Alzheimer's disease(AD) is a progressive dementia characterized by global cognitive decline and is defined pathologically by amyloid plaques and neurofibrillary tangles. In the past 10 years, important progress has been made in the understanding of the pathogenic mechanism of AD, and new therapeutic targets have become available that should allow the underlying disease process to be tackled directly. In this respect, the 'amyloid hypothesis' has been become the dominant theory in the cause of AD. New strategies for conquering the AD include attempts to stop the production of beta-amyloid protein(Abeta), increasing Abeta clearance, or interfere with Abeta aggregation and precipitation into fibril or plaques. This review summarizes recent advances in research on AD and inspects the perspective of research in potential therapies of AD.
Aged ; Alzheimer Disease* ; Amyloid ; Dementia ; Humans ; Neurofibrillary Tangles ; Plaque, Amyloid

Alzheimer's disease, the most common cause of dementia, is characterized by two major pathological hallmarks: amyloid plaques and neurofibrillary tangles. Based on these two indicators, an amyloid cascade hypothesis was proposed, and accordingly, most current therapeutic approaches are now focused on the removal of beta-amyloid peptides (Abeta from the brain. Additionally, strategies for blocking tau hyperphosphorylation and aggregation have been suggested, including the development of drugs that can block the formation of tangles. However, there are no true disease-modifying drugs in the current market, though many drugs based on theories other than Abeta and tau pathology are under development. The purpose of this review was to provide information on the current development of AD drugs and to discuss the issues related to drug development.
Alzheimer Disease ; Amyloid ; Brain ; Dementia ; Neurofibrillary Tangles ; Peptides ; Plaque, Amyloid

Secondary localized cutaneous amyloidosis appears in association with a variety of inflammatory skin diseases and skin tumors. The presence of dermal amyloid deposits in lesions of porokeratosis has rarely been described in the literature. We describe a Korean case of disseminated superficial porokeratosis, with clear histologic evidence of amyloid deposition in the upper dermis.
Amyloid* ; Amyloidosis ; Dermis ; Plaque, Amyloid* ; Porokeratosis* ; Skin ; Skin Diseases

We examined the amyloid deposit in various malignant cutaneous epithelial tumors by using Dylon stain. Histochemically identifiable amyloid deposits associated with basal cell epitheliomas(BCEs), squamous cell carcinomas(SCCs) and Bowens diseases were studied with monoclonal cytokeratin antibodies and anti-amyloid P antibodies. The results were as follaws, l. Amyloid deposits were detected in 5 of 12 BCEs, 4 of 11 SCCs, 3 of 9 Bowens diseases and 1 of 8 actinic keratoses. Amyloid deposits were not detected in o keratoacanthomas, 2 verrucous carcinomas, 1. Pagets disease and 3 extramammary Pagets diseases. 2. Anti-keratin antibody 34BE12 and anti-amyloid P antibody reacted with amyloid deposits in 3 of 5 BCEs which showed abundant amyloid deposits by Dylon stain. 3. Of 4 SCCs which showed amyloid deposits by Dylon stain, anti-keratin ant.ibody 34pE12 reacted with amyloid deposits in 2 cases and anti-amyloid P antibody reacted with amyloid deposits in 3 cases. 4. Anti-amyloid P antibody reacted with arnyloid deposits in 3 of 3 Bowens diseases which showed arnyloid deposits by Dylon stain. Anti-keratin antibody 34pE12 reacted with amyloid deposits only 1 of them. These findings suggest that epidermal keratins are the percursor substance of amyloid in malignant cutaneous epithelial tumors. The difference of antikeratin staining pattern between BCE-associated amyloid and SCC or Bowens disease-associated amyloid may be the results of difference in development stage of cutaneous amyloids.
Amyloid* ; Antibodies ; Carcinoma, Verrucous ; Keratins ; Keratoacanthoma ; Keratosis, Actinic ; Plaque, Amyloid*

We examined the amyloid deposits in seborrheic keratosis by using Dylon stain. Histochemically identified amyloid deposits in seborrheic keratosis were studied with monoclonal cytokeratin antibodies. Amyloid deposits were detected in 2 of 22 seborrheic keratosis. Anti-keratin antibody 34E12 reacted with amyloid deposits shown by Dylon stain in 2 of 22 seborrheic keratosis. Anti-keratin antibody 34B4 did not react with amyloid deposits
Amyloid ; Amyloidosis* ; Antibodies ; Keratins ; Keratosis, Seborrheic* ; Plaque, Amyloid

