Table 1.

Summary of symptoms and affected neuroanatomy of common dementia diagnoses.

Diagnosis		Symptoms	Affected Neuroanatomy
Alzheimer’s disease (AD)		Progressive episodic and semantic memory loss is the first and major symptom. Executive dysfunction, impaired judgement, changes in mood, personality, and behaviour, and language deficits (aphasia) are seen as the disease progresses [12,13]. Visuospatial deficits are also observed, but tend to be less severe than other cognitive symptoms [13].	Degeneration of medial temporal lobe structures (hippocampus, entorhinal cortex) [13]. Hypometabolism in limbic system (posterior cingulate and parahippocampal gyri), precuneus, posterior parietal cortex, and bilateral middle and inferior temporal gyri [14,15]. Prefrontal association cortex, temporoparietal, and posterior cingulate regions are associated with dementia severity [16].
Atypical AD	Posterior cortical atrophy (PCA)	Subtle vision problems that worsen over time including facial/object agnosias and alexia, difficulty with spatial awareness and judging distance. Later stages are likely to include memory loss, confusion, and communication difficulties. Most often (but not always) associated with AD [13,17].	Hypometabolism in striatum, lateral occipital lobe, inferior parietal lobe, lingual gyrus, posterior cingulate, cuneus, precuneus, supramarginal gyrus, and thalamus [18].
	Frontal variant AD (fvAD)	Early memory complaints and semantic language impairment. Irritability, delusions, and movement disorders (myoclonus) are also common [19].	Symmetrical degeneration of temporal lobes, with additional atrophy in frontal lobes, posterior corpus callosum and perisylvian region [19].
Dementia with Lewy bodies		Deficits in attention and visuospatial and executive functions, poor regulation of bodily functions, visual hallucinations, movement disorders (e.g., Parkinsonism), [1].	Hypometabolism in occipital cortex (primary visual cortex, Brodmann areas 17–19), temporal and parietal cerebral cortices [10,20].
Frontotemporal lobar degeneration (FTLD)	FTLD (generally)	Gradual and progressive deficits in behaviour (bvFTLD), language (PPA), or movement. Memory is often spared [21].	Hypometabolism in ventromedial and anterior frontal lobe, ventral temporal, and medial thalamic regions [22,23].
	Behavioural variant FTLD, bvFTLD	Late memory complaints. Language impairment (socioemotional aspects and phonemic fluency). Changes in personality and inappropriate behaviour, compulsivity, difficulty planning and organizing, apathy, anhedonia, lack of sympathy/empathy [1,2,19].	Symmetric or asymmetric frontotemporal cortex degeneration [19,21].
Progressive supranuclear palsy, PSP		Difficulty with rigidity, walking, postural instability, and eye movements. Executive dysfunction (difficulty concentrating, problem-solving, decision-making, and planning), and language deficits are common (depending on subtype) while memory is often spared [2,24].	Tauopathy with accumulation/degeneration in basal ganglia, diencephalon, and brainstem [24]. Hypometabolism in insular cortex, lateral and midline frontal cortex, cerebellum, brainstem, and caudate nucleus [25].
Progressive primary aphasia (PPA)	PPA (generally)	Difficulty with language most prominent feature that impairs daily living [2,26].	Hypometabolism in left parietal and posterolateral temporal lobes [9].
	Semantic dementia	Speech is fluent but understanding of word meaning is impaired. Prosody and syntax are spared while emotionality may be impaired [21,26,27].	Anterior temporal cortex atrophy, hypoperfusion or hypometabolism [26].
	Progressive nonfluent aphasia	Speaking becomes effortful, motor-related speech deficits and loss of grammar are evident while word knowledge is spared [21,26].	Left posterior fronto-insular atrophy, hypoperfusion or hypometabolism [26].
	Logopenic aphasia	Speech becomes slow and hesitant, finding the correct word becomes difficult, and sentence repetition is difficult [21,26,28].	Left posterior perisylvian or parietal atrophy, hypoperfusion or hypometabolism [26]. These patients sometimes present with AD at autopsy, but results have been controversial [2,13]
Vascular dementia		Varies, depending on location of stroke/lesion [1].	Hypometabolism and lesions in focal cortical and subcortical regions [29].
Mixed dementia		Dementia attributed to more than one cause, as such, symptoms vary as per other diagnoses.	Depends on diagnoses.
Mild cognitive impairment 1		Cognitive function worse than normal for the individual, but not causing interruption to daily living [1]	Posterior cingulate, inferior parietal lobe, and precuneus [9].
Primary psychiatric disorder 1		Various, depending on the diagnosis. Memory complaints, depressive or anxious mood, altered sleep cycles, slowed processing speeds, executive dysfunction, difficulty concentrating, worry, irritability, fatigue, muscle tension [30,31].	Increased activity in amygdala, altered activity in anterior cingulate cortex and hippocampus, and reduced activity in prefrontal cortex, [32,33].

¹ Mild cognitive impairment (MCI) and primary psychiatric disorder are not classified as dementia although MCI can develop into dementia over time, and primary psychiatric disorders can mimic dementia symptoms.