Summary
Senile plaques and neurofibrillary tangles are the markers of Alzheimer’s disease. They are also found in old patients who have been considered to be intellectually normal throughout their life, a situation referred to as “physiological aging”. The neurofibrillary tangles are made of abnormally phosphorylated tau. The anti-tau antibody labels not only the neurofibrillary tangles, but also the crown of the senile plaques and the neuropil threads interspersed between the cell bodies and the plaques. The senile plaque comprises a core made of Aβ peptide surrounded by a neuritic crown. The anti-Aβ antibody also labels “diffuse deposits”, i.e. ill limited areas of immunoreactivity which lacks the characteristics of the amyloid substance. The intellectual deficit appears to be statistically linked with the density of the tau-positive alterations -tangles, threads and plaque crowns — which usually appear simultaneously in a given cortical area. In the entorhinal area, their density increases proportionally to the intellectual deficit without threshold, suggesting that ageing and disease are a continuum. In the isocortex, the progression of the tau positive alterations is, on the contrary, stepwise — in a “all or none” fashion — from the hippocampus to the primary cortices, through the associative multimodal areas. The tau positive lesions probably progress through connections: they indeed disappear from areas, that have been disconnected by additional lesions (such as infarcts).
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References
Alzheimer A (1911) Über eigenartige Krankheitsfälle des späteren Alters. Zbl Ges Neurol Psychiat 4: 356–385
Bancher C, Jellinger KA (1994) Neurofibrillary tangle predominant form of Alzheimer’s disease: a rare subtype in very old subjects. Acta Neuropathol 84: 565–570
Bancher C, Brunner C, et al (1989) Accumulation of abnormally phosphorylated tau precedes the formation of neurofibrillary tangles in Alzheimer’s disease. Brain Res 477: 90–99
Bancher C, Jellinger K, Lassmann H, Fischer P, Leblhuber F (1996) Correlations between mental state and quantitative neuropathology in the Vienna Longitudinal Study on Dementia. Eur Arch Psychiat Clin Neurosci 246: 137–146
Berg L, McKeel DW, Miller P, Baty J, Morris JC (1993) Neuropathological indexes of Alzheimer’s disease in demented and nondemented persons aged 80 years and older. Arch Neurol 50: 349–358
Blessed G, Tomlinson BE, Roth M (1968) The association between quantitative measures of dementia and of senile change in the cerebral grey matter of elderly subjects. Br J Psychiatry 114: 797–811
Braak H, Braak E (1991) Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 82: 239–259
Braak H, Braak E, Grundke-Iqbal I, Iqbal K (1986) Occurrence of neuropil threads in the senile human brain and in Alzheimer’s disease. A 3rd location of paired helical filaments outside of neurofilament tangles and neuritic plaques. Neurosci Lett 65: 351–355
Braak H, Duyckaerts C, Braak E, Piette F (1993) Neuropathological staging of Alzheimer-related changes correlates with psychometrically assessed intellectual status. In: Corain B, Iqbal K, Nicolini M, Winblad B, Wisniewski H, Zatta P (eds) Alzheimer’s disease: advances in clinical and basic reserch. Wiley, Chichester, pp 131–137
Brion JP, Passareiro H, Nunez J, Flament-Durand J (1985) Mise en évidence immunologique de la protéine tau au niveau des lésions de dégénérescence neurofibrillaire de la maladie d’Alzheimer. Arch Biol (Brux) 95: 229–235
Delaère P, Duyckaerts C, Brion JP, Poulain V, Hauw J-J (1989) Tau, paired helical filaments and amyloid in the neocortex: a morphometric study of 15 cases with graded intellectual status in aging and senile dementia of Alzheimer type. Acta Neuropathol 77: 645–653
Delaère P, Duyckaerts C, Masters C, Piette F, Hauw J-J (1990) Large amounts of neocortical βA4 deposits without Alzheimer changes in a nondemented case. Neurosci Lett 116: 87–93
Delaère P, Duyckaerts C, He Y, Piette F, Hauw J-J (1991) Subtypes and differential laminar distributions of βA4 deposits in Alzheimer’s disease: relationship with the intellectual status of 26 cases. Acta Neuropathol 81: 328–335
Dessi F, Colle MA, Hauw J-J, Duyckaerts C (1997) Accumulation of SNAP-25 immunoreactive material in axons of Alzheimer’s disease. Neuroreport 8: 3685–3689
