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PubMedDate not supplied

Progression of Alzheimer-related neuritic plaque pathology in the entorhinal region, perirhinal cortex and hippocampal formation.

Extracellular deposits of the beta-amyloid protein and intraneuronal neurofibrillary changes are hallmarks of Alzheimer's disease. Neurofibrillary changes in the cell body of neurons are the neurofibrillary tangles, while beta-amyloid deposits containing dystrophic neurites with neurofibrillary changes are called neuritic plaques. beta-Amyloid deposits and neurofibrillary tangles display a sequential accumulation in the cerebral cortex. In the present study, the topographical distribution of beta-amyloid deposits and neuritic plaques in the entorhinal region, perirhinal cortex and hippocampal formation was investigated in relationship to the amyloid and neurofibrillary staging proposed by Braak. The number of subregions displaying beta-amyloid deposits and neuritic plaques continuously increases in correlation with the amyloid stage (for beta-amyloid deposits r = 0.90, p < 0.0001, for neuritic plaques r = 0.74, p < 0.0001) and neurofibrillary stage (for beta-amyloid deposits r = 0.53, p < 0.0001, for neuritic plaques r = 0.68, p < 0. 0001). Parallel to the advancement in the neurofibrillary stage, early and late predilection sites of beta-amyloid deposits and neuritic plaques can be distinguished. The early predilection sites correspond to projection areas of regions which exhibit incipient neurofibrillary tangles. Furthermore, neuritic plaques only occur in the presence of neurofibrillary tangles in the areas investigated. The findings indicate that neuritic plaques gradually develop in the projection areas of tangle-bearing neurons.

Aged↗
PubMed1998

Progression of Alzheimer histopathological changes.

The clinical-pathological correlations that were prospectively obtained in a cohort of old patients (> 75 years of age) are reviewed. The pathological data were obtained in 31 cases, either normal or affected by Alzheimer disease of various degrees of severity. The density of the A beta peptide deposits was poorly linked with the intellectual status. One patient had a very high density of deposits, although she was considered intellectually normal. When present in a patient, the A beta deposits usually involved all the cortical samples; the samples devoid of deposits most often belonged to the limbic system. The distribution of the neurofibrillary tangles was highly selective: the primary areas (such as the visual cortex) were lesioned only in a few cases, invariably the most severely affected ones. Neurofibrillary tangles involved the associative cortices (sparing the primary areas) in the cases of intermediate severity. The hippocampal-parahippocampal areas contained at least a few neurofibrillary tangles in all the cases. The prevalence of the neurofibrillary lesions in that cohort of cases probably indicated the chronological (and hierarchical) order of involvement: from limbic to associative, from associative to primary areas. There was a linear relationship between the density of the neurofibrillary tangles and the intellectual deficit in the hippocampal-parahippocampal gyrus. The relationship was stepwise rather than linear in the isocortical samples, suggesting that the neurofibrillary tangles were a late phenomenon in those types of cortices. An accumulation of SNAP 25 immunoreactivity was found in some of the most severely affected cases, pointing to a deficit in axonal transport. The density and the total number of neurons were evaluated in a sample of the supramarginal gyrus. The neuronal loss was found to be severe, but only in the most affected cases, when the density of neurofibrillary tangles was higher than 5/mm2.

Aged↗
PubMed1987

Recognition of Alzheimer paired helical filaments by monoclonal neurofilament antibodies is due to crossreaction with tau protein.

Neurofibrillary tangles and senile plaques are the principal pathological features of Alzheimer disease. Neurofibrillary tangles and the neurites of senile plaques contain paired helical filaments (PHF) that consist of two 10-nm filaments twisted into a double helix. The precursor proteins of PHF are not fully known. To identify these precursors, numerous immunochemical studies have been carried out during the past decade. Two apparently conflicting results have been reported. (i) Some, but not all, monoclonal antibodies to neurofilaments stained neurofibrillary tangles. (ii) Polyclonal antibodies prepared to PHF purified in NaDodSO4 because of their unusual insolubility did not recognize normal proteins, including neurofilaments, on electrophoretic transfer blots of human brain homogenates. These results have been confirmed in several laboratories, including by the use of electron microscopic labeling. Recently, we reported that polyclonal PHF antibodies include antibodies to tau proteins, a family of heat-stable microtubule-associated phosphoproteins, and that antibodies to tau stain Alzheimer neurofibrillary tangles. Those monoclonal neurofilament antibodies that recognize tangles are reported to be directed against phosphorylated epitopes. These facts prompted us to reexamine certain neurofilament monoclonal antibodies that stain neurofibrillary tangles. All monoclonal neurofilament antibodies that stain tangles that we examined, including those initially reported, reacted with tau proteins. Our results suggest that these antibodies react with phosphorylated tau proteins in PHF, not neurofilament proteins, highlighting the problem of using antibodies to phosphorylated protein epitopes in immunochemical studies. Independent evidence for the presence of neurofilament proteins in human paired helical filaments is now required.

