The progression of cognitive impairment in dementia with Lewy bodies, vascular dementia and Alzheimer's disease

Ballard, Clive; O’Brien, John T.; Morris, Christopher M.; Barber, Robert; Swann, Alan; Neill, D. W.; McKeith, Ian G.

doi:10.1002/gps.381

Cited by 104 publications

(73 citation statements)

References 32 publications

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“…For example, AD and VaD share features involving cerebral hypoperfusion, white matter changes, [165][166][167] pathophysiological markers, 168 -172 genetic links, [173][174][175][176] overlapping symptomatology, and diagnostic criteria of dubious reliability. [177][178][179][180][181][182][183][184][185] Several objective clinical criteria are presently used to distinguish AD from VaD, such as the Alzheimer Disease Diagnostic and Treatment Centers, National Institute of Neurological Disorders and StrokeAssociation Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN), DSM-IV, and the Hachinski Ischemia Score. 186 Of these, the most useful in differentiating VaD from AD appears to be the Hachinski Ischemia Score, 187 if it is assumed that mixed pathology is minimally present.…”

Section: Ad-vad Correlatesmentioning

confidence: 99%

Alzheimer Disease as a Vascular Disorder

Torre

2002

Stroke

777

491

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Background-The main stumbling block in the clinical management and in the search for a cure of Alzheimer disease (AD) is that the cause of this disorder has remained uncertain until now. Summary of Review-Evidence that sporadic (nongenetic) AD is primarily a vascular rather than a neurodegenerative disorder is reviewed. This conclusion is based on the following evidence: (1) epidemiological studies showing that practically all risk factors for AD reported thus far have a vascular component that reduces cerebral perfusion; (2) risk factor association between AD and vascular dementia (VaD); (3) improvement of cerebral perfusion obtained from most pharmacotherapy used to reduce the symptoms or progression of AD; (4) detection of regional cerebral hypoperfusion with the use of neuroimaging techniques to preclinically identify AD candidates; (5) presence of regional brain microvascular abnormalities before cognitive and neurodegenerative changes; (6) common overlap of clinical AD and VaD cognitive symptoms; (7) similarity of cerebrovascular lesions present in most AD and VaD patients; (8) presence of cerebral hypoperfusion preceding hypometabolism, cognitive decline, and neurodegeneration in AD; and (9) confirmation of the heterogeneous and multifactorial nature of AD, likely resulting from the diverse presence of vascular risk factors or indicators of vascular disease. Conclusions-Since the value of scientific evidence generally revolves around probability and chance, it is concluded that the data presented here pose a powerful argument in support of the proposal that AD should be classified as a vascular disorder. According to elementary statistics, the probability or chance that all these findings are due to an indirect pathological effect or to coincidental circumstances related to the disease process of AD seems highly unlikely. The collective data presented in this review strongly support the concept that sporadic AD is a vascular disorder. It is recommended that current clinical management of patients, treatment targets, research designs, and disease prevention efforts need to be critically reassessed and placed in perspective in light of these important findings. Key Words: Alzheimer disease Ⅲ dementia Ⅲ microcirculation Ⅲ risk factors Ⅲ vascular disorders A lzheimer disease (AD) is an insidious disorder that progressively ravages the brain, destroying its memory, intellect, and dignity in the process. The main stumbling block in the clinical management and in the search for a cure of AD is that the cause of this disorder has remained uncertain until now. For more than 30 years, AD has been classified and managed as a neurodegenerative disorder, 1,2 following a report by Roth in 1955 3 that suggested that dementia should be classified into 2 distinct disorders according to the variable mental changes caused by each: vascular dementia (VaD), caused by vascular lesions, and AD, resulting from a neurodegenerative process.Most investigators in the field have supported Roth's notion that dementing processes will d...

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Section: Ad-vad Correlatesmentioning

confidence: 99%

Alzheimer Disease as a Vascular Disorder

Torre

2002

Stroke

777

491

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“…However, within DLB patients, apolipoprotein E4 may be an important predictor of more rapid decline. [40][41][42][43] Additionally, as discussed above, visual hallucinations and delusions are present in DLB, as well as parkinsonian motor features. Parkinsonism may be present at onset, or develop later, unlike in PD dementia (PDD) where motor symptoms tend to precede cognitive impairment.…”

Section: Clinical Coursementioning

confidence: 86%

“…26,69,70 Use of selective serotonin reuptake inhibitors (SSRIs) for symptoms of anxiety, emotional lability, and depression have also demonstrated benefit, though there is no peer-reviewed evidence. 22,43,71 Tricyclic antidepressants (TCAs) and antispasmotics should be avoided for the potential anticholinergic exacerbations. 70 For REM sleep behavior disorder, clonazepam may be beneficial though it could worsen dementia and alertness.…”

