Psychiatry Research 321 (2023) 115063

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Psychiatry Research
journal homepage: www.elsevier.com/locate/psychres

A longitudinal study on cognitive aging in autism

C. Torenvliet a, *, A.P. Groenman a, b, T.A. Radhoe a, J.A. Agelink van Rentergem a, W.J. Van der
Putten a, c, H.M. Geurts a, c
a
Dutch Autism and ADHD Research Center, Brain and Cognition, Department of Psychology, University of Amsterdam, Amsterdam, the Netherlands
b
Research Institute Child Development and Education, University of Amsterdam, the Netherlands
c
Leo Kannerhuis, autism clinic (Youz/Parnassia Group), Amsterdam, the Netherlands

A R T I C L E I N F O A B S T R A C T

Keywords: Longitudinal studies on cognitive aging in autism are scarce, and largely underpowered, yet essential to obtain
Aging more conclusive results on cognitive changes in autism during adulthood. In the largest longitudinal study on
Cognition cognition thus far, we aimed to get more insight into cognitive aging in autism. As pre-registered, we computed
Autism
reliable change indices (RCIs) and multilevel models to estimate cognitive changes in 128 autistic, and 112 non-
autistic adults (range: 24–85 yrs.) over two to three timepoints (average interval: 3.5 yrs.). Participants were
tested on 15 outcome measures, covering verbal memory, visual (working) memory, prospective memory, theory
of mind, fluency, response speed, inhibition, planning, and switching. RCIs showed no significant differences
between groups (autism/no-autism) in changes over time. Using multilevel models, most tasks showed sensitivity
to cross-sectional age-related effects, and/or longitudinal changes, with worse performance at older age, and
later timepoints. However, effects were not significantly different between the autism and no-autism group. This
lack of group differences was substantiated by additional Bayesian analyses. In sum, the current study provides
evidence for parallel (similar) cognitive aging in autism. Specifically, autistic individuals diagnosed in adulthood,
without intellectual disability, do not seem at risk for accelerated cognitive decline.

1. Introduction Lever and Geurts, 2016; Roestorf et al., 2019; Tse et al., 2019; Zivrali
Yarar et al., 2020). Longitudinal studies are warranted to determine
Autism can be described as a developmental difference, shaping the whether autistic adults are indeed not particularly at risk for increased
lives of autistic individuals from the first to the final stages of life. impact of cognitive aging or whether previous cross-sectional results are
However, research on the entire lifespan of autistic individuals is scarce. clouded by cohort effects.
On cognitive aging, specifically, longitudinal studies are needed to Cohort effects could have affected previous cross-sectional conclu­
elaborate on the inconsistent findings in cross-sectional studies thus far. sions, especially in studies where age of diagnosis, and age of cognitive
Some might argue that autistic individuals are more vulnerable for assessment were related. Even though numerous reasons for late di­
cognitive aging (Bowler, 2007; Braden et al., 2017; Geurts and Vissers, agnoses are possible, if an individual with autism is diagnosed at, or
2012), supported by epidemiological data indicating increased risks for after retirement age, this could imply that their autism affected their
certain neurodegenerative disorders (Bishop-Fitzpatrick and Kind, school, studies, or work differently compared to those diagnosed at
2017; Croen et al., 2015; Geurts, McQuaid, et al., 2020; Hand et al., younger ages. Possibly, certain genetic and/or environmental factors in
2019; Rydzewska et al., 2018; Vivanti et al., 2021) – and by higher rates these individuals allowed them to compensate for aspects that they
of self-reported cognitive difficulties in adults with autism (Geurts, Pol, might have struggled with throughout life. Such compensatory mecha­
et al., 2020; Klein et al., 2022; Lever and Geurts, 2016). However, nisms show parallels to cognitive reserve, which is known to mitigate
though not consistent, most cognitive research tends to observe a gentler the effects of neural decline (Cabeza et al., 2018; Stern et al., 2019). For
pattern in which cross-sectional age-related differences between autistic instance, individuals with high educational attainment are known to
and non-autistic individuals are minimal or even advantageous towards show less, or late cognitive decline (Habib et al., 2007). Although
autistic individuals (Ambery et al., 2006; Geurts and Vissers, 2012; speculative, compensatory mechanisms in late-diagnosed autistic

* Corresponding author.
E-mail address: [email protected] (C. Torenvliet).