Alzheimer Disease↗
PubMed1996

The neuropathological changes associated with normal brain aging.

Neurofibrillary tangles and senile plaques are common neuropathological features in both normal brain aging and Alzheimer's disease. In order to examine the patterns of lesion distribution in cerebral aging, we review the clinicopathological analysis of 1144 nondemented cases comparing their neuropathologic features to that reported in cases with mild cognitive impairment and cases with Alzheimer's disease. Regardless of cognitive status, layer II of the entorhinal cortex is involved with neurofibrillary tangle formation in all of the cases, while the CA1 field of the hippocampus and the subiculum are less consistently affected. Neocortical area 20 is particularly prone to develop neurofibrillary tangles in intellectually preserved elders, whereas other neocortical areas are relatively spared. Substantial senile plaque formation is seen in the neocortex of non-demented cases. Quantitatively, mild cognitive impairment is correlated with neurofibrillary tangle densities in layer II of the entorhinal cortex, and clinically overt Alzheimer's disease with neurofibrillary tangle densities in area 20. In non-demented centenarians, there is an early development of neurofibrillary tangles in areas usually spared in the course of the degenerative process in younger individuals. These observations demonstrate that mesial and inferior temporal lobe structures are affected more frequently than originally thought in normal brain aging. In this respect, neurofibrillary tangle formation in area 20 may represent a crucial step of the degenerative process, because it may precede the emergence of the neuropsychological deficits characteristic of Alzheimer's disease. In addition, this study reveals age-related heterogeneity in the regional vulnerability of the cerebral cortex during normal brain aging.

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PubMed2002

Parahippocampal tau pathology in healthy aging, mild cognitive impairment, and early Alzheimer's disease.

Abnormally phosphorylated tau accumulates as neurofibrillary tangles and neuropil threads in older persons with and without Alzheimer's disease. The relationship between neurofibrillary tangles and neuropil threads and how they relate to cognitive function is unknown. This study investigated the relationship between phosphorylated tau lesions and cognitive function in 31 persons participating in the Religious Orders Study, a prospective, longitudinal clinicopathological study of aging and Alzheimer's disease. All subjects underwent detailed neuropsychological performance testing within a year of death and evidenced a spectrum of cognitive performance ranging from normal abilities to mild dementia. Measures of neurofibrillary tangle density and phosphorylated tau immunoreactive structures (predominantly neuropil threads) in the entorhinal and perirhinal cortices by quantitative image analysis were significantly correlated (r = 0.5). In multiple linear regression analyses controlling for age, sex, and education, parahippocampal neurofibrillary tangles and neuropil threads were significantly lower in persons without cognitive impairment compared to those with mild cognitive impairment and/or Alzheimer's disease. Further, neurofibrillary tangles were significantly correlated to measures of episodic memory but not other cognitive abilities; neuropil tangles were not significantly related to memory or other cognitive functions. These data indicate that phosphorylated tau pathology in the ventromedial temporal lobe develop prior to the onset of clinical dementia and their presence is associated with cognitive impairment, particularly impairment of episodic memory.

Aged↗
PubMedDate not supplied

[Alzheimer's disease and the zinc theory].

