Sequence of neurofibrillary changes in aging and Alzheimer's disease: A confocal study with phospho-tau antibody, AD2

2001 ◽  
Vol 3 (4) ◽  
pp. 417-425 ◽  
Author(s):  
M. Galván ◽  
J.P. David ◽  
A. Delacourte ◽  
J. Luna ◽  
R. Mena
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Changes

Neuropathological Alzheimer’s Disease Lesions in Nasu-Hakola Disease with TREM2 Mutation: Atypical Distribution of Neurofibrillary Changes

2021 ◽  
Vol 79 (1) ◽  
pp. 25-30
Author(s):  
Emanuela Maderna ◽  
Silvia Visonà ◽  
Vittorio Bolcato ◽  
Veronica Redaelli ◽  
Paola Caroppo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Autosomal Recessive ◽  
Cerebral Atrophy ◽  
Autosomal Recessive Disorder ◽  
Homozygous Mutation ◽  
Neurofibrillary Changes ◽  
Axonal Spheroids ◽  
Temporal Structures ◽  
Cortical Involvement

Nasu-Hakola disease is a rare autosomal recessive disorder associated to mutations in TREM2 and DAP12 genes, neuropathologically characterized by leukoencephalopathy with axonal spheroids. We report the neuropathologic findings of a 51-year-old female with a homozygous mutation (Q33X) of TREM2 gene. Beside severe cerebral atrophy and hallmarks of Nasu-Hakola disease, significant Alzheimer’s disease lesions were present. Neurofibrillary changes showed an atypical topographic distribution being severe at spots in the neocortex while sparing the mesial temporal structures. Our finding suggests that TREM2 genetic defects may favor Alzheimer’s disease pathology with neurofibrillary changes not following the hierarchical staging of cortical involvement identified by Braak.

Receptor-G-protein signalling in Alzheimer's disease

2001 ◽  
Vol 67 ◽  
pp. 163-175 ◽  
Author(s):  
Richard F. Cowburn ◽  
Cora O'Neill ◽  
Willy L. Bonkale ◽  
Thomas G. Ohm ◽  
Johan Fastbom
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Kinase ◽  
G Protein ◽  
Radioligand Binding ◽  
Phosphoinositide Hydrolysis ◽  
Binding Studies ◽  
Neurofibrillary Changes ◽  
Hydrolysis Pathway ◽  
Stimulation Of

Based on radioligand binding studies, it has long been assumed that the neurochemical pathology of Alzheimer's disease (AD) does not involve widespread changes in post-synaptic neurotransmitter function. However, more recent studies suggest that receptor function in AD may be compromised due to disrupted post-receptor signal transduction, in particular that mediated by the G-protein regulated phosphoinositide hydrolysis and adenylate cyclase (AC) pathways. The phosphoinositide hydrolysis pathway has been shown to be altered at a number of levels in AD post-mortem brains, including impaired agonist and G-protein regulation of phospholipase C, decreased protein kinase C (PKC) levels and activity, and a reduced number of receptor sites for the second messenger, Ins(1,4,5)P3. Of these, loss of Ins(1,4,5)P3 receptors and PKC in the entorhinal cortex and hippocampus correlates with AD-related neurofibrillary changes, as staged according to Braak's protocol. Disregulation of the phosphoinositide hydrolysis pathway may therefore have consequences for the progression of AD pathology. In contrast to the extensive pattern of disruption seen with the phosphoinositide hydrolysis pathway, changes to AC signalling in AD appear more circumscribed. Disruptions include a lesion at the level of Gs-protein stimulation of AC and, at least in the hippocampus, reduced enzyme activities in response to forskolin stimulation. Of these, the latter change has been shown to precede neurofibrillary changes. Apart from a loss of calcium/calmodulin sensitive AC isoforms, other components of this signalling pathway, including G-protein levels, Gi-protein mediated inhibition and protein kinase A levels and activity, remain relatively preserved in the disorder.

Age, neurofibrillary changes, Aβ-amyloid and the onset of Alzheimer's disease

1996 ◽  
Vol 210 (2) ◽  
pp. 87-90 ◽  
Author(s):  
Heiko Braak ◽  
Eva Braak ◽  
Jürgen Bohl ◽  
Ralf Reintjes
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Changes ◽  
Aβ Amyloid

Alzheimer's Disease Confirmed by Cerebral Biopsy: a Therapeutic Trial with Cortisone and A.C.T.H.

1955 ◽  
Vol 101 (424) ◽  
pp. 604-609 ◽  
Author(s):  
M. Sim ◽  
W. Thomas Smith
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Senile Plaque ◽  
Senile Dementia ◽  
Specific Treatment ◽  
Silver Impregnation ◽  
Therapeutic Trial ◽  
Progressive Dementia ◽  
Neurofibrillary Changes ◽  
Cerebral Biopsy

This paper describes treatment with cortisone and A.C.T.H. of two patients in whom Alzheimer's Disease (A.D.) had been confirmed histologically by cerebral biopsy.A.D. is a progressive dementia which usually occurs between the ages of 40 and 60 years, and there is no known specific treatment. Intellectual deterioration, which progresses insidiously over a period of 2–10 years, leads to gross dementia, and the inevitable problems of care and supervision often necessitate removal to an institution. Histologically the disease is characterized by atrophy of cortical nerve cells and the presence within the cortex of argentophile plaques which are demonstrable by the silver impregnation techniques of Bielschowsky or von Braunmühl (see Fig. 1); these plaques have a mixed granular and fibrillary structure. The same silver methods also show irregular thickening and disorientation of the nerve cell fibrils, which form “tangles” and “loops” (see Fig. 2). Identical plaques and neurofibrillary changes are also seen in senile dementia, the term “senile plaque” being used in both diseases.

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