Canine Cognitive Dysfunction: Clinical Notes for Veterinary Teams
These are the clinical notes for the 1-hour continuing education lecture “Canine Cognitive Dysfunction: Can We Improve the Lives of Affected Dogs?” presented by Dr. Curtis W. Dewey, with a closing conversation with Dr. Terry Fossum, for the Dr. Fossum’s Pet Care veterinary CE series.
The notes are written for veterinarians and veterinary technicians: they follow the lecture chapter by chapter, keep the numbers and cutoffs you would want at the treatment table, and add the primary references. The full lecture carries 1 hour of RACE-approved CE credit; the notes stand on their own if you just need the clinical content.
Clinical bottom line
CCD is common, underdiagnosed, and manageable: the 2019 review describes several therapeutic approaches with published support for cognitive ability and quality of life, and expects the largest effect when they are started early (Dewey 2019). There is no cure.
Published prevalence runs 14 to 35 percent of the aged pet dog population, rising steeply with age. Diagnosis is historical and clinical in most practices, with MRI as a supportive tool, and a way to rule out structural mimics, where owners elect it.
The lecture’s plan is stepwise and additive: dietary approaches first, then the nutraceuticals discussed in the literature, then enrichment and, in selected cases, device therapies, chosen so the plan stays simple enough for an owner to follow. These notes describe that framework; they do not prescribe a regimen.
About the lecturer
Curtis W. Dewey, DVM, MS, DACVIM (Neurology), DACVS is a board-certified veterinary neurologist and surgeon, certified in veterinary acupuncture and Chinese herbal medicine, and lead author of the 2019 review of canine cognitive dysfunction in Veterinary Clinics of North America: Small Animal Practice. He presents this lecture for the Dr. Fossum’s Pet Care CE series; the closing conversation is with Dr. Terry Fossum, DVM, MS, PhD, DACVS, the company’s founder.
Financial disclosure: Dr. Dewey formulated a combination cognitive-support supplement for senior dogs that Dr. Fossum’s Pet Care sells and receives a percentage of its sales, and Dr. Fossum’s Pet Care sponsors and provides this CE program. These notes are educational.
Three misconceptions the lecture opens with (1:47)
Dewey names three common beliefs that keep CCD undertreated.
- “It’s not common.” It is. The prevalence data below say 14 to 35 percent of aged pet dogs, and the true figure is probably higher because early signs get filed under normal aging.
- “Senility is just normal aging.” Owners often attribute the changes to normal aging. Getting lost in the house and house-soiling after years of reliability are disease signs, not normal aging.
- “There’s nothing you can do.” The bulk of the lecture is a direct answer to this one: several interventions have published support, and affected dogs whose disease is managed do not lose appreciable lifespan compared with unaffected agemates (Fast 2013; Schutt 2015).
How common it really is (5:30)
These are the studies behind the lecture’s figures.
| Finding | Number | Source |
|---|---|---|
| Prevalence, aged pet dog population (published range) | 14 to 35 percent | Dewey 2019 review (range); lower bound from Salvin 2010 (14.2 percent of 497 dogs aged 8 and older, owner survey, provisional classification; only 1.9 percent had a veterinary diagnosis) |
| Dogs 11 to 12 years with at least one impairment category | 28 percent | Neilson 2001 (n = 80 in that age band) |
| Dogs 15 to 16 years | 68 percent | Neilson 2001 (n = 34 in that age band) |
| Cognitively normal dogs over 8 progressing to mild cognitive impairment during a 24-month observation period | 33 percent | Schutt 2015 (longitudinal, 51 dogs over 8 years: 21 normal, 17 MCI, 13 CCD at baseline) |
| Mildly impaired dogs progressing to CCD over the same period | 22 percent | Schutt 2015 |
| Normal dogs moving to borderline scores; borderline dogs moving to CCD, over a roughly three-year follow-up | 11 dogs (58 percent); 3 dogs (14 percent); none went from normal straight to CCD | Fast 2013 (87 dogs over 8 years, followed 2008-09 to 2012) |
Two practice-level implications. First, your geriatric caseload is aging into this disease faster than owners report it, so the screening question has to come from your side of the table.
