# Retention and longitudinal change in Insight 46, an intensive neuroscience sub-study of the 1946 British birth cohort

**Authors:** Sarah E. Keuss, Kirsty Lu, Sarah-Naomi James, Jennifer M. Nicholas, William Coath, Ashvini Keshavan, David M. Cash, Carole H. Sudre, Josephine Barnes, Heidi Murray-Smith, Andrew Wong, Rebecca Street, Marcus Richards, Jonathan M. Schott

PMC · DOI: 10.1186/s13104-025-07323-y · BMC Research Notes · 2026-01-22

## TL;DR

This study examines factors affecting retention and cognitive changes in a neuroscience sub-study of older adults over 2.5 years.

## Contribution

The study identifies specific factors influencing retention and longitudinal cognitive changes in a longitudinal neuroscience cohort.

## Key findings

- An 88% retention rate was achieved over 2.5 years in the Insight 46 cohort.
- Cognitive improvements and declines were observed across different tests during follow-up.
- Being β-amyloid positive and female sex were associated with lower retention odds.

## Abstract

Participant retention is a significant challenge in ageing and dementia research. This analysis investigated (a) factors associated with retention in Insight 46, a neuroscience sub-study of the 1946 British birth cohort, and (b) clinical and cognitive changes over 2.5 years of follow-up.

Of 502 participants assessed at baseline (mean[SD] age: 70.5[0.7] years), 442 returned for follow-up (mean[SD] interval: 2.5[0.3] years), representing a retention rate of 88%. Being β-amyloid positive (measures using positron emission tomography), female sex, and older age at baseline associated with lower odds of retention, while completion of neuroimaging and better cognitive performance at baseline– particularly on memory testing– related to higher odds of retention. By the time of follow-up, 14 participants were deceased, 12 of whom were female. Over follow-up, improvements were noted in certain cognitive tests (face-name test, logical memory delayed recall) with declines seen in others (mini-mental state examination, digit-symbol substitution test). Increases in self- and informant-reported cognitive complaints, cognitive disorder diagnoses, and motor abnormalities were also observed, alongside declines in blood pressure. These results have implications for the interpretation and generalisability of Insight 46 data and may be relevant to the planning of other longitudinal studies in this field.

The online version contains supplementary material available at 10.1186/s13104-025-07323-y.

## Linked entities

- **Diseases:** dementia (MONDO:0001627)

## Full-text entities

- **Genes:** LYST (lysosomal trafficking regulator) [NCBI Gene 1130] {aka CHS, CHS1, Mauve}, APOE (apolipoprotein E) [NCBI Gene 348] {aka AD2, APO-E, ApoE4, LDLCQ5, LPG}, APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}
- **Diseases:** motor abnormalities (MESH:D000014), death (MESH:D003643), cognitive complaints (MESH:D003072), cardiovascular disease (MESH:D002318), JMS (MESH:C567476), coronavirus (MESH:D018352), Alzheimer (MESH:D000544), MR (MESH:D008944), MCI (MESH:D060825), CVS (MESH:D003333), BaMoS (MESH:D004195), Parkinson's Disease (MESH:D010300), Anxiety (MESH:D001007), brain disorder (MESH:D001927), blood pressure (MESH:D006973), NSHD (MESH:D002658), claustrophobia (MESH:D010698), cancer (MESH:D009369), PACC (MESH:D058617), Dementia (MESH:D003704), WMHV (MESH:D056784)
- **Chemicals:** Florbetapir (MESH:C545186)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** V03863X, Ito E
- **Cell lines:** FNAME-12 — Mus musculus (Mouse), Hybridoma (CVCL_J992)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12837026/full.md

## References

5 references — full list in the complete paper: https://tomesphere.com/paper/PMC12837026/full.md

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Source: https://tomesphere.com/paper/PMC12837026