https://doi.org/10.1016/j.psychres.2023.115063
Received 1 November 2022; Received in revised form 10 January 2023; Accepted 14 January 2023
Available online 18 January 2023
0165-1781/© 2023 The Author(s). Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
C. Torenvliet et al. Psychiatry Research 321 (2023) 115063

individuals could have caused cross-sectional conclusions on cognitive 2. Methods

aging in autism to be too optimistic.
Longitudinal data on autistic cognitive aging is scarce. In the first 2.1. Design
longitudinal study that measured the development of IQ and language
over a 40-year follow-up period, most individuals (n = 45, 75%) showed We used a multistage overlapping cohort design, with two cohorts
improvements or stable performances from childhood (2–13 years) to included at different timepoints (see Geurts et al., 2021). Data collection
middle adulthood (29–64 years; Howlin and Magiati, 2017). However, included four waves; at Wave 2 no cognitive data was obtained, and is
those individuals who failed to progress in early language development, thus not part of this study. The first cohort was included at Wave 1, had
showed severe impairments in middle adulthood (n = 15, 23%). Two the second cognitive measurement at Wave 3, and some had a third
studies covering middle- and late adulthood show contrasting results. In measurement at Wave 4. The second cohort was included at Wave 3 and
one study (Roestorf et al., 2019) they observed no age-related changes had the second measurement at Wave 4. Three measures were added at
on general intelligence, memory, and language in both younger (18–49 Wave 3; for these measures data are only available in Wave 3 and 4, see
yrs.) and older (50–79 yrs.) autistic (n = 33) and non-autistic (n = 18) Fig. 1.
adults over a two-year time period. Yet in another study (Pagni et al.,
2022) they observed more extensive cognitive decline in short-term 2.2. Participants
memory, but not long-term memory, in a sample of 23 autistic and 22
non-autistic middle-aged adults (40–64 yrs.) over a two-to-three year Participants (n = 464; nautism=207 and nno-autism=257) between 24
time period. However, both studies (Roestdorf et al., 2019; Pagni et al., and 85 years were eligible for the current study. Autistic individuals
2022) failed to detect general changes over time (i.e., in both groups). were included if 1) they had a registered diagnosis according to the DSM
Furthermore, modest sample sizes limited the generalizability of these (American Psychiatric Association, 2013) criteria, and 2) they scored
results. As such, more extensive longitudinal studies are needed to above the Autism Diagnostic Observation Schedule [− 2] cut-off (ADOS
obtain conclusive results on cognitive aging in autism. [− 2], Bastiaansen et al., 2011; Bildt et al., 2013; Lord et al., 2012), or the
Next to these longitudinal studies on autism, we could build on Autism-spectrum Quotient (AQ, Baron-Cohen et al., 2001).1 Exclusion
studies describing cognitive aging in other developmental conditions, criteria for both groups were 1) a history of neurological disorders (e.g.,
such as schizophrenia, and Attention Deficit/Hyperactivity Disorder epilepsy, stroke, multiple sclerosis), schizophrenia or having experi­
(ADHD). Considering that schizophrenia, and ADHD show large diag­ enced more than one psychotic episode, 2) Wechsler Adult Intelligence
nostic overlap with autism, and parallels in cognitive development to Scale-IV (WAIS-IV; Wechsler, 2003) IQ <70 or Mini Mental State Ex­
autism (Antshel et al., 2016; Jutla et al., 2022), one might argue that amination (MMSE; Folstein et al., 1975) < 18,2 3) current alcohol or
cognitive ageing might occur similarly across these developmental drugs dependency as indicated by the administration of the MINI In­
conditions. In a review by Rund (2018) it was concluded that schizo­ ternational Neuropsychiatric Interview (MINI; Sheehan et al., 1997;
phrenia is mostly neurodevelopmental in nature, not neurodegenerative. Van Vliet et al., 2000). For the no-autism group four additional exclusion
Longitudinal data indicated that in schizophrenia, cognitive functions criteria were: 1B) a history of autism or AD(H)D), 2B) first-degree rel­