Second, the Copenhagen cohorts mean “cognitively normal today” is not a stable category in dogs over eight: in Schutt 2015 a third of the normal dogs moved to mild impairment within the 24-month observation period, and in Fast 2013 more than half of the normal group had moved to borderline scores by the roughly three-year follow-up. That is the argument for making cognition a standing item in senior wellness visits.
Pathophysiology: the Alzheimer’s parallel, and where it breaks (2:29, 7:05)
CCD tracks Alzheimer’s disease closely: it affects the elderly, progresses gradually, and shares much of the pathologic signature of beta-amyloid deposition, tau protein changes, hippocampal atrophy, and microvascular disease in brain parenchyma.
Tau behaves somewhat differently in dogs (tangle formation is less prominent than in people), and, in the lecturer’s experience, affected dogs generally do not reach the end-stage pharyngeal and laryngeal dysfunction that drives aspiration pneumonia in human patients. That last difference matters for prognosis conversations: managed CCD dogs typically die with the disease, not of it.
The mechanistic threads the lecture pulls together: cerebrovascular disease and amyloid deposition feed each other in a vicious circle (vascular damage promotes deposition; amyloid is itself vasculotoxic), oxidative damage and failing mitochondria degrade neuronal energetics, and neuronal glucose utilization declines. That last point is the hypothesis behind the medium-chain triglyceride diet studies: an aging brain that handles glucose poorly can still run on ketones. A mechanism is a rationale for a study, not evidence of benefit.
The gut-brain wrinkle (28:30)
The newer layer is upstream of the amyloid story, and the lecture presents it as a hypothesis: with age the intestinal barrier and then the blood-brain barrier become leaky, the gut microbiome shifts, and bacterial products (and sometimes bacteria) reach the brain. Its causal role in naturally occurring CCD is unresolved.
Beta-amyloid has antimicrobial activity, and the inflammatory (or antimicrobial-protection) theory of Alzheimer’s disease treats its deposition as a response to microbes or their products rather than a starting point; the lecture builds on that theory. In human work, Porphyromonas gingivalis, the periodontal pathogen, has been identified in autopsied Alzheimer’s brains (Dominy 2019).
Dewey’s group ran a preliminary version of the same question in dogs (Dewey and Rishniw 2021): in 21 aging dogs (11 with presumptive CCD, 10 without), blinded 0-to-4 scoring of dental photographs against a 0-to-54 cognitive questionnaire found a significant association (p < 0.05) between periodontal disease severity and cognitive score, with no association between age and either. Correlation, not proven causation, and the paper says so, but it makes dental disease in a senior dog harder to dismiss as cosmetic, and it puts diet and microbiome maintenance inside the CCD conversation.
Diagnosis: history first, imaging where elected (16:26)
In most practices CCD is a historical and clinical diagnosis plus rule-outs for other encephalopathies. MRI is supportive rather than confirmatory: it rules out structural mimics and shows the age-associated changes below, but cost and general anesthesia keep it from being routine.
The history-taking pearl is the most immediately usable thing in the lecture: owners pre-interpret. They answer “is he avoiding the stairs?” with “yes, but I think it’s his joints,” or explain circling and getting stuck in corners as failing eyesight, even though blind dogs in a familiar house usually navigate on their mental map. Record the observation separately from the owner’s explanation, then evaluate pain, sensory loss and neurologic causes yourself.
The four complaints that recur most, the lecture’s big four (19:26): anxiety that can tip into frantic; disrupted sleep-wake cycles with night pacing; reduced interaction with people and other pets; and confusion or apparent senility. A structured instrument helps make this repeatable: the DISHAA categories (disorientation, interactions, sleep-wake, house-soiling, activity, anxiety) give owners a scoring framework you can trend between visits, and it is the outcome measure Dewey uses in his own trial work. We host an owner-facing version: the dog dementia self-check.
