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Alzheimer's disease : towards an understanding of the aetiology and pathogenesis / edited by D. C. Davies.

Alzheimer's disease / Linda C. Lu and Juergen H. Bludau.

The experience of Alzheimer's disease : life through a tangled veil / Steven R. Sabat.

Dementia [electronic resource].

Aluminum in biology and medicine.

Plague time : how stealth infections cause cancers, heart disease, and other deadly ailments / Paul W. Ewald.

Gale Encyclopedia of Science.

Niemann-Pick Type C (NPC) disease is a neurodegenerative disease that is characterized by the accumulation of cholesterol and glycosphingolipids in the late endocytic pathway. The majority of NPC cases are due to mutations in the NPC1 gene. The precise function of this gene is not yet known.
Using cDNA microarrays, we analyzed the genome-wide expression patterns of human fibroblasts homozygous for the I1061T NPC1 mutation that is characterized by a severe defect in the intracellular processing of low density lipoprotein-derived cholesterol. A distinct gene expression profile was identified in NPC fibroblasts from different individuals when compared with fibroblasts isolated from normal subjects. As expected, NPC1 mutant cells displayed an inappropriate homeostatic response to accumulated intracellular cholesterol. In addition, a number of striking parallels were observed between NPC disease and Alzheimer's disease.
Many genes involved in the trafficking and processing of amyloid precursor protein and the microtubule binding protein, tau, were more highly expressed. Numerous genes important for membrane traffic and the cellular regulation of calcium, metals and other ions were upregulated. Finally, NPC fibroblasts exhibited a gene expression profile indicative of oxidative stress. These changes are likely contributors to the pathophysiology of Niemann-Pick Type C disease.

PloS one, 2006-12, Vol.1 (1), p.e19-e19

Clues to neuro-degeneration in Niemann-Pick type C disease from global gene expression profiling

Objective To identify the midlife risk factors for subtypes of dementia newly developed later in life. Methods A nested case-control study was conducted on 157 demented cases and 628 comparison cases selected from 40,636 men and women who were enrolled from 1982 to 1992. Four comparison cases were frequency-matched on age, time at enrollment (within 6 months), gender, and residential township. Midlife risk factors included vascular risk factors (body mass index [BMI], total cholesterol, total triglycerides, blood glucose, cerebrovascular accident [CVA] history, diabetes mellitus history, and hypertension history), cigarette smoking, and alcohol consumption. Dementia assessments were ascertained through the computerized data linkage from National Health Insurance Database from 2000 to 2002 and clinically confirmed by neurologists or psychiatrists. Conditional logistic regression analysis was used to estimate the matched odds ratio (OR) and its 95% confidence intervals (CI) for each risk factor. Results A J-shaped relationship was observed between BMI (kg/m2 ) and dementia. The multivariate-adjusted ORs (95% CI) of developing dementia were 1.84 (1.02–3.33), 1.87 (1.08–3.23) and 2.44 (1.39–4.28), respectively, for BMIs of <20.5, 23.0–25.4, ≥25.5 compared with a BMI of 20.5–22.9 as the referent group (OR = 1.0). Similar findings were observed for Alzheimer disease (AD) and vascular dementia (VaD). The association between obesity (BMI ≥25.5) and both AD and VaD was statistically significant among cigarette smokers but not among nonsmokers. Additionally, history of CVA was a significant risk factor for VaD, but not for AD. Conclusion Being underweight, being overweight, and a cerebrovascular accident in midlife may increase the risk of dementia in late life.