are relatively stable throughout adulthood, yet more extensive brain atives (i.e., parents, children, siblings) with autism or AD(H)D, 3B) AQ >
changes seem present - hypothetically related to medication use. In 32, 4B) ADHD-SR symptoms in childhood ≥ 7 and/or adulthood ≥ 6.
ADHD, aging research is complicated by the interrelationships between Exclusion criteria were checked at each timepoint.
the core aspects of ADHD and the characteristics of cognitive aging.
Some ADHD symptoms might be expressed differently after childhood
2.3. Materials
(hyperactivity), whilst others might co-occur with old-age disease
(inattention/impulsivity) (Moffitt et al., 2015). To date, it is therefore
Eleven cognitive tests with 15 outcome variables were administered,
unclear whether ADHD is an actual risk factor for dementia, or merely a
see Table 1 for a brief description and references. This test battery in­
“phenotypic mimic” (Callahan et al., 2017). In sum, studying cognitive
cludes measures which are either particularly sensitive to cognitive
aging in developmental conditions is complicated, as brain and cogni­
decline, such as memory and processing speed (Salthouse, 2019) and/or
tive changes can be misaligned and, developmental changes in (late)
thought to be different in autistic adults, such as verbal fluency, and
adulthood complicate the study of developmental differences. However,
Theory of Mind (Torenvliet et al., 2021). Raw test scores were converted
in line with preliminary evidence on cognitive aging in autism, neither a
to z-scores, using baseline test scores (T1) of all participants in the
diagnosis of ADHD nor schizophrenia seems to be an obvious risk factor
no-autism group to compute means and standard deviations (n = 257).
for accelerated cognitive decline.
After recoding, higher z-scores indicated better performance.
The current study investigates longitudinal cognitive aging in a
Next to the cognitive variables, we administered the Cognitive
sample of autistic (n = 128) and non-autistic adults (n = 112) between
Failures Questionnaire (CFQ; Broadbent et al., 1982) measuring
24 and 85 years, extending our previous cross-sectional work (Lever and
self-reported cognitive functioning, the AQ measuring autism-related
Geurts, 2016; Torenvliet et al., 2021). A comprehensive cognitive test
traits (Baron-Cohen et al., 2001), WAIS III/IV matrix reasoning and
battery (k = 15) is administered in three waves in two, overlapping,
vocabulary subtests as a proxy for IQ (Wechsler, 1997a, 2003), and the
cohorts. Using reliable change indices (RCIs), frequentist multilevel
MMSE (Folstein et al., 1975) measuring global cognitive impairments.
regression, and Bayesian statistics cognitive changes are assessed. We
All these measures have sufficient (AQ; Baron-Cohen et al., 2001) to
expect that older participants perform worse compared to younger
good (CFQ; Broadbent et al., 1982, WAIS; Wechsler 1997a, 2003,
participants (cross-sectional age effect), and that performance declines
MMSE; Folstein et al., 1975) psychometric properties, and have been
over time (longitudinal interval effect) on nearly all cognitive tasks.
used widely in autism and/or aging research.
Also, the possibility that older individuals decline faster than younger
participants over time (age*interval interaction) is assessed. Most
importantly, we expect a parallel aging pattern between autistic and 1
In Cohort 1, 25% (N=13) of the followed-up autistic participants scored
non-autistic adults, hence, we hypothesize that reliable change rates are
below the ADOS cut-off (total < 7), in Cohort 2, 20.5% (N=15) scored below
similar across groups, and that cross-sectional age, and longitudinal
the ADOS-2 cut-off (total < 9). These participants all scored above the AQ cut-
interval effects are similar for autistic and non-autistic individuals. off. Rates are very similar to our results at T1, which were not changed by
including only ADOS+ participants (see Lever et al., 2016; Torenvliet et al.,
2021). Therefore, results are reported as pre-registered.
2
None of our participants scored below 25 on the MMSE.