MRI findings that discriminate CCD (17:19)
| Finding | Detail | Source |
|---|---|---|
| Generalized brain atrophy | Present, but also present in successfully aging dogs; not discriminating on its own | Lecture; Dewey 2019 review |
| Hippocampal atrophy | Total hippocampal volume, normalized to brain volume, significantly smaller in 16 CCD dogs than in 26 successfully aging controls, all 9 years or older (p = 0.04) | Dewey group, comparative MRI study (2020) |
| Interthalamic adhesion thinning | Mean thickness 6.79 mm (SD 0.70) in 66 normal dogs aged 0.6 to 15 years vs 3.82 mm (SD 0.79) in 12 demented dogs aged 12 to 18 years (Hasegawa 2005); thickness also falls weakly with age in normal dogs, so the lecture’s rule of thumb of 5 mm or less is a working cutoff, not a validated threshold; Noh 2017 (113 dogs) confirmed lower IA thickness and IA-to-brain-height ratios in dementia | Hasegawa 2005; Noh 2017 |
| Leukoaraiosis | Periventricular white-matter hyperintensities at the ependymal margin | Lecture; Dewey 2019 review |
| Cerebral microhemorrhages | 80 percent of CCD dogs (12 of 15) vs 12 percent of controls (3 of 25); the lecture attributes them to amyloid in vessel walls, the cerebral amyloid angiopathy pattern seen in people | Dewey group, PeerJ 2020 |
A microhemorrhage caveat from the same study: some aged dogs carry microbleeds without cognitive signs (presenting instead with vestibular signs or new-onset seizures), so microbleeds alone are not a CCD diagnosis; they may represent a related but distinct category.
Treatment: the stepwise framework (21:23)
The organizing problem in CCD therapy is not a shortage of options; it is that the options discussed number a dozen or more, and complex regimens reduce adherence. The lecture’s answer is a stepwise, additive plan: start with one or two interventions, reassess with a scored instrument, add the next layer based on response and owner bandwidth.
Step 1: diet, or MCT supplementation (26:56)
The lecture’s slide shows four commercial diets marketed for cognitive support (Purina Pro Plan Veterinary Diets NC NeuroCare, Hill’s Prescription Diet b/d, Purina Pro Plan Bright Mind, and Annamaet Re-juvenate); most carry medium-chain triglycerides at meaningful inclusion, and all carry an antioxidant package. Dewey’s read: all four are reasonable products, and two have published trials behind their formulations.
The NeuroCare approach (MCT plus a “brain protection blend” of antioxidants, B vitamins, arginine and fish oil) was tested in a 90-day double-blinded placebo-controlled study of 87 client-owned dogs with cognitive signs (Pan 2018), building on an 8-month MCT-supplementation study in aged laboratory beagles (Pan 2010). The antioxidant-fortified approach behind b/d comes from a two-year laboratory beagle study of dietary fortification with and without behavioral enrichment (Milgram 2005).
Availability moves: b/d shows as discontinued at US retailers and Hill’s now lists Prescription Diet Brain Care + j/d for cognitive dysfunction, so check what is actually orderable before it goes on a discharge sheet.
Where a diet change is off the table, MCTs can be added as a supplement. The mechanistic case is the glucose-to-ketone switch described above; the lecture also points to newer work suggesting direct effects of MCTs on brain function.
Step 2: nutraceuticals (32:57)
The lecture’s slide lists omega-3 fatty acids, MCTs, curcumin, resveratrol, green tea catechins and SAMe, and notes that the literature behind them is mixed in kind: some canine work, some rodent Alzheimer’s models, some human data. The lecture does not walk through those studies and neither do these notes.
The point it makes about the list is practical: it is long, complex regimens reduce adherence, and that is why combination products exist. (See the disclosure above; product specifics are deliberately out of scope for these notes.)
A drug note: levetiracetam, anecdotal (34:23)
Flagged exactly as the lecture flags it: nothing published in dogs for this indication. Dewey reports several years of anecdotal use with apparent cognitive improvement and good tolerability (occasional drowsiness). File it as experienced-clinician anecdote awaiting a study, not as an evidence-backed recommendation.
Human-style cholinergic drugs, by contrast, get a thumbs-down for gastrointestinal adverse effects and little uptake in dogs. Selegiline, the one FDA-approved drug for this indication in dogs, sits outside this lecture’s scope; our owner-facing medication guide covers it.
Step 3: enrichment and device adjuncts (22:49, 23:38)
Environmental enrichment (exercise, novelty, social interaction, new toys) has evidence of improving cognition in both impaired people and impaired dogs; the working theory is recruitment of quiescent brain regions to compensate for damaged ones. Tailor it to the patient’s mobility, senses and tolerance; it belongs in most plans.