The American journal of geriatric psychiatry, 2007-09, Vol.15 (9), p.762-771

Midlife Risk Factors for Subtypes of Dementia: A Nested Case-Control Study in Taiwan

MMW Fortschritte der Medizin, 2014-12, Vol.156 (21-22), p.83-84

Role of cardiovascular risk factors in the etiology of dementia

BMJ, 2005-08, Vol.331 (7514), p.455-455; author reply 455

Obesity in middle age and future risk of dementia: Midlife obesity increases risk of future dementia

MMW Fortschritte der Medizin, 2011-09, Vol.153 (38), p.86-9; quiz 90

Early diagnosis and treatment of dementia

MMW Fortschritte der Medizin, 2010-11, Vol.152 (44), p.54-7; quiz 58

Treatment of dementia

MMW Fortschritte der Medizin, 2009-06, Vol.151 (24), p.36-40; quiz 41

Management and therapy of Alzheimer's disease. Recommendations of a general practitioners' guideline

MMW Fortschritte der Medizin, 2008-09, Vol.150 (36-37), p.38-40

The benefits of physical activity

MMW Fortschritte der Medizin, 2007-08, Vol.149 (33-34), p.14-14

Mild cognition disorders signal increased risk of dementia. How can mental decline be stopped?

Alzheimer disease is caused by the development of senile plaques, which is responsible for neuronal destruction and accumulation of Beta Amyloid and synovial tangles formation (fig1) [1]. Because these tangles tigers the inflammation in the brain and progressively this inflammation is caused by neuronal atrophy, which is responsible for the death of nerve cell (fig1-2). Diagnosis The main components to diagnosis of Alzheimer Disease are: * Self-Reporting regarding symptoms too family members either friend can provide symptoms and their impact on daily routine (10). * Diagnosis Alzheimer on the basis of asses, memory and thinking skills (11). * Clinical test and imaging test also helps them to understand the causes, stage or define the characteristic of mental illness (12). * Actually Alzheimer diseases can be diagnosed after death, when microscopic examination or autopsy of brain done. MANAGEMENT OF ALZHEIMER'S DISEASE Pharmacological Approach Drugs which are used for dementia and cerebral disorder in Alzheimer Disease The indications of cognition enhancer are as follows: * Alzheimer Disease or multiple infarct dementia * Mild cognitive impairment and episodic memory lapses * Mentally retard children, learning defects, attention deficit disorder or personality disorder * Sequel of head injury or brain surgery Drugs used for the treatment of Alzheimer Disease (12, 13) Cholinergic Activators * Rivastigmine * Donepezil * Galantamine * Tacrine Glutamate Antagonists (NMDA) * Memantine Miscellaneous Drugs * Piracetam * Dihydroergotoxine * Pyritinol * Citicoline * Piribedil * Ginkgo biloba Individual drug Rivastigmine Carbamate derivative of physostigmine which inhibits or bloke both acetylcholine-esterase and butyrylcholine- esterase (14). Ginkgo biloba The Dried extract or isolated from of Chinese plant which contains several mixtures of ginkgoflavone glycoside (e.g. ginkgolide B) and some PAF (platelet activating factor) antagonistic action (8).Ginkgo biloba is well treated cerebral deterioration in cerebrovascular insufficiency and it has been promotes a diversification of cognitive or behavioral disorder (9, 10).Adverse effect is upper g.i.t symptoms and increased risk of bleeding.

Annals of the Romanian society for cell biology, 2021-01, Vol.25 (1), p.3548-3556

Alzheimer Disease –Etiology, Pathophysiology and Treatment: An Overview

Alzheimer's disease (AD) is the most common type of dementia, accounting for 60% to 80% of all cases [...].

