GC241 Reference (2) - New Vascular Neurocognitive Disorder Criteria JAMA
The 2023 JAMA consensus criteria provide an updated diagnostic framework for vascular cognitive impairment, integrating neuroimaging biomarkers of cerebrovascular disease with cognitive assessment to classify vascular contributions to cognitive impairment and dementia.
VasCog-2-WSO Criteria: Revised Diagnostic Criteria for Vascular Cognitive Impairment and Dementia (VCID)
This JAMA Neurology 2025 reference paper is paired with the GC 241 dementia lecture series. It presents the VasCog-2-WSO criteria — the most current international consensus diagnostic framework for vascular cognitive impairment and dementia (VCID). For exams, you need to understand:
- Why new criteria were needed — historical inconsistency in terminology and lack of operationalized thresholds
- The diagnostic hierarchy — first establish cognitive impairment (MCI vs dementia), then establish vascular etiology
- The terminology consensus — VCID as the umbrella, with vaMCI and VaD as severity levels
- The 6 cognitive domains aligned with DSM-5
- The neuroimaging thresholds (Fazekas scoring, lacune counts, strategic infarcts)
- How to distinguish vascular memory impairment from AD memory impairment — retrieval vs consolidation
- The new preclinical/at-risk VCID category
- How biomarkers for AD and DLB are used — not to diagnose VCID, but to suggest alternative/additional etiologies
- Probable vs possible VCID — neuroimaging or genetics required for "probable"
This paper is one of three GC 241 references. The GC 241 lecture summary slide explicitly lists "Vascular neurocognitive disorder" as a core exam topic alongside AD and DLB [1].
Vascular dementia (VaD) is the second most common form of dementia, accounting for 15%–20% of cases, and cerebrovascular disease (CeVD) may contribute to cognitive and functional decline in up to 75% of all persons with dementia. [2]
Despite this importance, the field has been hampered by:
| Problem | Explanation |
|---|---|
| No consensus terminology | Multiple competing terms: VCI, VaD, vascular cognitive disorder, vascular neurocognitive disorder (DSM-5), VCID |
| Inconsistent assessment guidelines | Some criteria require informant concern (VasCog-1, DSM-5), others don't (VICCCS-2, AHA-ASA) |
| Lack of neuroimaging operationalization | Older criteria gave vague imaging thresholds; new small-vessel disease standards (STRIVE-2) needed incorporation |
| No biomarker guidance | AD and DLB biomarkers have advanced enormously; VCID criteria needed to address mixed pathology |
| Subtype confusion | Terms like "multi-infarct dementia," "subcortical ischemic vascular dementia," "post-stroke dementia" used inconsistently |
The VasCog-1 criteria (2014) had better sensitivity and predictive validity than older criteria but still needed updating [2]. The VasCog-2-WSO used a Delphi consensus process with 70 international experts, 3 survey rounds, and a ≥75% agreement threshold [2].
Core Concepts and Mechanisms
The brain depends entirely on a reliable blood supply. Cerebrovascular disease damages the brain through two fundamental mechanisms:
- Large vessel disease → cortical infarcts, strategic infarcts (e.g., thalamus, angular gyrus) → domain-specific deficits depending on location
- Small vessel disease → diffuse white matter ischemia, lacunar infarcts, microbleeds → disrupts subcortical-cortical circuits → affects processing speed, executive function, attention
Why attention/processing speed and executive function are hit first in small vessel disease: The frontal-subcortical circuits (connecting prefrontal cortex → caudate → globus pallidus → thalamus → back to cortex) run through deep white matter. When small vessel disease damages white matter, these long-range circuits are interrupted early, well before cortical neurons themselves are lost. This is why the VasCog-2-WSO criteria recognize that attention and processing speed and executive function are affected early in the disease process and are helpful in identifying small vessel disease–related impairment in the early stages [2].
This is an exam favourite discriminator:
| Feature | VCID Memory Pattern | AD Memory Pattern |
|---|---|---|
| Core deficit | Inefficient encoding and/or retrieval | Impaired consolidation and storage |
| Free recall | Poor (but improves with cues) | Poor (does NOT improve with cues) |
| Recognition | Relatively preserved | Impaired |
| Forgetting rate | Slow (information is "in there" but hard to access) | Rapid (information is lost from storage) |
| Helpful test | Repeated supra-span word list with learning trials, free recall, and recognition | Same test shows flat learning curve, rapid forgetting, failed recognition |
Memory impairment in early VCID typically involves inefficient encoding and/or retrieval, vs consolidation and storage in Alzheimer disease. [2]
This distinction matters clinically: a patient with VaD who has trouble spontaneously recalling a word list but then recognizes the words when given choices likely has a retrieval deficit (subcortical pattern), while an AD patient fails both free recall and recognition (hippocampal/cortical pattern).