The device tier is more preliminary and mostly extrapolated from rodent models and human work: acupuncture and electroacupuncture (mechanistic support includes improved neuronal glucose utilization, reduced amyloid accumulation, neurotrophic factor production); transcranial photobiomodulation (near-infrared wavelengths targeting cytochrome c oxidase in the mitochondrial respiratory chain, a rational fit for a disease with documented mitochondrial dysfunction); and targeted pulsed electromagnetic field therapy, which has a small evidence base for cognition. Honest framing for owners: adjuncts with a mechanistic rationale and thin dog-specific data.
The TCVM lens (8:40, 36:07)
Dewey is certified in Chinese herbal therapy and spends a chapter mapping TCVM pattern language onto conventional CCD pathophysiology: phlegm (abnormal accumulation) maps to amyloid, blood and qi stagnation to vascular pathology and failing mitochondrial energetics, shen disturbance to disordered mentation, and the recurring yin-deficiency theme to the restless, anxious, worse-at-night presentation every CCD clinician recognizes.
The herbs on the lecture’s slide, chosen because they have been studied in Alzheimer’s models or in people, translate to conventional mechanisms vets can evaluate: huperzine A (from Huperzia serrata) is procholinergic, and other commonly used botanicals show antioxidant, anti-glutamate, anti-apoptotic, and amyloid-inhibiting activity in model systems. The lecture proposes these interpretive mappings; the useful part is that they convert an unfamiliar vocabulary into checkable pharmacology.
What to watch, and when to rescore (from the closing conversation with Dr. Terry Fossum, 46:34)
The item to watch first is the sleep-wake cycle. In the closing conversation Dewey and Fossum single it out as the sign owners notice soonest when anything changes, in either direction, because it is the one that changes the owner’s own nights; it is also the most frequently reported sign in the Copenhagen CCD cohort (57 percent in Fast 2013).
Score it with the rest of DISHAA at baseline and again at one and two months, the rescoring interval Dewey uses in his own open-label work. Set expectations honestly: this is a progressive disease being managed, not cured, and the realistic goal is a measurable change on the score, not resolution.
On timing of intervention: the preventive question (can starting at middle age, around six or seven years, delay onset?) has no controlled answer yet. The reasoning offered for earlier starts is that the pathologic processes are time-based, laboratory dogs show measurable cognitive decline from about age six, and that he considers the interventions discussed low in risk. That is a rationale, not proof, and the lecture is explicit about the difference; these notes make no preventive recommendation.
Frequently asked questions
Can CCD be diagnosed without MRI?
Yes, and in most practices it is: characteristic history in an aged dog (the big four: anxiety, night waking, reduced interaction, confusion), a structured score such as DISHAA to quantify and trend it, and rule-outs for other encephalopathies and for the medical mimics owners misattribute (pain, sensory loss, endocrine disease; Fast 2013 excluded severe cardiac, liver and kidney disease and hypothyroidism before calling CCD, and the lecture flags brain tumor as the main structural mimic).
MRI adds supportive findings (hippocampal atrophy, interthalamic adhesion thinning, microhemorrhages) and excludes structural mimics where owners elect imaging; none of them is a validated confirmatory test in an individual dog.
Does a CCD diagnosis shorten a dog’s life?
Two observational cohorts did not detect a survival difference by cognitive category (Fast 2013: 87 dogs, 6 of 37 CCD dogs euthanized for CCD; Schutt 2015: 51 dogs); their size, selection, management and euthanasia patterns limit the inference. The lecture adds that dogs rarely progress to the pharyngeal and laryngeal dysfunction and aspiration pneumonia that drive end-stage mortality in people. Quality of life, the owner’s and the dog’s, is what the plan is for.
How should a first plan and its follow-up be organized?
Simple enough for the household to keep up: a dietary approach (a cognitive diet or MCT supplementation), one or two nutraceuticals from the lecture’s list, and enrichment; the lecture’s point about combination products is adherence, not a product recommendation. Score with DISHAA at baseline, recheck at one to two months, and add the next layer based on response.
Earn the CE credit
This page summarizes the lecture; the full hour goes deeper on every chapter, with the imaging examples and the complete herb-mechanism tables. Watch it free and earn 1 hour of RACE-approved CE: Canine Cognitive Dysfunction: Can We Improve the Lives of Affected Dogs? (1 CE hour). Registration takes a minute; pass the short quiz afterward and your certificate is emailed to you.