UNLABELLED: In Alzheimer's disease, the Primum Movens is amyloid production on precapillaries: dysphoric angiopathy, and capillaries: senile plaques. Cerebral amyloid alone may be asymptomatic. Clinical symptoms of amnesia appear when amyloid induces neighbouring neuritic alterations: paired helical filaments and distant neuronal body lesions: neurofibrillary tangles. HYPOTHESIS: the amyloid induces zinc deficiency which produces the tangles. In Alzheimer's disease, cerebral zinc decreases particularly in the hippocampus. Without amyloid, neurofibrillary tangles are produced by metalotoxicity and therefore probably brain zinc displacement: by lead: encephalopatia saturnica, by calcium deficiency: Guam's encephalopathy, by aluminium, by blood-brain-barrier disturbances probably leading to an abnormal entry of metals in the brain (dementia pugilistica, viral encephalitides). Neurofibrillary tangles may be produced by deficiency of the following zinc enzymes: 1) those of DNA metabolism inducing abnormal DNA and therefore abnormal protein synthesis: paired helical filaments and neurofibrillary tangles; 2) of glutamate-dehydrogenase resulting in an excitotoxic increase of glutamate, which may produce neurofibrillary tangles, particularly in the hippocampus rich in glutamate pathways; 3) those of neuronal detoxication: superoxide-dismutase, carbonic anhydrase, lactate-dehydrogenase leading to neuronal toxicity particularly in the hippocampus normally rich in superoxide dismutase; 4) those of neurotransmitters metabolisms (opioid peptides, GABA, acetylcholine). Therapeutic implication: a non-toxic zinc complex crossing the Blood-Brain-Barrier should be useful.

Adult↗
PubMed1999

Agrin is a major heparan sulfate proteoglycan accumulating in Alzheimer's disease brain.

Heparan sulfate proteoglycans (HSPGs) have been suggested to play an important role in the formation and persistence of senile plaques and neurofibrillary tangles in dementia of the Alzheimer's type (DAT). We performed a comparative immunohistochemical analysis of the expression of the HSPGs agrin, perlecan, glypican-1, and syndecans 1-3 in the lesions of DAT brain neocortex and hippocampus. Using a panel of specific antibodies directed against the protein backbone of the various HSPG species and against the glycosaminoglycan (GAG) side-chains, we demonstrated the following. The basement membrane-associated HSPG, agrin, is widely expressed in senile plaques, neurofibrillary tangles and cerebral blood vessels, whereas the expression of the other basement membrane-associated HSPG, perlecan, is lacking in senile plaques and neurofibrillary tangles and is restricted to the cerebral vasculature. Glypican and three different syndecans, all cell membrane-associated HSPG species, are also expressed in senile plaques and neurofibrillary tangles, albeit at a lower frequency than agrin. Heparan sulfate GAG side chains are also associated with both senile plaques and neurofibrillary tangles. Our results suggest that glycosaminoglycan side chains of the HSPGs agrin, syndecan, and glypican, but not perlecan, may play an important role in the formation of both senile plaques and neurofibrillary tangles. In addition, we speculate that agrin, because it contains nine protease-inhibiting domains, may protect the protein aggregates in senile plaques and neurofibrillary tangles against extracellular proteolytic degradation, leading to the persistence of these deposits.

Aged↗
PubMed2000

Neurofibrillary tangle-associated collapsin response mediator protein-2 (CRMP-2) is highly phosphorylated on Thr-509, Ser-518, and Ser-522.

3F4, a monoclonal antibody raised against partially purified paired helical filaments (PHFs), strongly labeled neurofibrillary tangles and some plaque neurites but barely labeled neuropil threads. The levels of the 65-kDa antigen were significantly increased in the soluble fraction of the brains affected by Alzheimer's disease (AD), as compared with that in the case of control brains. The antigen was previously identified as human collapsin response mediator protein-2 (hCRMP-2) by sequencing the immunoaffinity-purified 65-kDa antigen [Yoshida, H., Watanabe, A., and Ihara, Y. (1998) J. Biol. Chem. 273, 9761-9768]. Here, we show that the 3F4 antigen represents a highly phosphorylated form of CRMP-2. The 3F4-reactive phosphoepitope was localized to the carboxyl-terminal portion of hCRMP-2, and was created by a novel 45-50-kDa protein kinase in rat brain extract. Site-directed mutagenesis of this portion showed that multiple sites of CRMP-2 are differentially phosphorylated within residues 507-522, and that phosphorylation of three sites, Thr-509, Ser-518, and Ser-522, is required for full 3F4 binding. The phosphorylation of this particular portion carboxyl-terminal to the basic region of CRMP-2 may play an important role in regulating its activity, and may be involved in the formation of degenerating neurites in AD brain.

Alzheimer Disease↗
PubMed1995

Alzheimer's changes in non-demented and demented patients: a statistical approach to their relationships.

