Dementia Characterized by Abundant Neurofibrillary Tangles and Scarce Senile Plaques: A Quantitative Pathological Study

Itoh, Yoshinori; Yamada, Masahisa; Yoshida, Ryoichi; Suematsu, Naomi; Oka, Takuro; Matsushita, M.; Otomo, E

doi:10.1159/000117216

Cited by 21 publications

(17 citation statements)

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“…A subset of patients with PART (previously referred to as SD-NFT, TPSD, etc.) display marked clinical impairment in the absence of any other recognizable substrate for dementia [14, 21, 39, 60, 66, 72, 99, 142]. The average age of death is generally higher for these patients than those with AD pathology [37, 79, 107].…”

Section: Clinical Featuresmentioning

confidence: 99%

“…Patients with mild-to-moderate AD-type neurofibrillary degeneration in the medial temporal lobe, but lacking Aβ plaques, have been described in European, Japanese, North and South American cohorts [2, 3, 14, 51, 52, 58, 69, 72, 79, 81, 82, 126, 142, 147, 149, 151]. NFT are practically universal in older persons' brains [22, 30, 108, 132], and are also observed in a more limited distribution in many younger individuals [30, 32, 42].…”

Section: Introductionmentioning

confidence: 99%

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Primary age-related tauopathy (PART): a common pathology associated with human aging

et al. 2014

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We recommend a new term, “primary age-related tauopathy” (PART), to describe a pathology that is commonly observed in the brains of aged individuals. Many autopsy studies have reported brains with neurofibrillary tangles (NFT) that are indistinguishable from those of Alzheimer's disease (AD), in the absence of amyloid (Aβ) plaques. For these “NFT+/Aβ−” brains, for which formal criteria for AD neuropathologic changes are not met, the NFT are mostly restricted to structures in the medial temporal lobe, basal forebrain, brainstem, and olfactory areas (bulb and cortex). Symptoms in persons with PART usually range from normal to amnestic cognitive changes, with only a minority exhibiting profound impairment. Because cognitive impairment is often mild, existing clinicopathologic designations, such as “tangle-only dementia” and “tangle-predominant senile dementia”, are imprecise and not appropriate for most subjects. PART is almost universally detectable at autopsy among elderly individuals, yet this pathological process cannot be specifically identified pre-mortem at the present time. Improved biomarkers and tau imaging may enable diagnosis of PART in clinical settings in the future. Indeed, recent studies have identified a common biomarker profile consisting of temporal lobe atrophy and tauopathy without evidence of Aβ accumulation. For both researchers and clinicians, a revised nomenclature will raise awareness of this extremely common pathologic change while providing a conceptual foundation for future studies. Prior reports that have elucidated features of the pathologic entity we refer to as PART are discussed, and working neuropathological diagnostic criteria are proposed.

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Section: Clinical Featuresmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Primary age-related tauopathy (PART): a common pathology associated with human aging

et al. 2014

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“…Outside the collateral sulcus, the AD pa- tients presented with abundant NFTs in the lateral occipitotemporal gyrus and inferior temporal gyrus compared with SD-NFT. The NFTs in SD-NFT were labelled by the antibodies to tau [phosphorylation-dependent (AT8, AT100, AT180, and AT270) and independent (TAU-2 and anti-human tau)], PHF, and ubiquitin as found in AD [9] (fig. 4).…”

Section: Neuropathologic Findingsmentioning

confidence: 99%

“…We studied demented elderly patients with such neuropathologic features [9,10], and compared them with agematched AD patients in clinicopathologic and genetic aspects [10]; our results indicated that this neuropathologic condition would represent a disease entity different from AD [10]. Therefore, we have proposed the term, 'senile dementia of the NFT type' (SD-NFT), which is distinguished from late-onset AD, i.e., senile dementia of the Alzheimer type [10].…”

Section: Introductionmentioning

confidence: 99%

Senile Dementia of the Neurofibrillary Tangle Type: A Comparison with Alzheimer’s Disease

Yamada

Itoh²,

Sodeyama

et al. 2001

Dement Geriatr Cogn Disord

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A subset of senile dementia, ‘senile dementia (SD) of the neurofibrillary tangle (NFT) type’ (SD-NFT), is characterized by numerous NFTs in the hippocampal region and absence or scarcity of senile plaques throughout the brain. To elucidate the pathogenesis of SD-NFT in comparison with Alzheimer’s disease (AD), we investigated the hippocampal lesions and analyzed the tau gene. The hippocampal regions from 5 patients with SD-NFT were neuropathologically evaluated in comparison with AD and nondemented control subjects. The tau gene was analyzed in 3 patients with SD-NFT. The densities of NFTs in the CA1/subiculum and entorhinal cortex of SD-NFT were significantly higher than those in AD. However, hippocampal atrophy, neuronal and synaptic loss, and astrocytic and microglial proliferation in SD-NFT were significantly mild compared with AD. There was no significant difference between SD-NFT and AD in the immunoreactivities of NFTs with different anti-tau antibodies. No mutation was found in the tau gene from the SD-NFT patients. Our results indicate that the neurodegenerative process with NFT formation of the hippocampal region in SD-NFT would be different from that in AD.

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“…However, all cases with neuritic plaques have neuropil threads and neurofibrillary tangles both in the entorhinal region and amygdala, indicating that neuropil threads and neurofibrillary tangles might be a prerequisite for the development of neuritic plaques (table 1). Recent reports on a rare form of senile dementia of the Alzheimer type characterized by the absence or near absence of senile plaques [Ulrich et al, 1992;Bancher and Jellinger, 1994;Itoh et al, 1996], as some cases at limbic stages, show (table 1, neurofibrillary stages III-IV) that even an advanced neurofibrillary pathology may remain devoid of neuritic plaques ( fig.¤1).…”

Section: Discussionmentioning

confidence: 99%

Alzheimer’s Disease

Yilmazer-Hanke¹

1998

Cells Tissues Organs

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The gradual development of Alzheimer-related neurofibrillary changes and β-amyloid deposits have been investigated in the amygdala and cerebral cortex with advanced silver methods. Neurofibrillary tangles occur within the somata of nerve cells, while neuropil threads are located in nerve cell processes. In neuritic plaques, there are both neuronal processes containing neurofibrillary changes and extracellular deposits of β-amyloid protein. The amygdala early displays Alzheimer-type pathology and is typically rich in neuritic plaques. Neuritic plaques do not occur in the amygdala in the absence of neuropil threads and neurofibrillary tangles in the entorhinal region and amygdala. In contrast to the gradual increase in the number of neurofibrillary tangles and neuropil threads, neuritic plaques grow in size and number along with advancement in the neurofibrillary and β-amyloid pathology. The findings indicate that neuropil threads and neurofibrillary tangles in the entorhinal region and amygdala precede neuritic plaques in the amygdala, and the density of neuritic plaques is related both to the degree of neurofibrillary and β-amyloid pathology in the cerebral cortex.

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Dementia Characterized by Abundant Neurofibrillary Tangles and Scarce Senile Plaques: A Quantitative Pathological Study

Cited by 21 publications

References 0 publications

Primary age-related tauopathy (PART): a common pathology associated with human aging

Primary age-related tauopathy (PART): a common pathology associated with human aging

Senile Dementia of the Neurofibrillary Tangle Type: A Comparison with Alzheimer’s Disease

Alzheimer’s Disease

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