The VasCog-2-WSO criteria follow a two-step process:
- Step 1: Establish cognitive impairment (MCI or Dementia) — using Box 1 criteria
- Step 2: Establish vascular etiology — using Box 2 criteria
- Additional: Determine certainty level, subtypes, mixed causation — using Box 3 criteria
Box 1: Diagnostic Criteria for MCI and Dementia
A.1. Concerns of the person, knowledgeable informant, or a clinician of mild levels of decline from a previous level of cognitive functioning. [2]
A.2. Evidence of modest deficits on objective cognitive assessment — typically in the range between 1 and 2 SDs below appropriate norms (between the 3rd and 16th percentiles). [2]
B. The cognitive deficits are not sufficient to interfere with independence (ie, instrumental activities of daily living are preserved), but greater effort, compensatory strategies, or accommodation may be required to maintain independence. [2]
A.1. Concerns of the person, a knowledgeable informant, or the clinician, of significant decline in specific abilities. [2]
A.2. Clear and significant deficits in objective assessment — test performance typically falls ≥ 2 SDs below appropriate norms (or below the third percentile). [2]
B. The cognitive deficits, in isolation from physical deficits, are sufficient to interfere with independence (eg, at a minimum requiring assistance with instrumental activities of daily living). [2]
Critical Exam Point: MCI vs Dementia
The single most important discriminator between MCI and dementia is functional independence. MCI = preserved independence in daily activities. Dementia = requires assistance with at least instrumental ADLs (managing finances, medications, etc.). The cognitive thresholds (1-2 SD vs ≥ 2 SD) are guides, but functional impairment is the defining feature.
Comparison with DSM-5 Framework (from GC lecture):
| Feature | VasCog-2-WSO MCI | DSM-5 Minor NCD | VasCog-2-WSO Dementia | DSM-5 Major NCD |
|---|---|---|---|---|
| Cognitive threshold | 1-2 SD below norms | 1-2 SD below norms | ≥ 2 SD below norms | ≥ 2 SD below norms |
| Functional impairment | Independence preserved | Independence preserved | Interferes with independence | Interferes with independence |
| Subjective concern required? | Yes | Yes | Yes | Yes |
| Objective testing required? | Yes | Yes | Yes | Yes |
These are essentially aligned — the VasCog-2-WSO criteria were designed to be consistent with DSM-5 [2][3].
The DSM-5 domains replace the VasCog-1 domains (80% consensus in round 2). [2]
| Domain | Subdomains/Description | Why It Matters in VCID |
|---|---|---|
| 1. Attention and processing speed | Sustained, divided, selective attention; processing speed | Most commonly affected early in subcortical small vessel disease — frontal-subcortical circuits disrupted |
| 2. Executive function | Planning, decision-making, working memory, inhibition, flexibility, responding to feedback | Second most commonly affected early — same circuit vulnerability |
| 3. Learning and memory | Free recall, cued recall, recognition memory, semantic and autobiographical long-term memory, implicit learning | Present but pattern differs from AD (retrieval > consolidation deficit) |
| 4. Language | Object naming, word finding, fluency, grammar and syntax, receptive language | Less prominently affected than in AD or FTD, but verbal fluency can be impaired |
| 5. Perceptual-motor function | Visual perception, visuoconstructional reasoning, perceptual-motor coordination | Replaces older "praxis-gnosis-body schema" |
| 6. Social cognition | Recognition of emotions, theory of mind, insight | Can be affected in frontal circuit damage |
Domain Name Change Alert
VasCog-1 used "complex attention" — VasCog-2-WSO renamed it to "attention and processing speed" and subsumed "praxis-gnosis-body schema" into "perceptual-motor function". If an exam asks about cognitive domains in VCID, use the updated DSM-5–aligned terminology.
Box 2: Establishing Vascular Etiology
Both A and B are required. C suggests mixed or alternative pathology.
