrograde amnesia)
Confusion deepens
( Easily overwhelmed by sensory stimulation )
* May become combative, suspicious, or hostile -> results from anosagnosia
Possible psychosis

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Severe Alzheimer’s Disease

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*Decline continues, basic activities of life now severely affected
* Loss of language/communication

* Require intensive help with daily living

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Neuropathology of alzheimer's

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* Widespread cortical atrophy (shrinkage)
* Cholinergic Disruption

* Abnormal protein deposits
*

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Widespread cortical atrophy

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(shrinkage)  particularly in language centers in temporal lobes and hippocampus (memory)
Not homogenous cerebral atrophy

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Cholinergic Disruption

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* Projections (Acetylcholine) of the basal forebrain degenerate
* Loss of acetylcholine -> acetylcholinesterase inhibitors used (increase levels of acetylcholine b/c of less breakdown of Ach)
* Stop working after 2-4 years b/c Ach is no longer produced

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Abnormal protein deposits (Amyloid plaque)

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-> most likely cause
* Extracellular accumulation of beta-amyloid protein (Aβ plaques) -> accumulate on outside of neural cells
* Toxic to neurons (cause neurons to die)
* Have APO E4 gene -> higher risk of developing sporadic Alzheimer’s disease, also respond better to drugs for disease
* Occurs in first in default network (opposite of paying attention in the world) -> first area affected in Alzheimer’s disease
* These deposits are also seen in healthy individuals

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Abnormal protein deposits: (Tau Protein)

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* rarely seen in healthy brains, key to Alzheimer’s
Intracellular accumulation of tau protein (neurofibrillary tangles)
* Tau: microtubule integrity in neurons
(allows cell body to perform basic functions)
* Tau becomes pathologically altered, accumulates in neurons, walls begin to collapse and neuron cannot perform functions and dies

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Bio marks of AD

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Biomarkers:
Hippocampal volume (hippocampus degenerates early in the disease)
CSF markers: Tau (higher in people w/ Alzheimer’s) and Aβ (lower in people w/ Alzheimer’s) in CSF (lumbar puncture) -> most promising diagnostic tool