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C. Torenvliet et al. Psychiatry Research 321 (2023) 115063

Fig. 1. Illustrative display of the study design.

Note. AUT, autism; avg., average; yrs., years; RAVLT, Rey Auditory Verbal Learning Test; WMS-III, Wechsler Memory Scale 3rd edition; CRT, choice response task;
ABT, Amsterdam Breakfast Task; TMT, trail making test; ToL, tower of London.

think tank, and approved by the ethical review board of the Department
Table 1
of Psychology of the University of Amsterdam (2011-PN-1952;
Overview of cognitive outcome variables.
2018-BC-9285).
Task Outcome Additional information Test-retest
(score range) reliability

RAVLTa Verbal Recall I Immediate recall trial 1–5 0.80 2.5. Analyses
(0–75)
Verbal Recall II Delayed recall (0–15) 0.83 Our pre-registered analyses plan (https://aspredicted.or
WMS-IIIb Visual Recall I Immediate recall (0–104) unavailable
g/VVZ_MHZ) consists of five parts. First, attrition analyses were per­
Visual Recall II Delayed recall (0–104) unavailable
ABTc Event Based PM Total correct (0–3) unavailable formed. We investigated differences between those who participated at
Time Based PM Total correct (0–3) unavailable follow-up and those who did not in group (autism/no-autism), cohort,
N-backd Working Accuracy difference score unavailable and sex-ratio across groups, and differences in baseline age, IQ, AQ
memory (− 1.0–1.0) score, CFQ score, and MMSE score for both groups (autism/no-autism)
Faux- Theory of Mind Total score (0–38) unavailable
separately.
Pase
DATf Letter Fluency Nr. of correct words 0.80 Second, reliable change indices (RCIs) were estimated to assess the
GITg Category Nr. of correct words 0.92 extent of change from T1 to T2 in two ways. In method 1, RCIs on all
Fluency outcomes were calculated based on average difference scores (Frerichs
Go- Inhibition (Accuracy NoGo/mean RT unavailable
and Tuokko, 2005)3:
NoGoh Go)*100
ToLi Planning Total Move Score (# excess unavailable x2 − x1 − (m2 − m1 ) 1 ∑
moves) RCISE = , sediff = (zi − zi )2
sediff n− 1 i
TMTj Set-shifting Total Time B/Total Time A unavailable
CRTk Response speed Mean reaction time unavailable
Response Standard deviation reaction unavailable
Chi-squared tests assessed group differences (autism vs. non autism,
variability time and improvement vs. stable vs. decline), using Holm-corrected p-values
(k = 15). In method 2, RCIs were calculated with previously observed
Note. RAVLT, Rey Auditory Verbal Learning Test; WMS-III, Wechsler Memory
test-retest reliabilities (i.e., independent of the current sample);
Scale; ABT, Amsterdam Breakfast Task; GIT, Groninger Intelligentie Test; ToL,
Tower of London; TMT, Trail Making Test; CRT, Choice Response Task; Nr.,
commonly used in clinical practice (Jacobson and Truax, 1991)4:
Number. x2 − x1 − (m2 − m1 ) √̅̅̅̅̅̅̅ √̅̅̅̅̅̅̅̅̅̅̅̅̅̅
a
Saan and Deelman (1986). RCIRxx = , sediff = 2s2e , Se = s1 1 − rxx
b sediff
Wechsler (1997b).
c
in house development (based on Altgassen et al., 2019). These were calculated for outcomes with the most comparable
d
in house development (see Lever et al., 2015). available samples, namely RAVLT recall I and II, and both fluency tasks
e
Baron-Cohen et al. (1999), Spek et al. (2010). (see Table 1). Holm corrected chi-squared tests assessed group differ­
f
Schmand et al. (2010). ences (k=4). Both methods were assessed separately in the two cohorts
g
Mulder et al. (2006). (Wave 1–3, and Wave 3–4), with a 1.645 cut-off for reliable change
h
in house development (see Torenvliet et al., 2023, preprint).
i (90% CI; Duff, 2012). Method 2 was expected to be more sensitive than
Shallice, 1982. ToL completion time was recorded, and limited to 120 s per
method 1, as test-retest reliabilities are based on shorter intervals, and
trial. After 120 s, the trial was ended and the maximum number of moves (20)
was administered for this trial. larger samples, resulting in smaller sediff.
j
in house development (based on Reitan and Wolfson, 1985). Third, multilevel regression analyses (R-package lme4; Bates et al.,
k
in house development (see Lever et al., 2015). 2015; R Version 3.6.1) were performed to identify the effects of age and
interval. Outcome variables were the z-scores on each cognitive mea­
2.4. Procedure sure. Interval effects were estimated in each individual (random in­
tercepts and slopes). In Model 1, effects of interval (between timepoints)
The screening procedure and corresponding materials are described were estimated to assess longitudinal changes across groups on each
in the study protocol paper, see Geurts et al. (2021). Cognitive tasks
were administered during 2–2.5 h testing sessions in counterbalanced
3
order. All participants received monetary compensation (€30,-) for their m2, m1, and sediff were estimated in the no-autism group from Cohort 2
(n=76).
participation, and (partial) reimbursement of their travelling costs. The 4
S1 were estimated in the no-autism group at T1, and rxx were the reported
set-up and results of this study were discussed with our older/autistic
test re-test reliabilities, see Table 1.

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C. Torenvliet et al. Psychiatry Research 321 (2023) 115063