The anterior hippocampus and the entorhinal cortex of 167 non-demented individuals (controls) and 22 patients with Alzheimer's dementia were investigated. Senile plaques and neurofibrillary tangles were counted on paraffin sections stained with methenamin silver and Gallyas silver iodide, respectively. The results showed that both senile plaques and neurofibrillary tangles areal densities (lesions per mm2) correlated significantly with age in the control collective. No significant correlation between Alzheimer's disease lesions and age was found in patients with Alzheimer's dementia. Positive and significant correlation between senile plaques and neurofibrillary tangles was found in the control group but not in the Alzheimer group. Control individuals (n = 43, matched for age with the Alzheimer group) displayed both plaques and tangles. In this subgroup neither plaques nor tangles correlation with age; however, there was a significant correlation between senile plaques and neurofibrillary tangles. We hypothesize that the continuous activity of underlying processes associated with senile plaques and neurofibrillary tangles formation or resolution might lead to the unbalanced production of these lesions in Alzheimer's disease.

Adult↗
PubMed2001

Neuronal and glial advanced glycation end product [Nepsilon-(carboxymethyl)lysine]] in Alzheimer's disease brains.

The cellular distribution of an advanced glycation end product [Nepsilon-(carboxymethyl)lysine (CML)] in aged and Alzheimer's disease (AD) brains was assessed immunohistochemically. CML was localized in the cytoplasm of neurons, astrocytes, and microglia in both aged and AD brains. Glial deposition was far more marked in AD brains than in aged brains, and neuronal deposition was also increased. On electron microscopic immunohistochemistry, neuronal CML formed granular or linear deposits associated with lipofuscin, and glial deposits formed lines around the vacuoles. Neuronal and glial deposits were prominent throughout the cerebral cortex and hippocampus, but were sparse in the putamen, globus pallidus, substantia nigra, and cerebellum, with glial deposits being far more prominent in AD brains. The distribution of neuronal and glial deposits did not correspond with the distribution of AD pathology. The extent of CML deposits was inversely correlated with neurofibrillary tangle formation, particularly in the hippocampus. Most hippocampal pyramidal neurons with neurofibrillary tangles did not have CML, and most of the neurons with heavy CML deposits did not have neurofibrillary tangles. In the hippocampus, neuronal CML was prominent in the region where neuronal loss was mild. These observations suggest that CML deposition does not directly cause neurofibrillary tangle formation or neuronal loss in AD.

Aged↗
PubMed1989

Aluminum-induced neurofibrillary degeneration affects a subset of neurons in rabbit cerebral cortex, basal forebrain and upper brainstem.

Neurofibrillary tangles in Alzheimer's disease show a predilection for cortical pyramidal and subcortical projection neurons. The antigenic composition, neuronal specificity and distribution of aluminum-induced neurofibrillary degeneration were examined in regions of rabbit brain analogous to those that develop neurofibrillary tangles in Alzheimer's disease. Neurofibrillary degeneration was induced by intraventricular instillation of aluminum chloride. In aluminum-treated rabbits, intensely immunoreactive filamentous aggregates were seen in affected neuronal perikarya after staining with an antiphosphorylated neurofilament antibody (SMI 31), while in controls immunoreactivity was confined to axon-like elements. Monoclonal antibodies against Microtubule-associated protein 2 and tau, which stain human neurofibrillary tangles, did not stain aluminum-induced neurofibrillary degeneration. Pyramidal neurons exhibiting neurofibrillary degeneration formed a discrete linear pattern in layers III and V of cortex. Cortical somatostatin and nicotinamide adenine dinucleotide phosphate diaphorase-reactive neurons identified in double-stained sections were unaffected. Large perikarya in the vicinity of the globus pallidus, some of which contained acetylcholinesterase, were frequently SMI 31-immunoreactive. Among the cell groups affected in the upper brainstem were the nucleus raphe dorsalis and locus coeruleus. These findings show that aluminum-induced neurofibrillary degeneration differs antigenically from neurofibrillary tangles in Alzheimer's disease. Nevertheless, many neuronal subsets that are particularly susceptible to Alzheimer's disease, including cortical pyramidal neurons, basal forebrain cholinergic neurons and upper brainstem catecholaminergic neurons, are also affected by aluminum-induced neurofibrillary degeneration.

Aluminum↗
PubMed1994

Neuropathological changes in the cerebral cortex of 1258 cases from a geriatric hospital: retrospective clinicopathological evaluation of a 10-year autopsy population.

