Related to neuronal death due to plaques and neurofibrillary tangles
Possibilities include tau proteins and beta-amyloid as culprits
Genetic link postulated
Symptoms
Memory impairment (short-term initially, progressing to longer-term)
Visuospatial impairment (difficulties with car parking, dropping items)
Planning (meal-cooking, complex tasks)
Word-finding problems
Disorientation to time and place
Labile mood as disease progresses with occasional delusions and dangerous behaviour
Diagnosis of Alzheimer’s dementia
The staging of the level of severity of Alzheimer’s as a disease process can be broken down into 3 separate entities:
Alzheimer’s Dementia
Alzheimer’s related mild cognitive impairment (MCI)
Pre-clinical Alzheimer’s
The criteria from each stage is based on recommendations from the National Institute on Aging -Alzheimer’s Association workgroups; full studies can be found here.
In summary, to diagnose dementia the follow need to be present:
Interferes with activities of daily living (ADLs)
A decline in function noted over time
This decline is not attributable to short-term or reversible causes (e.g. delirium)
The impairment in cognition is obtained (as described in the general dementia section) via history, collateral history, and bedside cognitive testing.
Multi-domain impairment documented in cognition, of at least two of:
Memory impairment
Reasoning and judgement
Visuospatial
Language
Behaviour/personality
With regards to a specific diagnosis of Alzheimer’s dementia, this is again sub-divided into 3 separate categories:
Probable Alzheimer’s Dementia
Possible Alzheimer’s Dementia
Probably or possible Alzheimer’s Dementia with evidence of pathophysiological process
Each sub-category has been defined as detailed below (each with the pre-requisite of a diagnosis of all-cause dementia as detailed above).
Probable Alzheimer’s Dementia
Insidious onset over months to years, rather than more acutely of hours to days
Definitive history of worsening of cognition over time
One of the following categories are present as the most prominent finding during clinical assessment:
Amnesic presentation (most common)
Non-amnesic presentations:
Language (e.g. word/name finding difficulties)
Visuospatial (e.g. facial recognition deficit)
Executive (e.g. impairment judgement and task planning)
Without any of the following findings present:
Significant cerebrovascular disease (e.g. significant stroke associated contemporaneously with onset of cognitive impairment)
Findings of the core features of Lewy Body Dementia (e.g. hallucinations, Parkinsonism etc… for more details see the LBD section)
Findings in keeping with fronto-temporal dementia
Findings in keeping with progressive aphasia
Concurrent neurological disease
Possible Alzheimer’s Dementia
Atypical Course
Clinical findings and features of Alzheimer’s Dementia but with an unusual time course (e.g. fast onset, rapid decline)
Mixed Presentation
Mixed with signs of Vascular Dementia
Mixed with signs of LBD
Mixed with other concurrent neurological disease
Probable Alzheimer’s Dementia with evidence of pathophysiological process
If the additional pathophysiological processes are identified, it increases the likelihood of the underlying disease process being that of an Alzheimer’s Dementia (remembering that a true diagnosis can only be confirmed at autopsy!)
It is not recommended that these biomarkers are routinely looked for in the diagnosis, due to ongoing research into the pathological process and the variability in availability and sensitivities of appropriate assays to detect them. More information is included for reference only.
Biomarkers of brain amyloid-beta protein deposition:
Low CSF Aβ42
Positive PET amyloid imaging
Biomarkers of downstream neuronal injury or degeneration:
Elevated CSF Tau
Decreased fluorodeoxyglucose (FDG) uptake on PET in temporal-parietal cortex