outcome. In Model 2, age (centered) and the age*interval interaction Table 2

were added to assess cross-sectional age effects, and whether the effects Descriptive statistics of the autism and no-autism group.
of interval were different for individuals of younger/older baseline age. Descriptive Autism (n = 128) No-autism (n =
Model 2 describes the interval effect only for the sample mean age (e.g., 112)
50 yrs.). Therefore, longitudinal effects (interval) were obtained from Cohort (1/2, 54/74, 42% 36/76, 32% χ2=2.57
Model 1 (Goh et al., 2012). In Model 3, group was added Model 1 to 1%)
assess group differences in longitudinal change. In Model 4, group was Sex (M/F, M%) 84/44, 65% 72/40, 64% χ2=0.03
added to Model 2 to assess group differences in cross-sectional age ef­ Educationa 35/49/43 16/53/43 χ2=6.32*
Mean (SD), min- Mean (SD), min- t-value Cohen’s
fects and/or age*interval interactions. In addition (not pre-registered), max max d
we conducted Bayesian analyses to quantify the evidence for multi­ Age T1 (yrs.) 52.2 (14.2), 55.4 (14.1), − 1.73 -0.23
level models without an interval*group, and age*interval*group inter­ 24.3–79.3 30.4–85.3
action, i.e., testing the null hypothesis of no differential aging effect. Time T1-T2 3.5 (2.0), 1.6–7.0 3.0 (1.8), 1.4–7.6 2.44* .26
(yrs.)
Bayes factors (BF01) were computed based on BIC values (Wagen­
Time T1-T3 8.1 (0.7), 7.1–9.4 7.6 (0.7), 6.7–9.0 4.05** .71
makers, 2007). BF01 > 3 indicated substantial evidence in favor of the (yrs.)
null model (Jarosz and Wiley, 2014). IQb 114.7 (15.5), 115.4 (16.0), − 0.33 -0.04
Fourth, simple regression analyses were performed to predict which 84–153 73–155
c
factors could explain individual differences in changes over time. Indi­ MMSE 29.0 (1.1), 25–30 29.1 (1), 26–30 0.06 <0.01
AQd 34.9 (7.3), 8–48 13.0 (5.8), 2–28 25.88** 3.32
vidual beta coefficients extracted from Model 1 (interval only) were CFQe 47.0 (14.6), 30.1 (10.0), 8–53 10.54** 1.35
used as outcome variables, with sex, baseline CFQ and baseline IQ as 15–80
predictors in each group. All regression analyses were Holm corrected
Note. M, male; F, female; **=p<.01; *=p<.05.
(k = 15). a
Level of education was determined by the Verhage Coding System, between
Fifth, sensitivity analyses for parts three and four were performed, slashes: junior secondary or practical education / senior secondary education or
only including participants of Cohort 2, because intervals, and sample vocational college / university degree.
sizes were expected to be more similar between the two groups (autism b
IQ was estimated at baseline by using two subtests (matrix reasoning and
vs. no-autism) within this cohort. vocabulary) of the Wechsler Intelligence Scale-III or IV (WAIS-III, WAIS-IV;
Wechsler, 1997, 2003).
c
3. Results Mini Mental State Examination (MMSE; Folstein et al., 1975) measured
global cognitive impairments at baseline. Individuals scoring below 25 were
At the first follow up (T2), the total sample consisted of 240 partic­ excluded (n = 0).
d
ipants (nautism=128, nno-autism=112), and at the second follow up (T3) 73 Autism Quotient (AQ) measured self-reported autism characteristics. In the
autism group, 9% (N = 12) scored below the AQ cut-off. These participants all
participants (nautism=46, nno-autism=27) were included. Cohort 1 con­
scored above the ADOS or ADOS-2 cut-off.
sisted of 90 participants; Cohort 2 consisted of 150 participants (see e
Cognitive failures questionnaire (CFQ) measured self-reported cognitive
Fig. 1). Autistic and non-autistic participants were equally divided be­ functioning.
tween the cohorts. Characteristics of the total sample are described in
Table 2. Education differed significantly between groups, with more
− 4.48, p <0.01), and those with lower estimated IQ participated less in
people with practical education in the autism group than in the no-
the follow-up study (IQ: µdropout=110.9, µfollow-up=115.4, t[463] =
autism group. MMSE score (global cognitive functioning) and esti­
− 2.17, p=.03). Other differences were not significant (p’s>0.25).
mated IQ did not differ significantly, yet AQ score (autism characteris­
tics), and CFQ score (self-reported cognitive difficulties) were
significantly higher in the autism group, and the average time interval 3.2. Reliable change indices
(T1-T2, and T1-T3) was significantly longer in the autism group.
Assessing the two cohorts seperately reduced the variance in intervals, RCIs based on method 1 (average difference scores) showed no sig­
yet they were still significantly longer in the autism group (see nificant differences in reliable changes between the autism, and no-
Tables S1A, and B). autism group, in neither cohort (all uncor. p’s>0.15, see Fig. 2a,
Table S2A). Across groups, percentages of individuals who reliably
3.1. Attrition analyses declined ranged from 0–22% in Cohort 1, and 0–7% in Cohort 2, per­
centages of individuals who improved ranged from 0–18% in Cohort 1,
Reasons for drop-out were mostly that no consent was given to be and from 0–10% in Cohort 2. Rates of decline were highest on visual/
contacted for future research5 (only in Cohort 1; n = 121, nautism=31) or verbal memory I and II, and both fluency tasks. Rates of improvement
that participants were not willing to participate when contacted (n = 64, were highest on theory of mind, and inhibition. RCIs based on method 2
nautism=35). Sixteen (nautism =12) participants could not be contacted, (test-retest reliabilities from previous studies) led to higher change rates
three passed away (nautism =2), 20 (nautism =9) were excluded at T2 for than using average difference scores. Across groups, percentages of in­
various reasons. dividuals who declined ranged from 15–34% in Cohort 1, and 1–13% in
Drop-out rates were significantly higher in the no-autism group Cohort 2, percentages of individuals who improved ranged from 0–9%
compared to the autism group (ndropout autism=80 [38%], ndropout no- in Cohort 1, and 1–22% in Cohort 2. No significant differences in reliable
2 changes were observed between the autism, and no-autism group, in
autism=144 [56%], χ [464] = 14.28, p<.01) and higher in Cohort 1 than
in Cohort 2 (ndropout C1=180 [67%], ndropout C2=44 [23%], χ 2[464] = neither cohort (see Fig. 2b, Table S2B).
87.05, p<.01). No significant difference in sex ratio was observed. In the In sum, most of the expected decline over time was observed in
autism group, no significant differences between the drop-out and Cohort 1 and based on test-retest reliabilities. The majority of in­
followed-up group were observed on baseline age, IQ, AQ score, CFQ dividuals performed consistently over time. Changes over time did not
score, or MMSE score (all p’s>0.10). In the no-autism group, those who significantly differ between autistic and non-autistic individuals.
were younger at baseline (age: µdropout=46.6, µfollow-up=55.3, t[463] =
3.3. Multilevel modeling

5
At the first stage of cohort 1, the study was not yet conceptualized as lon­ To analyze the effects of cross-sectional age, and changes over time
gitudinal, thus, some participants were not informed about future research. in a continuous manner, we performed multilevel regression analyses on

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C. Torenvliet et al. Psychiatry Research 321 (2023) 115063

Fig. 2a. Percentage of cognitive increases and decreases per cognitive outcome, group, and cohort reflected by Reliable Change Indices (RCI’s) based on average
difference scores.