To examine the neuropathological and clinical characteristics of cerebral aging, we evaluated retrospectively a non-selected autopsy population of 1258 patients from the Geriatric Hospital of the University of Geneva School of Medicine. The prevalence of Alzheimer's disease increased with age below 90 years of age. In the nonagenarians and centenarians, there was a decline in the number of affected cases. The distribution with age of neurofibrillary tangles and senile plaques varied among the cortical areas studied. The CA1 field of the hippocampus and the inferior temporal cortex displayed increasing densities of neurofibrillary tangles with age, whereas the superior frontal and the occipital cortex were relatively spared, especially in patients in their tenth and eleventh decade. The percentage of cases presenting with senile plaques in the neocortex and hippocampal structure increased with age with a marked predominance of cases with moderate to high senile plaque densities. Neurofibrillary tangles were often observed in the CA1 field and the inferior temporal cortex of non-demented individuals and were present in most cases with Alzheimer's disease. Conversely, the involvement of the superior frontal and occipital cortex was moderate even in demented patients. The distribution of senile plaques was homogeneous in all of the neocortical areas independently of the clinical diagnosis. Moreover, there was no correlation between the presence of neurofibrillary tangles and senile plaques in the cerebral regions studied. These results indicate a differential topography of neurofibrillary tangles and senile plaques, and suggest that overt clinical signs of Alzheimer's disease are linked to the progression of the neurodegenerative process in neocortical areas.

Age Factors↗
PubMed1980

Alzheimer's disease: X-ray spectrometric evidence of aluminum accumulation in neurofibrillary tangle-bearing neurons.

The elemental content of neurons of the hippocampus was studied by a combination of scanning electron microscopy and x-ray spectrometry in autopsy-derived brain tissue from three cases of senile dementia (Alzheimer type) and three nondemented elderly controls. Foci of aluminum were detected within the nuclear region of a high percentage of neurons containing neurofibrillary tangles from the cases of senile dementia as well as the elderly controls. The adjacent normal-appearing neurons from both groups of patients were virtually free of detectable aluminum. These findings suggest that the association of aluminum to Alzheimer's disease extends to the neuronal level.

Aluminum↗
PubMed1994

Clinical correlates of cortical and nucleus basalis pathology in Alzheimer dementia.

OBJECTIVE: We correlated severity of dementia in Alzheimer's disease with the degree of neuropathology in cortical and subcortical brain regions. METHODS: In 13 patients with Alzheimer's disease who underwent neuropsychological testing before death, we assessed neurofibrillary tangles, senile plaques, and neuronal and synaptic density in the midfrontal cortex and the nucleus basalis of Meynert. RESULTS: In the midfrontal cortex, synapse density was the strongest correlate of dementia severity, followed by neurofibrillary tangles. In the nucleus basalis, by contrast, neurofibrillary tangles were the strongest correlate, followed by synapse density. Stepwise regression analyses showed midfrontal synapse density to be the strongest predictor of tests emphasizing higher cortical functions, but neurofibrillary tangles in the nucleus basalis were the strongest predictor on memory-oriented tests. CONCLUSIONS: The specificity of pathology in cortical vs subcortical locations for predicting a particular quality of neuropsychological deficit probably reflects disruption of corticocortical connections vs derangement of the basal forebrain cholinergic system.

Aged↗
PubMed1995

Age-related distribution of neuropathologic changes in the cerebral cortex of patients with Down's syndrome. Quantitative regional analysis and comparison with Alzheimer's disease.

OBJECTIVE: To investigate whether changes in the cerebral cortex exhibit similar distribution patterns in both disorders of Down's syndrome and Alzheimer's disease, we performed a comparative neuropathologic study of patients with these disorders to further clarify the possible relationships between these dementing conditions. DESIGN: The regional and laminar distribution and density of neurofibrillary tangles and senile plaques were analyzed in the cerebral cortex of a series of 16 patients (aged 6 to 74 years) with Down's syndrome and in 10 elderly individuals with Alzheimer's disease. RESULTS: Quantitative analyses revealed that the time course of neurofibrillary tangle formation in Down's syndrome displays regional patterns comparable with those observed in aging and Alzheimer's disease with layer II of the entorhinal cortex being affected first in Down's syndrome, followed by the hippocampus proper and neocortex. The oldest patients with Down's syndrome had neurofibrillary tangle densities sometimes higher than in patients with Alzheimer's disease. At variance with Alzheimer's disease, amyloid deposition was widespread in all of the cortical areas investigated and was observed much earlier than neurofibrillary tangle formation. Patients with Down's syndrome also frequently had higher senile plaque densities than patients with Alzheimer's disease. CONCLUSIONS: These results indicate that the development of pathologic changes in patients with Down's syndrome does not parallel that observed in elderly individuals and patients with Alzheimer's disease in all respects. However, the comparable development patterns of neurofibrillary tangle formation suggest that detailed analysis of patients with Down's syndrome may be useful to further our knowledge of the mechanisms underlying the installation of the neuropathologic alterations leading to the demonstrated loss of select neuronal populations in Alzheimer's disease.