International journal of molecular sciences, 2022-12, Vol.24 (1), p.107

Pathogenesis of Alzheimer's Disease

Key Points
The phenomenon of amyloid formation is associated with protein misfolding disorders, including Alzheimer's disease, Parkinson's disease and type II diabetes.
The amyloid state is a 'generic state' of proteins and its study can provide great insight into the nature of functional structures and into that of disease-related assemblies.
A multitude of quality control, or 'housekeeping', mechanisms exist in living organisms to prevent the conversion of normally soluble proteins into the aberrant amyloid state and to maintain protein homeostasis.
The failure of these quality control mechanisms can give rise to 'protein metastasis', the uncontrolled conversion of these molecules into aberrant self-propagating assemblies that ultimately lead to a cascade of cytotoxic processes.
Our increasing ability to monitor and characterize the molecular structures and formation mechanisms of the protein species that are involved in amyloid formation is suggesting novel strategies to treat or prevent protein misfolding disorders.
Ultimately, the results of this field of research will result in great changes in the way we are able to manage modern lifestyles and maintain healthy ageing.
Protein aggregation and amyloid deposition are associated with a wide range of medical disorders, including Alzheimer's disease and type II diabetes. Studies into the amyloid state are revealing fundamental principles that underlie the maintenance of protein homeostasis, and the origins of aberrant protein behaviour and disease.
The phenomenon of protein aggregation and amyloid formation has become the subject of rapidly increasing research activities across a wide range of scientific disciplines. Such activities have been stimulated by the association of amyloid deposition with a range of debilitating medical disorders, from Alzheimer's disease to type II diabetes, many of which are major threats to human health and welfare in the modern world. It has become clear, however, that the ability to form the amyloid state is more general than previously imagined, and that its study can provide unique insights into the nature of the functional forms of peptides and proteins, as well as understanding the means by which protein homeostasis can be maintained and protein metastasis avoided.

Nature reviews. Molecular cell biology, 2014-06, Vol.15 (6), p.384-396

The amyloid state and its association with protein misfolding diseases

Hypertension affects two-thirds of people aged >60 years and significantly increases the risk of both vascular cognitive impairment and Alzheimer’s disease. Hypertension compromises the structural and functional integrity of the cerebral microcirculation, promoting microvascular rarefaction, cerebromicrovascular endothelial dysfunction and neurovascular uncoupling, which impair cerebral blood supply. In addition, hypertension disrupts the blood–brain barrier, promoting neuroinflammation and exacerbation of amyloid pathologies. Ageing is characterized by multifaceted homeostatic dysfunction and impaired cellular stress resilience, which exacerbate the deleterious cerebromicrovascular effects of hypertension. Neuroradiological markers of hypertension-induced cerebral small vessel disease include white matter hyperintensities, lacunar infarcts and microhaemorrhages, all of which are associated with cognitive decline. Use of pharmaceutical and lifestyle interventions that reduce blood pressure, in combination with treatments that promote microvascular health, have the potential to prevent or delay the pathogenesis of vascular cognitive impairment and Alzheimer’s disease in patients with hypertension.
Hypertension and ageing have deleterious effects on the cerebral microcirculation that can lead to cognitive dysfunction. This Review discusses cerebrovascular maladaptation to hypertension and microvascular contributions to hypertension-induced cognitive impairment in ageing, as well as the role of hypertension in the pathogenesis of Alzheimer’s disease.
Key points
Hypertension is associated with ageing and significantly increases the risk of vascular cognitive impairment and Alzheimer’s disease.
In older individuals, hypertension leads to maladaptation of the cerebral circulation, resulting in dysregulation of cerebral blood flow, microvascular rarefaction, blood–brain barrier disruption, oxidative stress and impaired neurovascular coupling.
Hypertension causes pathological alterations in cerebral microvessels that damage microvascular structure, network architecture and function, and contribute to the genesis of cerebral microhaemorrhages, lacunar infarcts and white matter injury; these factors are associated with cognitive decline.
Potential mechanisms by which hypertension could exacerbate the progression of Alzheimer’s disease include increased oxidative microvascular damage, brain inflammation and blood–brain barrier disruption, as well as impaired glymphatic (also known as glial-lymphatic) clearance of amyloid-β.
Use of pharmaceutical and/or lifestyle interventions that reduce blood pressure in combination with treatments that promote microvascular health could potentially prevent or delay cognitive decline in patients with hypertension.

Nature reviews. Nephrology, 2021-10, Vol.17 (10), p.639-654

Hypertension-induced cognitive impairment: from pathophysiology to public health