Model 3 (interval, group, and their interaction) showed no signifi­

cant interval*group interactions. Hence, no significant group differences
in longitudinal change were observed. Model 46 (interval, age, group,
and their interactions) showed no significant age*group interactions,
and no significant age*interval*group interactions meaning that in­
dividuals with and without autism showed no significant difference in
age-related effects (cross-sectional) or age-related changes over time
(longitudinal). Models 3 and 4 are summarized in Fig. 3b; statistical
details are provided in Table S3B. A graphical display of the group, age,
and interval effects is provided in Fig. 4.
In sum, multilevel models showed clear age-related effects, and
modest effects of interval. None of the cross-sectional age effects or
longitudinal changes over time were significantly different between
autistic, and non-autistic individuals.
Fig. 2b. Percentage of cognitive increases and decreases per cognitive
outcome, group, and cohort reflected by Reliable Change Indices (RCI’s) based 3.4. Bayesian analyses
on Test-Retest Reliabilities.
Note. Error bars reflect 95% confidence intervals. Group differences were all BIC Bayes Factors indicated substantial to very strong evidence in
non-significant. For figural clarity, those who remained stable are omitted. VisI, favor of the models without group interactions (all BF01 > 28, see
visual recall I; VisII, visual recall II; VerbI, verbal recall I; VerbII, verbal recall II; Table S3c, and Fig. S1), substantiating the absence of significant group
ToM, theory of mind; LeFl, letter fluency; CaFl, category fluency; VWM, visual differences in the effect of interval, and age*interval.
working memory; MRT, mean reaction time; SDRT, reaction time variability;
Inhb, inhibition; Shft, set shifting; Plan, planning; EBPM, event-based pro­
3.5. Sensitivity analyses
spective memory; TBPM, time-based prospective memory.

Learning effects (i.e., improvement in performance over time) might

all 15 outcomes. As the models allowed intercepts and slopes to vary
have obscured previous interval effects, and possibly also interval*group
between participants, we first assessed the added value of these pa­
interactions, because (1) we did not observe interval effects for some
rameters. Random intercepts significantly improved all models, yet
age-sensitive measures (e.g., visual/verbal recall), and (2) intervals for
random slopes did not, except for response speed, and visual recall I, and
cohort 2 were shorter than intended due to COVID restrictions. There­
II. As random slopes could not be reliably estimated for some models and
fore, we extended the pre-registered sensitivity analyses to analyze the
the models hardly improved when adding random slopes, subsequent
data from both cohorts separately, instead of only for cohort 2.
planned analyses on these slopes were omitted, including analyses on
Multilevel results of the separate cohorts showed better fit of the
the predictive value of sex, baseline IQ, and baseline CFQ. Removing
interval-only models (higher marginal R2) as compared to the combined
random slopes did not change the parameters of the fixed factors.
cohort models. With time, individuals from cohort 1 significantly
Model 1 (interval only) showed a significant effect of interval for
declined in performance on verbal recall I and II, category fluency, and
category fluency, response speed, inhibition, and event-based prospec­
response speed, whereas individuals from cohort 2 significantly
tive memory. Participants generally declined in performance over time,
improved on verbal recall I and II, visual working memory, and event-
but improved in performance on event-based prospective memory.
based prospective memory. In cohort 2, significant declines were still
Model 2 (interval, age, and their interaction) showed that, baseline age
observed on inhibition and processing speed. Both cohorts showed no
effects (cross-sectional) were present in visual/verbal memory, category
significant interval*group interactions. The significant interval*age
fluency, response speed, response variability, and both event-/time-
interaction on letter fluency and set shifting remained significant in
based prospective memory. Older individuals generally scored worse
cohort 1 and 2, respectively, and showed the same pattern as in the
than younger individuals at baseline. A significant age*interval inter­
combined cohort. Age*group interactions, and age*interval*group in­
action was observed on letter fluency, and set shifting. Those older at
teractions were all not significant. Statistical details can be found in
baseline declined significantly more over time compared to those
Table S4A and S4B, and Fig. S2, B and C (cohort 1), and Table S5A and
younger at baseline. Models 1 and 2 are summarized in Fig. 3a; statis­
S5B and Fig. S3A, B and C (cohort 2). Of note, BIC bayes factors in the
tical details can be found in Table S3A.
separate cohorts yielded similar results as compared to the combined

6
As the data were previously analysed in a cross-sectional manner (Lever and
Geurts, 2016; Torenvliet et al., 2021), cross-sectional effects are only briefly
noted.

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Fig. 3a. Effects of age, interval, and their interactions on each cognitive outcome measure obtained from the multilevel models independent of group.

