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.

scholarly journals Alzheimer's 100th anniversary of death and his contribution to a better understanding of Senile dementia

2015 ◽  
Vol 73 (2) ◽  
pp. 159-162 ◽  
Author(s):  
Eliasz Engelhardt ◽  
Marleide da Mota Gomes
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Tangles ◽  
Senile Dementia ◽  
100Th Anniversary ◽  
Silver Impregnation ◽  
New Disease ◽  
Impregnation Technique ◽  
Alois Alzheimer

Initially the trajectory of the historical forerunners and conceptions of senile dementia are briefly presented, being highlighted the name of Alois Alzheimer who provided clinical and neuropathological indicators to differentiate a group of patients with Senile dementia. Alzheimer's examination of Auguste D’s case, studied by him with Bielschowsky’s silver impregnation technique, permitted to identify a pathological marker, the intraneuronal neurofibrillary tangles, characterizing a new disease later named after him by Kraepelin – Alzheimer’s disease. Over the time this disorder became one of the most important degenerative dementing disease, reaching nowadays a status that may be considered as epidemic.

Familial Pre-senile Dementia: The Relevance of a Histological Diagnosis of Pick's Disease

1973 ◽  
Vol 122 (571) ◽  
pp. 671-673 ◽  
Author(s):  
Myre Sim ◽  
R. N. Bale
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Diagnostic Criteria ◽  
Clinical Features ◽  
Senile Dementia ◽  
Histological Diagnosis ◽  
Pick's Disease ◽  
Pick’S Disease ◽  
Familial Cases ◽  
Cerebral Biopsy

The literature of familial pre-senile dementia is adequately reviewed by McMenemey (1963) and Pratt (1967) and that on familial forms of Alzheimer's disease by Tandy and Bain (1970). In non-familial cases of Alzheimer's disease it has been possible to correlate the clinical features with the histological diagnosis obtained from cerebral biopsy (Sim and Sussman, 1962; Sim et al., 1966), and the present paper is an attempt to see whether, by using similar diagnostic criteria as listed in Table I, including cerebral biopsy, a similar consistency could be demonstrated in the affected members of each family.

Characteristics of Insulin-degrading Enzyme in Alzheimer's Disease: A Meta-Analysis

2018 ◽  
Vol 15 (7) ◽  
pp. 610-617 ◽  
Author(s):  
Huifeng Zhang ◽  
Dan Liu ◽  
Huanhuan Huang ◽  
Yujia Zhao ◽  
Hui Zhou
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Enzyme Activity ◽  
Protein Level ◽  
Senile Plaque ◽  
Meta Analysis ◽  
Cochrane Library ◽  
Insulin Degrading Enzyme ◽  
Degrading Enzyme ◽  
Significant Difference

Background: β-amyloid (Aβ) accumulates abnormally to senile plaque which is the initiator of Alzheimer's disease (AD). As one of the Aβ-degrading enzymes, Insulin-degrading enzyme (IDE) remains controversial for its protein level and activity in Alzheimer's brain. Methods: The electronic databases PubMed, EMBASE, The Cochrane Library, OVID and Sinomed were systemically searched up to Sep. 20th, 2017. And the published case-control or cohort studies were retrieved to perform the meta-analysis. Results: Seven studies for IDE protein level (AD cases = 293; controls = 126), three for mRNA level (AD cases = 138; controls = 81), and three for enzyme activity (AD cases = 123; controls = 75) were pooling together. The IDE protein level was significantly lower in AD cases than in controls (SMD = - 0.47, 95% CI [-0.69, -0.24], p < 0.001), but IDE mRNA and enzyme activity had no significant difference (SMD = 0.02, 95% CI [-0.40, 0.43] and SMD = 0.06, 95% CI [-0.41, 0.53] respectively). Subgroup analyses found that IDE protein level was decreased in both cortex and hippocampus of AD cases (SMD = -0.43, 95% CI [-0.71, -0.16], p = 0.002 and SMD = -0.53, 95% CI [-0.91, -0.15], p = 0.006 respectively). However, IDE mRNA was higher in cortex of AD cases (SMD = 0.71, 95% CI [0.14, 1.29], p = 0.01), not in hippocampus (SMD = -0.26, 95% CI [-0.58, 0.06]). Conclusions: Our results indicate that AD patients may have lower IDE protease level. Further relevant studies are still needed to verify whether IDE is one of the factors affecting Aβ abnormal accumulation and throw new insights for AD detection or therapy.

