Cambridge Adult ADHD & ASD Clinic

24/12/2025

03/10/2025

This post is meant to be thought provoking, a 'what if'' perspective.
Autism has too often been described as a disorder. But what if it is something else entirely, not a deficit, but an evolutionary pathway shaping the future of human cognition?

Enjoy the reading...

https://cambridgeadhdclinic.com/autism-disorder-difference-evolution/

16/09/2025

In this post, I address the issue of misdiagnosis and delayed diagnosis in autistic adults, and why so many still wait years before receiving clarity. Despite broader criteria and greater awareness, autism in adulthood continues to be overlooked, mislabelled, or recognised only late in life.

Why does this happen?
Several barriers stand out. Childhood history may be unavailable, diagnostic tools are not always sensitive to adult presentations, and coping strategies such as masking can hide traits for years. Overlap with other conditions makes matters harder still: anxiety, depression, ADHD, OCD, bipolar disorder, psychosis, and personality disorders can all resemble autistic traits, leading to partial or mistaken diagnoses.

The personal cost is high. Many adults spend decades navigating services under the wrong label, receiving treatments that ease some symptoms but never address the whole picture. Women in particular are at greater risk, with some studies suggesting that nearly half were given a different psychiatric diagnosis before autism was recognised, compared with fewer men. Other research indicates that around one in four autistic adults report at least one prior misdiagnosis, especially where autistic traits overlap with anxiety, depression, ADHD, or personality disorders.

Improving recognition requires more than structured tools alone. A reliable assessment must explore a detailed neurodevelopmental history, trace lifelong patterns of traits and adaptations, and carefully separate autism from other conditions with overlapping features. Only this breadth of evaluation can reduce the risk of autism being missed, overlooked, or misdiagnosed.

Read the full article:
👉 https://cambridgeadhdclinic.com/adult-autism-delayed-missed-diagnosis/

Kentrou V et al. (2024) EClinicalMedicine • Dufour I et al. (2025) J Neurodev Disord • Gesi C et al. (2021) Brain Sci

Author:
Dr Valentino A. Pironti
Senior Clinical Psychologist | Cognitive Neuroscientist
Specialist in Adult ADHD & Autism
Clinical Director, Cambridge Adult ADHD & ASD Clinic

30/08/2025

Another 5 star review from one of our clients!

https://share.google/nkEBpIXWXWjc1BGKW

25/08/2025

Brain filter's dysregulation and inattention across ADHD and autism.

Enjoy the reading, Dr Valentino

https://cambridgeadhdclinic.com/sensory-gating-and-inattention-across-adhd-and-autism-clinical-insights/

05/08/2025

📘 Still relevant today:
The Updated European Consensus Statement on diagnosis and treatment of adult ADHD — senior-authored by Dr Valentino Pironti, our founder and director, together with sixty-two other leading ADHD experts from the UK and across Europe — continues to provide clinicians with a unified, gold-standard framework.

First published in 2019, the statement remains highly relevant in today’s fragmented and fast-changing diagnostic landscape, where reliable, evidence-based guidance is more important than ever.

If you're seeking clarity around adult ADHD diagnosis, our team is here to help.

https://cambridgeadhdclinic.com/

26/07/2025

Can autism present in biologically distinct subtypes?

A new study in Nature Genetics suggests it can — identifying four robust phenotypic clusters, each with its own genetic fingerprint.

Using item-level data from over 5,000 autistic children in the SPARK cohort, researchers applied unsupervised clustering to 239 behavioural and developmental items from parent-report questionnaires, without relying on diagnostic scores or subscale totals.

🧩 They found four subtypes:

Social/Behavioural (37%) – High core autism traits (social communication and restricted behaviours), plus elevated ADHD, mood, and disruptive symptoms, but no developmental delay.
🔹 Genetically enriched for ADHD polygenic scores; rare mutations in genes linked to chromatin structure, DNA repair, and microtubule activity.

Moderate Challenges (34%) – Milder, balanced profile with low severity across domains.
🔹 Served as the reference group; no specific polygenic or rare variant enrichments.

Mixed ASD with Developmental Delay (19%) – Core symptoms plus language and cognitive delays, and elevated self-injury.
🔹 Higher burden of rare mutations in genes affecting neuronal firing and sodium channel activity; lower polygenic scores for cognition and educational attainment.

Broadly Affected (10%) – Severe difficulties across all domains: social, cognitive, behavioural, and emotional.
🔹 Genetically enriched for major depressive disorder; widespread rare variant impact with no dominant pathway, consistent with broad impairment.

🧬 Each subtype also showed distinct gene expression patterns across developmental stages and brain cell types, some prenatal, others postnatal, further supporting divergent biological underpinnings.

This is one of the clearest demonstrations to date that autism is not biologically monolithic, but rather, a construct encompassing multiple genetically and developmentally distinct profiles.

👉 Notably, the largest group showed clear overlap with ADHD traits and polygenic architecture, raising the possibility that ADHD research may also benefit from similar subtype-focused methodologies, helping move beyond broad diagnostic labels toward more precise, biologically grounded frameworks.

🔬 These findings offer robust support for the existence of distinct autism subtypes, each underpinned by specific genetic and developmental mechanisms, challenging the notion of autism as a single, uniform condition and opening the door to more biologically grounded classifications and targeted interventions.