Fig. 3b. Effects of interval, and age and interval interactions per group.
Note. Left-sided bars indicate a decline with age, or interval (negative betas), whereas right-sided bars indicate an improvement with age, or interval (positive betas).
*=Holm corrected p-value 〈.05. In 3b all Holm corrected p-values were 〉.05. B, standardized beta; VisI, visual recall I; VisII, visual recall II; VerbI, verbal recall I;
VerbII, verbal recall II; ToM, theory of mind; LeFl, letter fluency; CaFl, category fluency; VWM, visual working memory; MRT, mean reaction time; SDRT, reaction
time variability; Inhb, inhibition; Shft, set shifting; Plan, planning; EBPM, event-based prospective memory; TBPM, time-based prospective memory.

cohorts. accelerated or protective aging in autistic adults. Bayesian analyses

In sum, sensitivity analyses showed that splitting the cohorts was confirmed that evidence was robustly in favor of the null hypotheses
useful for inspecting some contrasting patterns between our two cohorts that specified no differences in age-related decline between those with-
(improvement vs. decline), especially for verbal recall. Both in and without autism. When comparing clinically relevant changes over
improvement and decline over time, autistic individuals seemed to time, group differences were minimal, and if anything, autistic in­
change similarly to non-autistic individuals. dividuals seemed to decline less over time. Given that this is the first
larger-scale cognitive study that assesses cognitive aging in autism
4. Discussion longitudinally, and aging effects were generally modest, these conclu­
sions have to be interpreted with care. However, it seems that in autism,
The current study provides evidence against accelerated cognitive age-related longitudinal changes are similar to previously observed par­
decline in autistic adults. Although nearly all cognitive measures seemed allel age-related cross-sectional effects.
sensitive to either cross-sectional age-related effects or longitudinal age- If replicated, these findings can have valuable contributions to the
related changes, none of the models indicated significant evidence for autism field. Even on cognitive domains where autistic adults generally

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Fig. 4. Graphical display of the effects of interval, age, group, and their interactions of the combined cohorts.
Note. Age was categorized only for visual purposes, in all analyses age was added as a continuous predictor. Intervals were shorter (max. 2.5 years) for outcomes in
the bottom row (Shft, Plan, EBPM, TPBM) as these tasks were not administered at Wave 1. VisI, visual recall I; VisII, visual recall II; VerbI, verbal recall I; VerbII,
verbal recall II; ToM, theory of mind; LeFl, letter fluency; CaFl, category fluency; VWM, visual working memory; MRT, mean reaction time; SDRT, reaction time
variability; Inhb, inhibition; Shft, set shifting; Plan, planning; EBPM, event-based prospective memory; TBPM, time-based prospective memory.

seem to experience more difficulties compared to non-autistic adults mimic. Thus, it could be that autistic people resemble or report char­
(fluency, theory of mind), and on tasks where longitudinal changes were acteristics that are typical in old-age disease without the same biological
most prominent across groups (response speed, fluency, inhibition, mechanisms underlying these characteristics. Moreover, based on the
verbal memory) no significant differences in cognitive change between aforementioned epidemiological studies it is unclear whether most
those with, and without an autism diagnosis were observed. Thus, dif­ autistic individuals might show altered cognitive aging, or if only a
ferences in development in various cognitive domains observed in the subgroup of autistic individuals is particularly vulnerable for cognitive
first stages of life of autistic individuals do not seem to persist or retrace decline. Consistent with the very first longitudinal study of cognitive
in later stages of life. Therefore, autism seems to show parallels to aging in autism, in which they observed cognitive decline only for 23%
schizophrenia, being best described by differences in neurodevelopment, of autistic individuals (Howlin et al., 2014), the current study seems to
not neurodegeneration (Rund, 2018). indicate that an increased risk of late life (cognitive) disease might be
However, disregarding accelerated cognitive decline in autism might true for a subgroup of autistic individuals, whereas generally accelerated
contrast with the reported increased risk of old-age disease. It remains aging in autism may be less likely.
puzzling why in autism increased rates of, for instance, dementia, and As rates of age-related disease are known to show steep increases at
Parkinson’s disease are reported in epidemiological studies (Bishop-­ the final stages of life (70+), patterns of cognitive decline might be
Fitzpatrick and Kind, 2017; Croen et al., 2015; Geurts, McQuaid, et al., different in an older autism cohort. While the current cohort is one of the
2020; Hand et al., 2019; Rydzewska et al., 2018; Vivanti et al., 2021), oldest cohorts described in the autism literature, compared to other
without observing differences in cognitive decline. However, neurode­ aging cohorts, the current cohort is still relatively young. Therefore,
generative disorders are, like developmental conditions, hard to classify more research on old-age trajectories is essential to capture all phases of
correctly and heterogeneous in nature, with misdiagnoses of Alz­ cognitive aging in autism. The feasibility of including older adults might
heimer’s Disease (AD) occurring up to 30% (Magnin, 2021). Like in increase naturally, given the increasing trends in (late) adult autism
ADHD (Callahan et al., 2017), it is therefore unclear whether autism is diagnoses (Russell et al., 2022), and the aging of autistic adults who are
indeed a risk factor for old-age disease, or more likely to be a phenotypic currently diagnosed. Of note, based on the current results, old age did

