Alzheimer's disease: an animated, cited guide

This page needs JavaScript for its animations. The outline and key answers are below, and every claim in the full version carries a numbered citation.

Not medical advice. Alzheimer's Companion is an educational synthesis of published literature. It does not replace a clinician.

What is in it

What Alzheimer's is Dementia versus Alzheimer's, who it affects, the numbers.
The brain that forgets Where it starts and how it spreads, stage by stage.
Amyloid, animated From one protein cut to a plaque, and the debate about it.
Tau and the tangle How a scaffold protein turns into a tangle and spreads.
Microglia and the lost synapse Inflammation, pruning, and the strongest link to memory loss.
Genes and inheritance APOE, the dominant families, Down syndrome, and what a test means.
Twenty years before symptoms The biomarker cascade, in order.
Stages and symptoms From no symptoms to severe dementia, function by function.
Diagnosis and biomarkers Criteria, scans, spinal fluid, blood tests and screening tools.
The differential Delirium, vascular, Lewy body, frontotemporal and reversible causes.
Cholinesterase inhibitors and memantine Inside the synapse, and what the benefit really is.
Anti-amyloid antibodies over time Lecanemab and donanemab over 18 months, ARIA and the debate.
Beyond memory Agitation, mood, psychosis and sleep, and the drug cautions.
Lowering the risk The 14 modifiable risk factors and what trials show.
Living with dementia and caregiving Planning, safety, caregivers and the end of life.
Nursing care Assessment, giving the medicines, communication, documentation.
Toward a cure The pipeline, prevention trials, and the evidence for each route.
History and people From Auguste Deter in 1901 to the antibodies.
Flashcards and mnemonics Flip cards by topic.
Quiz Questions with explanations.
Glossary Every term, searchable.
Sources Every reference behind the app.

Part 1 · The disease

The brain that forgets

Tau tangles and amyloid plaques both spread through the brain in a fixed order, but not the same order. Step through the tangle stages, then switch to amyloid and compare where each one starts.

Map

Spread

Schematic outlines. Deep structures are dashed. Regions outside a scheme are left unshaded; that does not mean they are spared.

Why memory goes first

The first tangles form where the hippocampal memory circuit begins. Follow a signal around the loop, then watch which neurons are lost, in the order the studies report.

Disease course

Schematic. Dots on the loop are signals; faded dashed cells are lost neurons. The MRI shapes compound the published yearly rates, for illustration.

Scoring a brain at autopsy: the ABC score

The 2012 NIA-AA guidelines rate three things and combine them into one level of Alzheimer's neuropathologic change. Choose a rating for each and read the result. ^246,366

A · amyloid plaques (Thal phase)

B · tangles (Braak stage)

C · neuritic plaques (CERAD)

How the levels combine

Not, Low, Intermediate, High

A0 is always "Not". With B0 or B1 the level is at most "Low". "High" needs A3, B3 and C2 or C3 together. "Intermediate" or "High" is considered a sufficient explanation for dementia. ³⁶⁶

The guidelines recognise that Alzheimer's changes can be present without cognitive impairment, and they set protocols for common co-pathologies: Lewy body disease, vascular brain injury, hippocampal sclerosis and TDP-43 inclusions. ^246,366

In plain wordsAfter death, a pathologist scores how much amyloid, how far the tangles have spread and how many damaged plaques there are. Together they say how likely Alzheimer's explains the dementia.

Exam hookA = Thal (amyloid), B = Braak (tangles), C = CERAD (neuritic plaques). A0 → Not. B0–1 → at most Low. High = A3 + B3 + C2–3.

Table after Montine 2012, Table 3. B0 and B1 share a column in the original.