Criterion A: Clinical Features (A.1 or A.2)
The onset of the cognitive deficits is temporally related to ≥ 1 clinical strokes. Onset is abrupt and cognitive deficits persist beyond 3 months after the stroke. [2]
Why 3 months? After an acute stroke, many patients have transient cognitive deficits that improve with recovery. By 3 months, post-stroke delirium and acute metabolic disturbance have resolved, and residual cognitive deficits are more likely to represent true vascular cognitive impairment rather than acute confusional states. Consensus was not reached on a specific time frame (3 months had 39% agreement, 6 months had 30%), so the 3-month guidance from VasCog-1 was retained as the most supported option [2].
Evidence of stroke can be:
- Documented history of a stroke with cognitive decline temporally associated [2]
- Physical signs consistent with stroke (even without known stroke history): hemiparesis, lower facial weakness, Babinski sign, pronator drift, sensory deficit, visual field defect, pseudobulbar syndrome, cerebellar signs [2]
- Covert neuroimaging evidence of CeVD (brain infarct or hemorrhage) may be present in the absence of clinical stroke history [2]
Multiple strokes may produce a stepwise or fluctuating course — classic "stepwise deterioration" of vascular dementia [2].
In the absence of history of stroke or TIA, evidence for decline from subcortical ischemic pathology may be associated with gradual onset and slowly progressive course, typically predominant in some combination of attention and processing speed, and/or executive functioning, with additional domains potentially affected to a lesser extent. [2]
This is the "Binswanger-type" or subcortical pattern — the patient has extensive white matter disease causing a slowly progressive dementia that can mimic AD. The key differentiator is the predominance of attention/processing speed and executive dysfunction rather than the memory-first presentation of AD.
Supportive features:
Personality and mood changes, particularly apathy, depressive symptoms and emotional lability, and gait-balance disorders are common in VCID. [2]
Features Removed from VasCog-2-WSO
Gait disturbance and urinary frequency were removed from the supportive clinical features because they were considered too nonspecific to be diagnostic [2]. Major depression was removed from the exclusion criteria because of considerable overlap between depression and VCID symptoms in later life [2]. These are important changes from VasCog-1.
MRI is preferable to CT. At least 1 of the following is required: [2]
| Neuroimaging Finding | VasCog-2-WSO Threshold | Why This Matters |
|---|---|---|
| Multiple infarcts or a single extensive/strategically placed infarct | Strategic locations (e.g., thalamus) may be sufficient alone | Thalamus is a critical relay station for memory and executive circuits; a single thalamic infarct can cause significant cognitive impairment |
| Multiple lacunes (≥ 2) outside the brainstem | 1 lacune may suffice if strategically placed or combined with extensive WMH | Brainstem lacunes are common but rarely cause cognitive impairment on their own |
| White matter hyperintensities (WMH) | Extensive and confluent: Fazekas score 2 or 3; or periventricular Fazekas = 3 and/or deep Fazekas = 2 or 3 | WMH are ubiquitous with aging; only extensive/confluent WMH correlate meaningfully with cognitive impairment |
| Intracerebral hemorrhage (ICH) | 1 may suffice if large and/or lobar or strategically placed; or ≥ 2 ICH | Lobar ICH suggests cerebral amyloid angiopathy (CAA); deep ICH suggests hypertensive microangiopathy |
Supportive but not sufficient alone:
- Cerebral microbleeds and cortical superficial siderosis [2]
- Abnormalities meeting criteria for cerebral amyloid angiopathy (Boston criteria v2.0) [2]
The STRIVE-2 definitions and guidelines of measurement of cerebrovascular lesions and changes should be adopted for all imaging evidence. [2]
Fazekas Score — Must Know for Exams
The Fazekas scale rates white matter hyperintensities on MRI:
| Score | Periventricular | Deep White Matter |
|---|---|---|
| 0 | Absent | Absent |
| 1 | Caps or pencil-thin lining | Punctate foci |
| 2 | Smooth halo | Beginning confluence |
| 3 | Irregular, extending into deep WM | Large confluent areas |
For VCID diagnosis: Periventricular Fazekas ≥ 3 and/or Deep Fazekas ≥ 2 meets the "extensive and confluent" threshold. Fazekas 1 alone is very common in healthy elderly and should NOT be used to diagnose VCID.
This is where the criteria handle mixed dementia (which is extremely common in practice — up to 75% of dementia cases have some vascular contribution [2]).