📖 Litman et al. Nature Genetics (2025)
PMID: 40634707

If you are seeking clarity about Autism, we are here to support you
https://cambridgeadhdclinic.com/

14/07/2025

🧠 Too Late for ADHD? Or Just Late to Be Seen?
Recent research is examining cases where ADHD-like symptoms appear to emerge in adulthood — raising important questions about so-called late-onset ADHD.

This short article reviews the evidence and considers whether early traits may have been masked, misattributed, or buffered by supportive environments.

🔗 https://cambridgeadhdclinic.com/late-onset-adhd-in-adults-what-is-the-evidence/

28/06/2025

🌌 Clues from the Edge of Science
Exploring early hypotheses and emerging evidence in ADHD and autism — not established facts, but possible new directions in science.
Each post in this series takes a closer look at ideas still under investigation — intriguing, thought-provoking, and worth watching.

🧠 Neuroinflammation and ADHD: A Possible Link?
When we think of ADHD, we often think of attention, impulsivity, or dopamine — not the immune system. But a growing body of early research is exploring something less obvious: neuroinflammation.

Neuroinflammation isn’t always harmful — in fact, it plays a critical role in brain health. Immune cells like microglia and astrocytes help maintain and repair the brain, support neuroplasticity, and guide synaptic pruning. This physiological neuroinflammation is part of normal brain function, especially during development.

But when this system becomes dysregulated, it may turn maladaptive. In this altered state, neuroinflammation can affect brain function in subtle but potentially important ways.

🔬 What do we know so far?

Emerging research has reported elevated levels of inflammatory molecules — such as IL-6, TNF-α, and CRP — in children and adults with ADHD. These cytokines can interact with neurons and glial cells, potentially influencing how neural networks and brain chemistry function.

In animal models, maternal immune activation (i.e., immune system stimulation during pregnancy) has been shown to affect offspring brain development and behaviour in ways that resemble ADHD phenotypes — including changes in activity, attention, and impulsivity.

🧪 One of the Possible Mechanisms

Several mechanisms have been proposed to explain how neuroinflammation might interact with ADHD. One of these hypotheses is that neuroinflammation alters neurotransmitter systems already implicated in ADHD — particularly dopamine, glutamate, and noradrenaline. For instance:

IL-6 can reduce dopamine synthesis and availability by lowering the availability of tyrosine hydroxylase, the key enzyme involved in dopamine production.

Chronic inflammation may disrupt the glutamate–GABA balance, which is critical for cognitive stability and attention.

Pro-inflammatory cytokines like TNF-α may interfere with dopamine transporter (DAT) and vesicular storage, altering dopamine signalling efficiency.

Microglial activation can increase extracellular glutamate and impair its uptake, contributing to excitotoxicity and further neurotransmitter imbalance.

So while inflammation may not cause ADHD, in some individuals it may modulate systems already involved in attention and self-regulation, adding a new layer to our understanding of how ADHD might work — at least in some cases.

This line of research is still young, and findings remain preliminary. But it opens an exciting new frontier in the biology of neurodevelopment.

https://cambridgeadhdclinic.com/adhd-neuroinflammation-link/

📚 For those of you who want to go further, see:

Oades, R. D., Dauvermann, M. R., Schimmelmann, B. G., Schwarz, M. J., & Myint, A. M. (2010). Attention-deficit hyperactivity disorder (ADHD) and glial integrity: An exploration of associations of cytokines and kynurenine metabolites with symptoms and attention. Behavioral and Brain Functions, 6(1), 32.

Corominas-Roso, M., Ramos-Quiroga, J. A., Palomar, G., Catalán, R., Rigau-Ratera, E., & Casas, M. (2017). Cortisol and inflammatory biomarkers in adults with attention-deficit hyperactivity disorder. Neuropsychobiology, 75(3), 159–168.

Donfrancesco, R., Nativio, P., Balia, C., Villa, M. P., & Andriola, E. (2023). Alterations in striatal architecture and biochemical marker levels in an animal model of ADHD: Focus on proinflammatory cytokines. Biomedicines, 11(6), 1556.

Reed, M. D., Yim, Y. S., Wimmer, R. D., Kim, T. K., Tooke, K. I., Pace, B. T., ... & Huh, J. R. (2020). IL-17a promotes sociability in mouse models of neurodevelopmental disorders. Nature, 577(7789), 249–253.

22/12/2024

🎄✨ Wishing You Serene Festivities ✨🎄

As the year draws to a close, we wish you peace, joy, and moments of serenity this festive season—and a stellar 2025 ahead.

Stay tuned for updates in March.

Warm regards,
Dr. Valentino Pironti and the Team.
Cambridge Adult ADHD & ASD Clinic

12/01/2024

Dear All,
colleagues at the University of Cambridge are conducting a research project. See the poster attached. If you can help, please do.

09/07/2023

Dear All,
Collegues at University Of Edinburgh, School of Health in Social Science are recruiting participants for an MSc project on self-harm and autistic women. The reseacrh is conducted by Samuel Thomas Whatnall, supervised by Dr Ewelina Rydzewska.

The project has received ethical approval and specific measures have been put in place to minimise risk to participants given the sensitivity of the topic in question. Evidence of this can be provided by the study team on request.

Please see further details below. If you are interested, please email
Samuel for more details.

er3research@gmail.com

Thank you, Cambridge Adult ADHD & ASD Team