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Amyloid-Beta: The 40- and 42-Amino-Acid Peptides Behind Alzheimer's Plaques — and the Antibodies Aimed at Them

Amyloid-beta is a peptide of 40 or 42 amino acids cut from a much larger brain protein, APP. It clumps into the plaques found in Alzheimer's disease and was first purified in 1984. The approved Alzheimer's drugs that target it are antibodies, not peptides; the largest trial showed moderately slower decline with brain-swelling side effects.

Made by the body40 or 42 amino acidsNot a medicine — the approved drugs are antibodies against it

Caroline S · Published 2026-10-04

Length

Mainly 40 or 42 amino acids (Aβ40 and Aβ42), depending on where the final cut falls

Sequence

Aβ42: DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA — residues 672–713 of the 770-residue amyloid-beta precursor protein, APP (UniProt P05067); Aβ40 ends two residues earlier, at 711

Origin

Cut from APP, a protein on the surface of nerve cells, by two enzymes in sequence (beta-secretase, then gamma-secretase). First purified from the blood-vessel amyloid of Alzheimer's brains and reported in 1984 by Glenner and Wong (PMID 6375662).

Last reviewed

2026-10-04

What is it good for?

Nothing as a product — it is not taken by anyone. In the body its normal role is unsettled: UniProt annotates it as a metal-binding peptide that binds copper, zinc and iron. Its notoriety is that it clumps into the plaques of Alzheimer's disease, which is why the approved Alzheimer's antibodies are designed to clear it.

Illustration: A clear glass flask, tilted, on a white surface with a copper sphere and green reflection.
Illustration

What it is

Amyloid-beta is a short peptide cut from a long protein. The parent is the amyloid-beta precursor protein, APP — 770 residues in its longest form, sitting in the membrane of nerve cells (UniProt P05067). Two enzymes cut it in sequence: beta-secretase makes the first cut, gamma-secretase the second. What falls out between them is amyloid-beta, mainly in two lengths:

Form Precursor residues Length
Aβ40 672–711 40
Aβ42 672–713 42

The full Aβ42 sequence is DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA. The peptide-chain entry explains how a sequence like this is read.

How it was found

In 1984 Glenner and Wong purified a protein from the amyloid deposits in the blood vessels of Alzheimer's brains and sequenced it. A computer search found no match with any protein sequenced up to then (Biochemical and Biophysical Research Communications, PMID 6375662). They suggested it might come from a unique precursor in the blood and might offer a diagnostic test.

What it does

Its normal job is not settled. UniProt annotates amyloid-beta peptides as metal chelators — binding copper, zinc and iron — that bind lipoproteins in spinal fluid and plasma, and annotates Aβ42 as the more effective reductant of the two forms. Some of these annotations come from laboratory studies.

What is not in doubt is the clumping: amyloid-beta is the main constituent of the amyloid plaques in Alzheimer's disease. Whether those plaques drive the disease or accompany it is debated; the antibody trials below test it directly in people.

What is described How firm
Main protein of Alzheimer's amyloid Biochemistry of human brain tissue (1984 onward)
Normal role in metal and lipoprotein binding UniProt annotation, partly in vitro
Removing it slows decline One large trial: a moderate difference, with side effects

The antibodies aimed at it

The approved Alzheimer's drugs connected with amyloid-beta are antibodies — large proteins — not peptides. FDA's records list three: aducanumab (Aduhelm, 2021-06-07), lecanemab (Leqembi, 2023-01-06) and donanemab (Kisunla, 2024-07-02).

The largest published result is lecanemab's Clarity AD trial (New England Journal of Medicine, 2023, PMID 36449413; funded by Eisai and Biogen):

18-month outcome, 1,795 people with early Alzheimer's Lecanemab Placebo
Change in CDR-SB (0–18; higher = worse) +1.21 +1.66
Brain amyloid (PET substudy, 698 people) −59.1 centiloids vs placebo —
Infusion-related reactions 26.4% —
Brain swelling or effusion on scans (ARIA-E) 12.6% —

The authors described moderately less decline with adverse events, and called for longer trials. These medicines are prescribed and monitored by specialists; this entry records the trial, not a recommendation.

Where it stands

Amyloid-beta is a target, not a treatment, and no product contains it (openFDA, 2026-10-04). PubMed returns 91,174 records for amyloid beta, 515 tagged as randomised controlled trials.

Another peptide that forms amyloid — in the pancreas rather than the brain — is amylin. For the compounds marketed on cognition claims, see peptides for focus and mood, and for one brain-peptide preparation with its own trial record, cerebrolysin.

What the research shows

Is the main protein of Alzheimer's amyloid

Purified and sequenced from Alzheimer's cerebrovascular amyloid in 1984 (Glenner and Wong, Biochem Biophys Res Commun, PMID 6375662)

Clearing it slows Alzheimer's decline

Moderately, in one 1,795-person trial: CDR-SB worsened 1.21 on lecanemab vs 1.66 on placebo over 18 months; brain swelling or effusion in 12.6% (Clarity AD, N Engl J Med 2023, PMID 36449413)

Has a defined normal function

Unsettled. UniProt annotates metal binding and lipoprotein binding, partly from laboratory studies

Bars show how much of the evidence is in humans, not how well anything works.

Where it stands

In the body

A fragment of the nerve-cell surface protein APP (UniProt P05067).

United States

Not a medicine. Antibodies against it are licensed: aducanumab (Aduhelm, BLA 761178, 2021-06-07), lecanemab (Leqembi, BLA 761269, 2023-01-06), donanemab (Kisunla, BLA 761248, 2024-07-02) (openFDA, 2026-10-04).

Published record

PubMed returns 91,174 records for amyloid beta, 515 tagged as randomised controlled trials (2026-10-04).

Frequently asked questions

What is amyloid-beta?

A peptide of 40 or 42 amino acids cut from a large protein on the surface of nerve cells, the amyloid-beta precursor protein (APP). It tends to clump, and its clumps form the amyloid plaques found in Alzheimer's disease.

What is the difference between Aβ40 and Aβ42?

Length: Aβ42 carries two extra amino acids at its end (isoleucine and alanine), because the final enzyme cut falls two positions later. UniProt annotates Aβ42 as the more effective metal reductant of the two.

Is amyloid-beta something people take?

No. It is not a supplement or a drug, and no product contains it. It is studied because of its role in Alzheimer's disease, and the medicines connected with it are antibodies designed to remove it from the brain.

Do the amyloid drugs work?

In the largest published trial, lecanemab's Clarity AD study of 1,795 people, decline on the CDR-SB scale over 18 months was 1.21 points on the drug and 1.66 on placebo — a difference the authors called moderate — with brain swelling or fluid on scans in 12.6% of treated participants. Decisions about these drugs belong with a specialist.

When was amyloid-beta discovered?

Glenner and Wong reported purifying it from the blood-vessel amyloid of Alzheimer's brains in 1984, noting that its sequence matched no known protein.