Clinical features suggesting alternative etiology:
| Feature | Suggests |
|---|---|
| Insidious early onset of cognitive, perceptual, and motor symptoms suggestive of AD without corresponding vascular lesions | AD as primary pathology |
| Early and prominent movement disorder | DLB, other α-synucleinopathy, or non-vascular movement disorder |
| Features of another primary neurological disorder (MS, encephalitis, toxic/metabolic) | Alternative cause |
Neuroimaging: Absent or minimal cerebrovascular lesions on CT or MRI → argues against VCID [2]
Biomarkers for alternative etiologies:
- AD biomarkers: CSF or plasma Aβ42:40 ratio, p-tau181, p-tau217; amyloid PET at accepted thresholds; autosomal AD mutation; homozygous APOE ε4 [2]
- DLB biomarkers: Dopamine transporter imaging (DaT scan); α-synuclein seed amplification assay in CSF [2]
- Other: FTD pathogenetic variants, brain tumor, traumatic brain injury [2]
Biomarkers in VCID Criteria — A Subtle but Important Point
AD and DLB biomarkers are included in the VCID criteria NOT to diagnose VCID, but to suggest an alternative or concomitant etiology. The presence of positive amyloid biomarkers in a patient with vascular lesions suggests mixed dementia (AD + VCID), and the clinician should state which etiology is clinically more salient.
Box 3: Miscellaneous Criteria
| Level | Requirement |
|---|---|
| Probable VCID | Clinical criteria supported by neuroimaging (a) OR both clinical and genetic evidence of CeVD (b) |
| Possible VCID | Clinical criteria met but neuroimaging and/or genetic evidence not available |
Genetic disorders qualifying for "probable" without neuroimaging:
CADASIL, CARASIL, HERNS, PADMAL, RVCL, COL4A1-related disorders [2]
| Genetic Disorder | Key Features |
|---|---|
| CADASIL (most important for exams) | Autosomal dominant, NOTCH3 mutation; recurrent subcortical infarcts, migraine with aura, progressive dementia, psychiatric disturbances |
| CARASIL | Autosomal recessive, HTRA1 mutation; alopecia, spondylosis, early dementia |
| COL4A1-related | Porencephaly, ICH, retinal vessel tortuosity |
State which etiology is clinically more salient: vascular or other. [2]
| Pattern | Example |
|---|---|
| VCID with concomitant neurodegenerative disease | "VCID [primary] with contribution from AD" or "AD [primary] with contribution from VCID" |
| VCID with nonneurodegenerative pathology | "VCID [primary] with contribution from traumatic brain injury" |
| VCID with contribution from depression | Recognizes depression-VCID overlap |
Associated behavioral/psychiatric symptoms: apathy, depressive symptoms, emotional lability, psychotic symptoms, agitation [2]
Requires (a) significant incidental neuroimaging evidence of CeVD satisfying criterion B AND (b) does not satisfy criteria for MCI or dementia, with no concerns of cognitive change. [2]
Why this matters: This category recognizes covert CeVD — incidentally discovered cerebrovascular disease in cognitively normal individuals. These patients are at elevated risk of future cognitive decline and stroke, and should be targeted for risk factor modification and monitoring. This parallels the "preclinical" stage concept in AD criteria (Reference 1 of GC 241) [2].
Integration with GC 241 Lecture and Related Material
The GC 241 summary slide lists the core topics as:
- DSM-V criteria of diagnosis
- Common etiologies: Alzheimer's disease, Vascular neurocognitive disorder, Lewy Body Dementia
- Imaging and fluid biomarkers
- New advances in Alzheimer's disease
The VasCog-2-WSO criteria directly address the "vascular neurocognitive disorder" component. For exam purposes, you should be able to:
- Define and differentiate MCI vs dementia (functional impairment is the key)
- List the 6 DSM-5 cognitive domains
- Describe the two clinical presentations of VCID (post-stroke vs gradual subcortical)
- List neuroimaging criteria including Fazekas thresholds
- Contrast memory impairment patterns between VCID and AD
Ryan Ho Neurology notes list vascular dementia as the second most common cause (10-20%) and note it as "multi-infarct dementia" [4]. The VasCog-2-WSO criteria dropped the term "multi-infarct dementia" as a formal subtype, preferring the broader ischemic/hemorrhagic/mixed classification [2].
Maksim Medicine Notes describe the approach to cognitive disorders and note that the predominant deficit in vascular dementia is executive dysfunction [5]. The VasCog-2-WSO criteria refine this by emphasizing attention and processing speed alongside executive function as the earliest affected domains [2].