Adolescent↗
PubMed1995

Distribution of tangles and threads in the cerebral cortex in progressive supranuclear palsy.

Recent studies have described silver- and tau-positive glia and threads in the degenerating lesions of progressive supranuclear palsy. In this study, Gallyas-Braak silver impregnation and several immunohistochemical techniques were employed to examine the distribution of tangles, abnormal glia and threads in the cerebral cortex of nine cases of progressive supranuclear palsy. In addition to neurofibrillary tangles, argentophilic glia and threads were impregnated exclusively by Gallyas-Braak technique. This technique demonstrated two types of glia profiles: tightly coiled intra-cytoplasmic profiles surrounding nuclei (coiled profiles) and thorn-like profiles with radial ramifications (thorn-like profiles). Thorn-like profiles are possibly in astrocytes and were detected in the cerebral cortex, while coiled profiles are possibly in oligodendroglia and were detected both in the cerebral cortex and subcortical white matter. Topographically, many neurofibrillary tangles were constantly seen in the frontal cortex and in the pre-central gyrus. Numerous neurofibrillary tangles were detected in the entorhinal cortex of the two brains. Argentophilic glia and threads were also frequent both in the frontal cortex and the precentral gyrus; however, they were more frequent in the pre-central gyrus that in the frontal cortex in four of the eight cases examined. In two brains, argentophilic threads were distributed widely in the cerebral cortex and white matter except for the temporal cortex. In immunohistochemical studies, argentophilic glia and threads were mostly positive for Tau 2, and a small number of them were weakly positive for ubiquitin and paired helical filament protein. The immunoproperties of these abnormal glia and threads seemed to be virtually identical to those of neurofibrillary tangles.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1997

[An elderly patient with progressive supranuclear palsy without neurological signs].

We report an elderly patient with progressive supranuclear palsy (PSP) who showed no neurological signs clinically. A 70-year-old man presented with irritation and poor hygiene, thereafter he showed excitement and violence. A cranial CT scan revealed bilateral moderate atrophy of the temporal lobes and slight enlargement of the lateral ventricle. The brain stem was slightly atrophic. Although he died at the age of 80 years, he had no neurological signs throughout the clinical course. Neuropathological study showed typical findings of PSP, neuronal loss with gliosis and neurofibrillary tangles in the basal ganglia, amygdala, midbrain, pons, dentate nucleus and inferior olivary nucleus. Staining by Gallyas-Braak methods revealed argyrophilic and tau-positive glial fibrillary tangles in the cerebral cortex. Neurofibrillary tangles showed greater frequency than usual for the physiological level in that age group in the hippocampus regions as well as in the amygdala. The possibility that the psychotic symptoms, mainly personality change, are connected with the degeneration of limbic system is indicated. Since there have not been any previous reports of PSP without neurological signs, this case represents an important in terms of clinico-pathological variation of PSP. We suggest that there is discrepancy between symptomatic and neuropathological aspects in elderly patients with PSP.

Aged↗
PubMed1992

The pathology of the neuronal cytoskeleton in Alzheimer's disease.

The two characteristic neuropathological lesions of Alzheimer's disease are the neurofibrillary tangles and the senile plaques. Neurofibrillary tangles are made of abnormal filaments (PHF) accumulating in neurons and mainly composed of a modified form of the microtubule-associated protein tau (PHF-tau). Senile plaques are composed of a cluster of dystrophic neurites surrounding an extracellular deposit of amyloid fibers made of a 42 amino-acid peptide (beta-amyloid peptide). The abnormal filaments contain the complete sequences of the different tau isoforms. The PHF-tau proteins can be distinguished from the normal tau proteins by the presence of several phosphorylated sites. One of these sites is phosphorylated by a calcium-calmodulin-dependent kinase. The relationship between PHF-tau and the cytoskeletal pathology in Alzheimer's disease is further discussed.

Aged↗