Section: Treatmentmentioning

confidence: 99%

Dementia with Lewy Bodies

Mayo

Bordelon

2014

Semin Neurol

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).Dementia with Lewy bodies (DLB) is an atypical parkinsonian disorder characterized as a synucleinopathy based on the cardinal pathologic finding, the Lewy body, a neuronal inclusion comprised of aggregated α-synuclein. Lewy bodies are found in brainstem nuclei in both Parkinson disease (PD) as well as in DLB, though in DLB there is a concomitant presence of Lewy bodies in the cortex and subcortical white matter. The cortical Lewy bodies may not demonstrate the classic structure of an eosinophilic core with surrounding halo; however, they contain α-synuclein. Clinically, DLB manifests with fluctuating alertness, visual hallucinations, and parkinsonian motor symptoms, and has features of both a cortical and a subcortical dementia. EpidemiologyDementia with Lewy bodies is the second most common pathologic diagnosis of dementia, next to Alzheimer disease (AD) and accounts for 25% of all dementias. 1 The prevalence of DLB is estimated to be 0.7% of the population over 65 years of age. 2 Given the challenge of clinical diagnostic accuracy in dementia, there is a wide variation in estimates of the prevalence among dementia patients, ranging from 3 to 26.3% in those over the age of 65 years. 3,4 The incidence of DLB is 3.5 per 100,000 person years and this increases with age. 5 There is a slightly greater male predominance of 1.9:1. 6 Risk factors of DLB include advanced age, hypertension, hyperlipidemia, and carriers of one or more APOE ε4 alleles. 7-9 As in PD, there is overrepresentation of the CYP2D6B allele, and a greater heterozygous frequency of glucocerebrosidase 1 (GBA1) estimated at 3.5% versus 2.9% in Parkinson disease dementia (PDD) and 0.4% in the general population. 10 A separate study also found a significant association between GBA1 mutation carrier status and DLB with an odds ratio of 8.28 versus 6.48 in PDD. 11 PathophysiologyDementia with Lewy bodies is considered a synucleinopathy, along with PD and multiple system atrophy (MSA). It is distinguished pathologically by the presence of Lewy bodies, which are intracellular inclusions with an eosinophilic core Keywords ► dementia with Lewy bodies ► Lewy body ► synucleinopathy ► dementia ► parkinsonism AbstractDementia with Lewy bodies (DLB) is the second most common diagnosis of dementia after Alzheimer disease (AD). The essential pathologic feature is the Lewy body, a neuronal inclusion containing α-synuclein, found in brainstem nuclei and the neocortex. Clinical features include early fluctuations in attention, hallucinations, and parkinsonism, with progression to a combined cortical and subcortical dementia. To distinguish it from Parkinson disease dementia, a time course of one year from cognitive changes to motor feature onset has been established. There is more severe impairment of verbal fluency, executive function, and visuospatial abilities in DLB patients. Both rapid eye movement sleep behavior disorder and neuroleptic sensitivity are notable in this patient group. Treatment is aimed at symptom management. Cholinesterase inhibitors can be bene...

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“…C. Ballard in his study on the progression of cognitive impairment in dementia with Lewy bodies, vascular dementia and Alzheimer disease reported that the magnitude of cognitive decline was similar in different types of dementia (20). On the other hand Sultzer DL, in his study entitled "A comparison of psychiatric symptoms in vascular dementia and Alzheimer disease" reported that patients with VD had more cognitive impairment compared to patients with DAT, as indicated by the neurobehavioral rating scale total scores (21).…”

Section: Discussionmentioning

confidence: 99%

A comparative study of behavioral and psychological symptoms in patients with vascular and Alzheimer dementia

Javed¹,

Gaur²,

Ibrahim³

et al. 2017

Sri Lanka J. Psyc.

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BackgroundDementia is a common, disabling disorder of the elderly. With the steady growth in the older population, the rate of dementia is expected to increase two fold by 2030 and three fold by 2050. Dementia of Alzheimer Type (DAT) and vascular dementia (VD) are among the most common types of dementia. Behavioral and psychological symptoms of dementia (BPSD) are associated with increased patient morbidity and carer burden.

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The progression of cognitive impairment in dementia with Lewy bodies, vascular dementia and Alzheimer's disease

Abstract: Over 1 year, DLB, VaD and AD patients had similar rates of cognitive decline overall. Apolipoprotein E4 may be an important predictor of more rapid decline in DLB.

Cited by 104 publications

References 32 publications

Alzheimer Disease as a Vascular Disorder

Alzheimer Disease as a Vascular Disorder

Dementia with Lewy Bodies

A comparative study of behavioral and psychological symptoms in patients with vascular and Alzheimer dementia

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