Cerebral amyloid angiopathy(CAA) is a nonspecific disease entity that has been associated with a number of neuropathologic conditions, the most prominent being dementia and cerebral hemorrhage. It occurs more commonly than is generally appreciated, with implications that may be overlooked. As amyloid deposits are found in the vessels of the leptomeninges and cerebral cortex, the location and size of the hematoma, with cortical and subarachnoid extension, help to differentiate amyloid angiopathy from other causes of intracerebral hemorrhage in the elderly. It has, in addition, characteristic pathological features, and the existence of these, together with the occurance of nontraumatic normotensive spontaneous primary cerebral hemorrhage in the elderly, should indicate the existence of CAA. The authors report a case of cerebral amyloid angiopathy-related intracerebral hemorrhage.
Aged ; Amyloid* ; Cerebral Amyloid Angiopathy ; Cerebral Cortex ; Cerebral Hemorrhage* ; Dementia ; Hematoma ; Humans ; Plaque, Amyloid

The pathophysiologic process of Alzheimer's disease (AD) begins years before the diagnosis of clinical dementia. This concept of preclinical AD has arisen from the observation of AD pathologic findings such as senile plaques and neurofibrillary tangles in the brains of people who at the time of death had normal cognitive function. Recent advances in biomarker studies now provide the ability to detect the pathologic changes of AD, which are antecedent to symptoms of the illness, in cognitively normal individuals. Functional and structural brain alterations that begin with amyloid-beta accumulation already show the patterns of abnormality seen in individuals with dementia due to AD. The presence of preclinical AD provides a critical opportunity for potential interventions with disease-modifying therapy. This review focuses on the studies of antecedent biomarkers for preclinical AD.
Aging ; Alzheimer Disease ; Biomarkers ; Brain ; Dementia ; Neurofibrillary Tangles ; Plaque, Amyloid

Amyloidosis, which refers to amyloid deposits accumulated in various organs, belongs to the same category as multiple myeloma; it can be accompanied by pathologic fracture. It is important to find out the exact cause of amyloidosis in order to decide treatment options and to predict prognosis. The authors described an amyloidosis case with multiple musculoskeletal involvements presented with pathologic fracture and arthrosis, and also reviewed the related articles.
Amyloidosis ; Fractures, Spontaneous ; Multiple Myeloma ; Plaque, Amyloid ; Prognosis

Lichen amyloidosis is a chronic intensely pruritic skin disorder characterized histologi-cally by the deposition of amyloid in the papillary dermis. Lichen amyloidosis has been reported in association with several pruritic skin disorders including atopic dermatitis, lichen planus, and mycosis fungoides. It is hypothesized that the scratching in pruritic skin diseases is the most important step in forming amyloid deposit. We report two cases of lichen amyloidosis occuring in two patients with atopic dermatitis.
Amyloid ; Amyloidosis* ; Dermatitis, Atopic* ; Dermis ; Humans ; Lichen Planus ; Lichens* ; Mycosis Fungoides ; Plaque, Amyloid ; Skin ; Skin Diseases

Nine cases of primary localized cutaneous amyloidosis were studied by immunoperoxidase technique (ABC method) employing anti-keratin antibodies. All specimens were examined using consecutive paraffin sections to confirm the correspondence between amyloid existing area and reactive sites. Anti-keratin antibody 34pE which recognize 68, 58, 56.5, 56kd keratin peptides reacted with amyloid deposits in both lichen amyloidosus and macular amyloidosis. However, anti-keratin antibodies 34pB4 and 35pH did not react with amyloids. In general, Dylon staining positive material, keratin reacted with 34pE and amyloid P showed similar distribution in serial sections, but did not show the same one. Several keratin bodies reacted with 34pE, which were not stained with Dylon staining or antiamyloid P were found in the dermis of one specimen. These results suggest that immunohistochemical staining with antikeratin antibody 34pE using formalin-fixed, paraffin-embedded sections appeared to be a useful method in studying the histogenesis of primary localized cutaneous arnyloidosis.
Amyloid* ; Amyloidosis* ; Antibodies* ; Catalytic Domain ; Dermis ; Immunoenzyme Techniques ; Lichens ; Paraffin ; Peptides ; Plaque, Amyloid*