Ryan Ho Psychiatry provides DSM-5 diagnostic criteria for major NCD and specifies vascular disease as one of the etiologies [3]. The VasCog-2-WSO criteria are fully harmonized with DSM-5 cognitive domains [2].
| Feature | VCID | Alzheimer's Disease | DLB |
|---|---|---|---|
| Onset | Abrupt (post-stroke) or gradual (subcortical SVD) | Insidious, gradual | Insidious |
| Course | Stepwise or slowly progressive | Progressively declining | Fluctuating cognition |
| Earliest cognitive domains | Attention/processing speed, executive function | Learning and memory | Attention, executive function, visuospatial |
| Memory pattern | Retrieval deficit (improves with cues) | Consolidation deficit (rapid forgetting, poor recognition) | Variable |
| Hallucinations | Uncommon | Late feature | Early, recurrent, well-formed visual hallucinations |
| Motor signs | Focal neurological signs (hemiparesis, Babinski) | Usually absent early | Parkinsonism |
| Neuroimaging | Infarcts, lacunes, WMH, ICH | Hippocampal/medial temporal atrophy | Relative preservation of medial temporal lobe |
| Key biomarkers | Neuroimaging (MRI); no specific fluid biomarker yet | Amyloid PET, CSF/plasma Aβ42:40, p-tau | DaT scan, α-synuclein SAA |
| Management | Vascular risk factor control; no specific pharmacotherapy | AChEI, memantine | AChEI (especially rivastigmine); avoid typical antipsychotics |
Clinical Approach Summary
- Onset pattern: Abrupt (suggests stroke-related VCID) vs gradual (suggests subcortical SVD or AD)
- Course: Stepwise decline (multi-infarct) vs slow progression (subcortical SVD) vs steady decline (AD)
- Cognitive domains affected: Executive function, attention, processing speed (VCID) vs memory (AD) vs visuospatial/hallucinations (DLB)
- Vascular risk factors: Hypertension, diabetes, smoking, AF, hyperlipidemia, prior stroke/TIA
- Stroke history: Any documented cerebrovascular events? Physical signs of stroke?
- Supportive features: Apathy, depressive symptoms, emotional lability, personality changes
- Functional status: Basic vs instrumental ADLs — determines MCI vs dementia
- Informant history: Essential; patient may lack insight
- Cognitive screening: MMSE, MoCA (note MoCA is more sensitive for executive/attention deficits — relevant to VCID)
- Neurological exam: Focal signs (hemiparesis, facial weakness, Babinski, pronator drift, sensory deficit, visual field defect, pseudobulbar palsy, cerebellar signs)
- Gait assessment: Frontal/apraxic gait in subcortical disease (small steps, wide base, magnetic gait)
- Mood assessment: Screen for depression/apathy (high overlap with VCID)
- MRI Brain (preferred over CT): Look for infarcts, lacunes, WMH (Fazekas score), ICH, microbleeds, cortical superficial siderosis
- Blood tests: Rule out reversible causes (TSH, B12, folate, LFT, RFT, CBC, glucose, syphilis serology, HIV)
- AD biomarkers if available: CSF Aβ42:40, p-tau; amyloid PET — to assess for mixed pathology
- DaT scan: If DLB suspected
- Genetic testing: If early-onset or family history suggests monogenic cause (CADASIL etc.)