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not seem an additional predictor of cognitive decline in autism specif­ decease) also did not differ between the groups. Therefore, it seems
ically. Also, research including only older adults (Geurts, et al., 2020; unlikely that differences in attrition have biased our results. Fourth, RCI
Geurts and Vissers, 2012) does not hint at distinctive age-related dif­ analyses have to be interpreted with care, as the average interval be­
ferences for autistic people. Therefore, although additional research is tween timepoints differed significantly between the autistic and
needed, we expect similar outcomes for longitudinal autistic cohorts of non-autistic group. However, as the autistic group had longer average
older age. time intervals, one might expect exaggerated group differences in reli­
The current study is distinctive in covering a wide range of cognitive able changes (i.e., larger decline in the autism group). As no group
functions, which nearly all showed either sensitivity to cross-sectional differences in reliable changes were observed, the differences in average
age-related effects or longitudinal age-related changes. However, some time intervals do not seem to be of major impact.
measures were less sensitive to longitudinal changes than expected
based on cross-sectional findings– i.e., visual (working) memory, and 5. Conclusions
planning. This pattern is consistent with the general aging literature, in
which longitudinal age effects are often smaller than cross-sectional Based on the current findings, age-related changes in cognition seem
patterns (Salthouse, 2003, 2010, 2019). It also highlights the difficulty similar in autistic- and non-autistic individuals. As this is the first large-
of longitudinal research in which the repetitive nature of data collection scale longitudinal study on cognitive aging in autism, these findings
(i.e., learning effects) might cloud age-related decline (Salthouse, 2019). contribute unique knowledge to the autism literature. However, careful
The inclusion of parallel test forms, additional timepoints, and longer interpretation of the current conclusions is essential, and more longi­
intervals between timepoints are key to capture cognitive aging effects tudinal research is key to understand cognitive decline in older autistic
more precisely. Acquiring long-term funding seems essential to enable adults precisely, and more generally throughout the autistic population.
more, and longer time intervals, and reduce rates of attrition.
The partial absence of age-related changes posed a challenge, yet CRediT authorship contribution statement
also provided an unexpected advantage. By splitting the cohort by those
with generally long intervals (cohort 1, ~5.8 yrs.), and those with C. Torenvliet: Visualization, Formal analysis, Data curation,
shorter intervals (cohort 2, ~1.9 yrs.), we were not only able to detect Conceptualization, Writing – original draft, Writing – review & editing.
similar rates of decline between autistic- and non-autistic individuals A.P. Groenman: Conceptualization, Writing – original draft, Writing –
(cohort 1), but we also observed that learning seemed to develop at review & editing. T.A. Radhoe: Data curation, Writing – original draft,
similar pace (cohort 2). In cohort 1, rates of cognitive decline on verbal Writing – review & editing. J.A. Agelink van Rentergem: Writing –
memory were significant, yet similar across the groups. Oppositely, in original draft, Writing – review & editing. W.J. Van der Putten: Data
cohort 2, we observed significant improvements in verbal memory curation, Writing – original draft, Writing – review & editing. H.M.
performance, indicating learning effects, which were also not signifi­ Geurts: Conceptualization, Funding acquisition, Writing – original
cantly different between autistic and non-autistic adults. These findings draft, Writing – review & editing.
further confirm the hypothesis that individuals with autism are not
particularly (in)sensitive to the effects of cognitive aging. Declaration of Competing Interest

4.1. Strengths & limitations None.

The study provides a unique insight into cognitive aging in autism in

Acknowledgements
various ways. First, the current study is the first to capture cognitive
decline in autism longitudinally in a relatively large sample on a wide
We would like to thank all our participants for the effort and time
range of cognitive abilities. Second, advanced statistical analyses were
they have put into this study, and the clinical institutions and organi­
used to account for heterogeneity within the sample, such as allowing
zations who actively helped recruiting our participants. Furthermore,
random parameters in the regression models, and investigating the
we would like to thank the students and research assistants involved in
extent of reliable change. Also, additional Bayesian analyses allowed
the project for their help with the recruitment of participants and data
quantifying evidence for the null hypotheses. We also provided scientific
collection. Lastly, we would like to thank our think tank of autistic/older
rigor by pre-registering our analyses, and adjusting for multiple
adults for their instrumental contributions to this work.
comparisons.
Some aspects of the current study limit the aforementioned in­
terpretations. First, as the autism group was mainly recruited via clinical Funding statement
institutions, we might have missed individuals from underserved pop­
ulations. Representative samples remain a persistent issue in autism This study was funded by the VICI Grant (Grant Number:
research (Giwa Onaiwu, 2020; Maddox et al., 2021), and the current 453–16–006) awarded to HMG by the Netherlands Organization for
study is, unfortunately, no exception as diversity regarding ethnicity and Scientific Research (NWO).
gender identity was limited. Second, educational attainment was rela­
tively high, limiting interpretations to those with practical education. Supplementary materials
Also, the average IQ was about one standard deviation above the global
mean, and we excluded those with an intellectual disability. Given the Supplementary material associated with this article can be found, in
current knowledge on cognitive reserve (e.g., Cabeza et al., 2018), the the online version, at doi:10.1016/j.psychres.2023.115063.
current sample might disregard those most vulnerable to cognitive
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