Dickson DW, Crystal HA, Mattiace LA, Masur DM, Blau AD, Davies P, Yen SH, Aronson MK (1991) Identification of normal and pathological aging in prospectively studied nondemented elderly humans. Neurobiol Aging 13: 179–189
Divry P (1927) Etude histochimique des plaques séniles. J Belge Neurol Psychist 9: 649–657
Duyckaerts C, Hauw J-J, Piette F, Rainsard C, Poulain V, Berthaux P, Escourolle R (1985) Cortical atrophy in senile dementia of the Alzheimer type is mainly due to a decrease in cortical length. Acta Neuropathol 66: 72–74
Duyckaerts C, Hauw JJ, Bastenaire F, Piette F, Poulain C, Rainsard V, Javoy-Agid F, Berthaux P (1986) Laminar distribution of neocortical plaques in senile dementia of the Alzheimer type. Acta Neuropathol 70: 249–256
Duyckaerts C, Brion J-P, Hauw J-J, Flament-Durand J (1987) Quantitative assessment of the density of neurofibrillary tangles and senile plaques in senile dementia of the Alzheimer type. Comparison of immunocytochemistry with a specific antibody and Bodian’s protargol method. Acta Neuropathol 73: 167–170
Duyckaerts C, Delaère P, Poulain V, Brion JP, Hauw J-J (1988) Does amyloid precede paired helical filaments in the senile plaque? A study of 15 cases with graded intellectual status in aging and Alzheimer disease. Neurosci Lett 91: 354–359
Duyckaerts C, Kawasaki H, Delaère P, Rainsard C, Hauw J-J (1989) Fiber disorganization in the neocortex of patients with senile dementia of the Alzheimer type. Neuropathol Appl Neurobiol 15: 233–247
Duyckaerts C, Uchihara T, Seilhean D, He Y, Hauw J-J (1997) Dissociation of Alzheimer type pathology in a disconnected piece of cortex. Acta Neuropathol 93: 501–507
Duyckaerts C, Dolle MA, Seilhean D, Hauw J-J (1997) La spongiose laminaire du gyrus denté: un signe de désafférentation observé dans la maladie d’Alzheimer. De la neurophysiologie à la maladie d’Alzheimer. In: Besson JM, Bassant MH, Calvino B, Epelbaum J, Forette F, Lamour M, Pierrot-Deseilligny C, Christen Y (eds) Symposium en hommage à Yvon Lamour. Solal, Marseille, pp 173–182
Duyckaerts C, Bennecib M, Grignon Y, Uchihara T, He Y, Piette F, Hauw J-J (1997) Modeling the relation between neurofibrillary tangles and intellectual status. Neurobiol Aging 18: 267–273
Fischer O (1907) Miliare Nekrosen mit drusigen Wucherungen der Neurofibrillen, eine regelmässige Veränderung der Hirnrinde bei seniler Demenz. Monatschr Psychiat Neurol 22: 361–372
Fischer O (1910) Die presbyophrene Demenz, deren anatomische Grundlage und klinische Abgrenzung. Z Ges Neurol Psychiatr 3: 371–471
Glenner GG, Wong CW (1984) Alzheimer’s disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. Biochem Biophys Res Commun 120: 885–890
Gomez-Isla T, Price JL, McKeel DW, Morris JC, Growdon JH, Hyman BT (1996) Profound loss of layer II entorhinal cortex neurons occurs in very mild Alzheimer’s disease. J Neurosci 16: 4491–4500
Grignon Y, Duyckaerts C, Bennecib M, Hauw J-J (1998) Cytoarchitectonic alterations in the supramarginal gyrus of late onset Alzheimer disease. Acta Neuropathol 95: 395–406
Hauw J-J, Uchihara T, He Y, Seilhean D, Piette F, Duyckaerts C (1997) The time course of lesions in the neocortex in ageing and Alzheimer disease. In: Iqbal K, Winblad B, Nishimura T, Takeda M, Wisniewski HM (eds) Alzheimer’s disease: biology, diagnosis and therapeutics. Wiley, Chichester
Masliah E, Terry RD (1993) Role of synaptic pathology in the mechanisms of denervation in Alzheimer disease. Clin Neurosci 4: 192–198
Terry RD, Gonatas JK, Weiss M (1964) Ultrastructural studies in Alzheimer presenile dementia. Am J Pathol 44: 269–297
Terry RD, Masliah E, Salmon DP, Butters N, DeTeresa R, Hill R, Hansen LA, Katzman R (1991) Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol 30: 572–580
Terry RD, Masliah E, Hansen LA (1994) Structural basis of the cognitive alterations in Alzheimer disease. In: Terry RD, Katzman R, Bick KL (eds) Alzheimer disease. Raven Press, New York, pp 179–196
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Duyckaerts, C., Colle, M.A., Dessi, F., Grignon, Y., Piette, F., Hauw, JJ. (1998). The progression of the lesions in Alzheimer disease: insights from a prospective clinicopathological study. In: Jellinger, K., Fazekas, F., Windisch, M. (eds) Ageing and Dementia. Journal of Neural Transmission. Supplementa, vol 53. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6467-9_10
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DOI: https://doi.org/10.1007/978-3-7091-6467-9_10
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