Biological Signatures of Alzheimer’s Disease

2020 ◽  
Vol 20 (9) ◽  
pp. 770-781 ◽  
Author(s):  
Poornima Sharma ◽  
Anjali Sharma ◽  
Faizana Fayaz ◽  
Sharad Wakode ◽  
Faheem H. Pottoo
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Senile Plaque ◽  
Senile Plaques ◽  
Amyloid Deposition ◽  
Immune Defense ◽  
Amyloid Angiopathy ◽  
Microvascular Changes ◽  
Β Amyloid

Alzheimer’s disease (AD) is the most prevalent and severe neurodegenerative disease affecting more than 0.024 billion people globally, more common in women as compared to men. Senile plaques and amyloid deposition are among the main causes of AD. Amyloid deposition is considered as a central event which induces the link between the production of β amyloid and vascular changes. Presence of numerous biomarkers such as cerebral amyloid angiopathy, microvascular changes, senile plaques, changes in white matter, granulovascular degeneration specifies the manifestation of AD while an aggregation of tau protein is considered as a primary marker of AD. Likewise, microvascular changes, activation of microglia (immune defense system of CNS), amyloid-beta aggregation, senile plaque and many more biomarkers are nearly found in all Alzheimer’s patients. It was seen that 70% of Alzheimer’s cases occur due to genetic factors. It has been reported in various studies that apolipoprotein E(APOE) mainly APOE4 is one of the major risk factors for the later onset of AD. Several pathological changes also occur in the white matter which include dilation of the perivascular space, loss of axons, reactive astrocytosis, oligodendrocytes and failure to drain interstitial fluid. In this review, we aim to highlight the various biological signatures associated with the AD which may further help in discovering multitargeting drug therapy.

scholarly journals Senile plaque calcification of the lamina circumvoluta medullaris in Alzheimer's disease

2021 ◽  
Author(s):  
Ralf Schober ◽  
Isabel Hilbrich ◽  
Carsten Jäger ◽  
Max Holzer
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Senile Plaque

scholarly journals Endophytic Fungal Community of Huperzia serrata: Diversity and Relevance to the Production of Huperzine A by the Plant Host

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 892
Author(s):  
Lingli Cui ◽  
Hamza Armghan Noushahi ◽  
Yipeng Zhang ◽  
Jinxin Liu ◽  
Andreea Cosoveanu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fungal Community ◽  
Slow Growth ◽  
Specific Treatment ◽  
Huperzine A ◽  
Ionization Mass ◽  
Correlation Index ◽  
Plant Host ◽  
Huperzia Serrata

As the population ages globally, there seem to be more people with Alzheimer’s disease. Unfortunately, there is currently no specific treatment for the disease. At present, Huperzine A (HupA) is one of the best drugs used for the treatment of Alzheimer’s disease and has been used in clinical trials for several years in China. HupA was first separated from Huperzia serrata, a traditional medicinal herb that is used to cure fever, contusions, strains, hematuria, schizophrenia, and snakebite for several hundreds of years in China, and has been confirmed to have acetylcholinesterase inhibitory activity. With the very slow growth of H. serrata, resources are becoming too scarce to meet the need for clinical treatment. Some endophytic fungal strains that produce HupA were isolated from H. serrate in previous studies. In this article, the diversity of the endophytic fungal community within H. serrata was observed and the relevance to the production of HupA by the host plant was further analyzed. A total of 1167 strains were obtained from the leaves of H. serrata followed by the stems (1045) and roots (824). The richness as well as diversity of endophytic fungi within the leaf and stem were higher than in the root. The endophytic fungal community was similar within stems as well as in leaves at all taxonomic levels. The 11 genera (Derxomyces, Lophiostoma, Cyphellophora, Devriesia, Serendipita, Kurtzmanomyces, Mycosphaerella, Conoideocrella, Brevicellicium, Piskurozyma, and Trichomerium) were positively correlated with HupA content. The correlation index of Derxomyces with HupA contents displayed the highest value (CI = 0.92), whereas Trichomerium showed the lowest value (CI = 0.02). Through electrospray ionization mass spectrometry (ESI-MS), it was confirmed that the HS7-1 strain could produce HupA and the total alkaloid concentration was 3.7 ug/g. This study will enable us to screen and isolate the strain that can produce HupA and to figure out the correlation between endophytic fungal diversity with HupA content in different plant organs. This can provide new insights into the screening of strains that can produce HupA more effectively.

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.

scholarly journals Caretaker Obstreperous Behavior Rating Scale

1997 ◽  
Vol 8 (S3) ◽  
pp. 321-324 ◽  
Author(s):  
Joan M. Swearer ◽  
David A. Drachman
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rating Scale ◽  
Late Onset ◽  
Senile Dementia ◽  
Medical Personnel ◽  
Original Description ◽  
Behavior Rating Scale ◽  
Large Patient ◽  
Number Of Patients

Although Alzheimer's original description of the dementing disorder that bears his name emphasized the prominence of troublesome and disruptive behaviors, a systematic investigation of behavioral disturbances of dementia did not begin in earnest until the 1980s. At that time, as the neuropathologic identity of presenile Alzheimer's disease and late-onset “senile dementia” was recognized, the redefinition of Alzheimer's disease abruptly increased the number of patients diagnosed with this condition. Physicians and other medical personnel working with Alzheimer's disease patients recognized both the importance of abnormal behaviors in this now large patient population and the need to describe, classify, and quantify these behaviors.

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