RACE program 20-1192320 (provider 50-29133), Medical category, non-interactive distance, approved through 2028-04-23. This program has been RACE approved for 1 hour of continuing education credit in jurisdictions that recognize RACE approval. RACE does not accredit, endorse, or certify any program or person, nor does RACE approval validate the content of the program.
References
- Dewey CW, Davies ES, Xie H, Wakshlag JJ. Canine cognitive dysfunction: pathophysiology, diagnosis, and treatment. Vet Clin North Am Small Anim Pract. 2019;49(3):477-499. PMID 30846383.
- Salvin HE, McGreevy PD, Sachdev PS, Valenzuela MJ. Under diagnosis of canine cognitive dysfunction: a cross-sectional survey of older companion dogs. Vet J. 2010;184(3):277-281. PMID 20005753.
- Neilson JC, Hart BL, Cliff KD, Ruehl WW. Prevalence of behavioral changes associated with age-related cognitive impairment in dogs. J Am Vet Med Assoc. 2001;218(11):1787-1791. PMID 11394831.
- Fast R, Schutt T, Toft N, Moller A, Berendt M. An observational study with long-term follow-up of canine cognitive dysfunction: clinical characteristics, survival, and risk factors. J Vet Intern Med. 2013;27(4):822-829. PMID 23701137.
- Schutt T, Toft N, Berendt M. Cognitive function, progression of age-related behavioral changes, biomarkers, and survival in dogs more than 8 years old. J Vet Intern Med. 2015;29(6):1569-1577. PMID 26463980.
- Dewey CW, Rishniw M, Johnson PJ, et al. Interthalamic adhesion size in aging dogs with presumptive spontaneous brain microhemorrhages: a comparative retrospective MRI study of dogs with and without evidence of canine cognitive dysfunction. PeerJ. 2020;8:e9012. PMID 32322448.
- Dewey CW, Rishniw M, Johnson PJ, et al. Canine cognitive dysfunction patients have reduced total hippocampal volume compared with aging control dogs: a comparative magnetic resonance imaging study. Open Vet J. 2020;10(4):438-442. PMID 33614439.
- Dewey CW, Rishniw M. Periodontal disease is associated with cognitive dysfunction in aging dogs: a blinded prospective comparison of visual periodontal and cognitive questionnaire scores. Open Vet J. 2021;11(2):210-216. PMID 34307077.
- Hasegawa D, Yayoshi N, Fujita Y, Fujita M, Orima H. Measurement of interthalamic adhesion thickness as a criteria for brain atrophy in dogs with and without cognitive dysfunction (dementia). Vet Radiol Ultrasound. 2005;46(6):452-457. PMID 16396259.
- Noh D, Choi S, Choi H, Lee Y, Lee K. Evaluation of interthalamic adhesion size as an indicator of brain atrophy in dogs with and without cognitive dysfunction. Vet Radiol Ultrasound. 2017;58(5):581-587. PMID 28707338.
- Dominy SS, Lynch C, Ermini F, et al. Porphyromonas gingivalis in Alzheimer’s disease brains: evidence for disease causation and treatment with small-molecule inhibitors. Sci Adv. 2019;5(1):eaau3333. PMID 30746447.
- Pan Y, Larson B, Araujo JA, et al. Dietary supplementation with medium-chain TAG has long-lasting cognition-enhancing effects in aged dogs. Br J Nutr. 2010;103(12):1746-1754. PMID 20141643.
- Pan Y, Landsberg G, Mougeot I, et al. Efficacy of a therapeutic diet on dogs with signs of cognitive dysfunction syndrome (CDS): a prospective double blinded placebo controlled clinical study. Front Nutr. 2018;5:127. PMID 30619873.
- Milgram NW, Head E, Zicker SC, et al. Learning ability in aged beagle dogs is preserved by behavioral enrichment and dietary fortification: a two-year longitudinal study. Neurobiol Aging. 2005;26(1):77-90. PMID 15585348.
Related owner-facing resources on this site: the dog dementia hub, stages guide, and owner self-check. Educational content provided by Dr. Fossum’s Pet Care.
These notes summarize a recorded continuing-education lecture for veterinary professionals. They are educational, not clinical guidelines; decisions about an individual patient belong to the attending veterinarian.