- Vascular risk factor workup: BP, HbA1c, lipid panel, ECG (AF screen)
- No specific pharmacotherapy for VCID — unlike AD (which has AChEI and memantine) [5]
- Primary strategy: aggressive vascular risk factor control
- Antihypertensives, statins, antiplatelet/anticoagulant therapy as indicated
- Glycemic control, smoking cessation, weight management
- AF management
- Cognitive rehabilitation and multidisciplinary support
- Treat associated symptoms: Antidepressants for depression; cautious use of antipsychotics for BPSD
- Prevent further strokes to halt stepwise decline
Exam Intelligence
| Trap | Correct Understanding |
|---|---|
| "Vascular dementia always has stepwise decline" | Not true — subcortical SVD pattern is gradual and slowly progressive, mimicking AD |
| "Memory is preserved in vascular dementia" | Not true — memory CAN be impaired in VCID, but the pattern differs (retrieval vs consolidation) |
| "Fazekas 1 WMH = vascular dementia" | Not true — Fazekas 1 is very common in healthy elderly; need Fazekas ≥ 2-3 for diagnostic significance |
| "Gait disturbance is a diagnostic feature of VaD" | Removed from VasCog-2-WSO supportive criteria (too nonspecific), though still commonly seen |
| "Major depression excludes VCID diagnosis" | Removed as exclusion criterion in VasCog-2-WSO due to significant overlap |
| "Multi-infarct dementia is the main subtype" | Dropped as a formal subtype — now classify as ischemic/hemorrhagic/mixed |
| "VCID is purely vascular" | Most elderly have mixed pathology — criteria explicitly address mixed causation and encourage stating predominant etiology |
| "Biomarkers diagnose VCID" | Currently no specific fluid biomarker for VCID — neuroimaging (MRI) remains the mainstay; AD/DLB biomarkers used to suggest alternative/additional etiologies |
| "Possible VCID means less severe" | "Possible" means imaging/genetic evidence is not available, not that the disease is milder |
| Parameter | Value |
|---|---|
| VaD as proportion of all dementia | 15-20% |
| CeVD contribution to all dementia | Up to 75% |
| MCI cognitive threshold | 1-2 SD below norms (3rd-16th percentile) |
| Dementia cognitive threshold | ≥ 2 SD below norms ( < 3rd percentile) |
| Cognitive deficit persistence after stroke | Beyond 3 months |
| Lacune threshold for VCID | ≥ 2 outside brainstem (or 1 if strategic/with extensive WMH) |
| Fazekas score threshold for WMH | Overall 2-3; or PV = 3 and/or Deep = 2-3 |
| Delphi consensus threshold | ≥ 75% agreement |
High Yield Summary
-
VasCog-2-WSO (2025)
- is the latest international consensus criteria for VCID:
-
Terminology
- VCID (umbrella) → vaMCI (mild) + VaD (major/dementia-level)
-
Two-step diagnosis
- First establish MCI or dementia (Box 1), then establish vascular etiology (Box 2)
-
MCI vs Dementia
- Differentiated by functional independence (preserved in MCI, impaired in dementia), not just cognitive test scores
-
Six cognitive domains
- (DSM-5 aligned): Attention/processing speed, executive function, learning/memory, language, perceptual-motor function, social cognition
-
Two clinical presentations
- Post-stroke (abrupt onset, stepwise, persists > 3 months) vs subcortical SVD (gradual, attention/executive predominance)
-
Memory in VCID = retrieval deficit
- (improves with cues) vs AD = consolidation deficit (rapid forgetting, fails recognition)
-
Neuroimaging thresholds
- Multiple/strategic infarcts, ≥ 2 lacunes outside brainstem, WMH at Fazekas ≥ 2-3, ICH
-
Probable VCID
- requires neuroimaging support or genetic evidence (e.g., CADASIL)
-
Possible VCID
- = clinical criteria met but no imaging/genetics available
- New preclinical/at-risk category
- Significant CeVD on imaging but no cognitive impairment — target for risk reduction
- AD/DLB biomarkers
- in VCID criteria: used to identify alternative/additional etiologies, NOT to diagnose VCID
- No specific pharmacotherapy for VCID
- management is aggressive vascular risk factor control and stroke prevention
- Gait disturbance, urinary frequency, and major depression
- removed from VasCog-2-WSO criteria (nonspecific or overlapping)
Active Recall - VasCog-2-WSO Criteria for VCID
[1] GC 241. A short course of dementia.pdf (Summary slide, p2) [2] GC 241. Reference (2) - New vascular neurocognitive disorder criteria JAMA.pdf (all pages) [3] Ryan Ho Psychiatry.pdf (p77, Approach to Dementia and DSM-5 criteria) [4] Ryan Ho Neurology.pdf (p128, Dementia and Dementia Syndromes) [5] Maksim Medicine Notes.pdf (p114-115, Geriatrics - Dementia section)
GC241 Reference (1) - Alzheimers Dementia - Revised Criteria For Diagnosis And Staging Of Alzheimer S Disease
The revised criteria for diagnosis and staging of Alzheimer's disease define it as a biological construct characterized by the presence of amyloid-beta and tau biomarkers, enabling classification across a clinical continuum from preclinical to dementia stages independent of symptom onset.
GC241 Reference (3) - Patel Dementia With Lewy Bodies
Dementia with Lewy bodies is a progressive neurodegenerative disorder characterized by cognitive decline, visual hallucinations, fluctuating attention, and parkinsonism due to abnormal alpha-synuclein protein deposits (Lewy bodies) in cortical and subcortical neurons.