Close-meshed prevalence rates of different stages as a tool to uncover the rate of Alzheimer's disease-related neurofibrillary changes

Ohm, Thomas G.; Müller, Holger M.; Braak, Heiko; Böhl, Jürgen

doi:10.1016/0306-4522(95)90397-p

Cited by 207 publications

(109 citation statements)

References 9 publications

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“…A rough estimate of the time scale of the overall progression (Fig. 3) was provided by Ohm et al (28). The findings of Scahill et al are broadly consistent with the scheme shown in Fig.…”

supporting

confidence: 69%

Imaging the progression of Alzheimer pathology through the brain

Smith

2002

Proc. Natl. Acad. Sci. U.S.A.

174

104

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“…A rough estimate of the time scale of the overall progression (Fig. 3) was provided by Ohm et al (28). The findings of Scahill et al are broadly consistent with the scheme shown in Fig.…”

supporting

confidence: 69%

Imaging the progression of Alzheimer pathology through the brain

Smith

2002

Proc. Natl. Acad. Sci. U.S.A.

174

104

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“…AD is slowly progressive and the underlying pathology is present for many years before the onset of dementia (Ohm et al, 1995;Braak and Braak, 1997). The clinical phase between normal functioning and dementia in AD may comprise: (1) an early stage marked by subjective memory complaints where early neuropathological changes are overcome by compensatory processes; and (2) a later phase where developing AD pathology is manifest as AMCI.…”

Section: Introductionmentioning

confidence: 99%

Subjective cognitive impairment: increased prefrontal cortex activation compared to controls during an encoding task

Rodda

Dannhauser

Cutinha

et al. 2009

Int J Geriat Psychiatry

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SUMMARYObjective Subjective cognitive impairment (SCI) has been proposed as a clinical stage which may precede mild cognitive impairment in the clinical continuum of AD, and is characterised by the presence of subjective memory complaints in the absence of objective cognitive deficits. Specific memory-related brain activation differences have been reported in mild cognitive impairment and in cognitively normal individuals at known genetic risk of AD; our objective was to determine whether similar differences are present in people with SCI. Methods We compared brain activation in a memory clinic sample of 10 SCI subjects and 10 controls during a verbal episodic memory encoding task using functional magnetic resonance imaging (fMRI). Results There were no differences between groups on measures of encoding success (recognition accuracy) nor was there evidence of altered semantic processing. Both groups activated left prefrontal cortex (PFC) and cerebellum during encoding. The SCI group also demonstrated activation in left medial temporal, occipitoparietal and medial frontal cortex. Group comparisons revealed increased activation in SCI in left PFC, where activation strength correlated with memory task performance. Conclusions The activation differences reported in this study may reflect the employment of compensatory strategies in the face of early AD pathology, although a number of alternative explanations need to be considered. Further studies with larger samples may help to determine whether the observed activation changes are likely to be associated with early neuropathological processes or with other unrelated factors.

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“…There is increasing evidence that the clinical syndrome of Alzheimer disease (AD) is preceded by a silent preclinical phase characterized by neuropathological change spanning over decades (Ohm et al, 1995;Braak et al, 1999;Corder et al, 2004). Both the apolipoprotein E (APOE) 4 allele (APOE4 or 4) and firstdegree family history (Fratiglioni et al, 1993) increase the preclinical prevalence of neurofibrillary tangles and amyloid plaques, the main pathology in AD (Ghebremedhin et al, 1998(Ghebremedhin et al, , 2001Corder et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

The Influence of Alzheimer Disease Family History and Apolipoprotein E ε4 on Mesial Temporal Lobe Activation

Johnson¹,

Schmitz²,

Trivedi³

et al. 2006

J. Neurosci.

143

152

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First-degree family history of sporadic Alzheimer disease (AD) and the apolipoprotein E 4 (APOE4) are risk factors for developing AD. Although the role of APOE4 in AD pathogenesis has been well studied, family history remains a rarely studied and poorly understood risk factor. Both putatively cause early brain changes before symptomatic disease, but the relative contribution of each to brain function is unknown. We examined 68 middle-aged participants with a parent diagnosed with AD [family history (ϩFH)] and 64 age-and educationmatched controls without a first-degree family history of any dementia [no family history (ϪFH)]. All underwent cognitive testing, APOE genotyping, and a functional magnetic resonance imaging encoding task that required discrimination of novel items from previously learned items. A 2 ϫ 2 factorial ANOVA (presence/absence of parental family history and presence/absence of the APOE4) was used to detect group effects. A greater response to novel items was detected in the mesial temporal lobe and fusiform gyrus bilaterally among persons without a first-degree family history of AD. In hippocampal areas, the ϪFH ϩ4 group exhibited the greatest signal change, and the ϩFH ϩ4 group exhibited the least. These findings indicate that FH of AD is an important predictor of hippocampal activation during encoding and that FH may modulate the effect of APOE4 in these middle-aged adults, suggesting that an as yet unspecified factor embodied in first-degree family history of AD is influencing the expression of APOE4 on brain function.

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Close-meshed prevalence rates of different stages as a tool to uncover the rate of Alzheimer's disease-related neurofibrillary changes

Cited by 207 publications

References 9 publications

Imaging the progression of Alzheimer pathology through the brain

Imaging the progression of Alzheimer pathology through the brain

Subjective cognitive impairment: increased prefrontal cortex activation compared to controls during an encoding task

The Influence of Alzheimer Disease Family History and Apolipoprotein E ε4 on Mesial Temporal Lobe Activation

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