scholarly journals Predicting memory decline as a risk factor for Alzheimer's disease in older post-menopausal women: quod erat demonstrandum?

2009 ◽  
Vol 22 (2) ◽  
pp. 332-335 ◽  
Author(s):  
Mark A. Rodrigues ◽  
Jonathan K. Foster ◽  
Giuseppe Verdile ◽  
Karen Joesbury ◽  
Richard Prince ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Neuronal Damage ◽  
Mixed Data ◽  
Memory Decline ◽  
Estrogen Production ◽  
Age Related ◽  
Menopausal Women ◽  
Post Menopausal

Alzheimer's disease (AD) is the major form of age-related dementia worldwide, accounting for more than two-thirds of all dementia cases. The disease is characterized by a progressive loss of cognitive and intellectual functioning (Gilman, 1997). A number of risk factors for AD have been identified. The prevalence of AD increases with age, diabetes, depression, family history of Parkinson's disease and following head injury or exposure to solvents (Jorm et al., 1991; van Duijn et al., 1991; Ott et al., 1995; Yoshitake et al., 1995; Devanand et al., 1996). Published research further suggests that low education levels are associated with increased prevalence of clinical AD (Gatz et al., 2001; Qiu et al., 2001; Ravaglia et al., 2002). Women also have a higher risk for developing the disease than men, with the risk being markedly increased following menopause (Sherwin, 2002; Sherwin 2003). Additionally, slightly more severe cognitive deficits have been reported in AD in women compared to men (Buckwalter et al., 1993, Henderson and Buckwalter, 1994). These epidemiological trends may be a consequence of reproductive hormonal changes. Specifically, menopause results in a marked diminution in gonadal estrogen production in women (see Sherwin, 2003, for a review). Estrogen plays a pivotal role in the maintenance and function of neuronal circuits in the brain and in resistance to neuronal damage (McEwen, 2001). The neuroprotective properties of estrogen are thought to be mediated at least in part by anti-amyloidogenic, anti-oxidative and ant-inflammatory mechanisms (reviewed in Barron et al., 2006a). However, limited and somewhat mixed data exist regarding the association between endogenous levels of estrogen and cognitive decline (Manly et al., 2000; Schupf et al., 2003). Based on some of our own findings, we here consider the factors that may be useful in predicting memory decline as a risk factor for Alzheimer's disease in older post-menopausal women.

scholarly journals Alzheimer's disease and age-related memory decline (preclinical)

2011 ◽  
Vol 99 (2) ◽  
pp. 190-210 ◽  
Author(s):  
Alvin V. Terry ◽  
Patrick M. Callahan ◽  
Brandon Hall ◽  
Scott J. Webster
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Memory Decline ◽  
Age Related

scholarly journals Age-Associated Epigenetic Alterations, Somatic Mutations, and Their Crosstalk in Alzheimer’s Disease

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 636-637
Author(s):  
Yaroslav Markov ◽  
Kyra Thrush ◽  
Morgan Levine
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Somatic Mutations ◽  
Brain Regions ◽  
Major Risk Factor ◽  
Postmortem Brain ◽  
Biological Aging ◽  
Learning Approaches ◽  
Age Related

Abstract Aging is the major risk factor for Alzheimer’s Disease (AD), and as life expectancy increases, neurodegeneration will continue to afflict an ever-increasing proportion of the population. While numerous theories are attempting to explain the drivers behind AD pathology, what unites them is the observation that AD is reliably associated with a progressive buildup of age-related molecular changes. Because of the varying clinical presentations of AD in patients with similar genetic backgrounds, it has been postulated that epigenetics may be implicated in its etiology. Building on our prior work showing that AD pathology is linked to alterations in age-related DNA CpG methylation (DNAme) across various brain regions, we use state-of-the-art machine learning approaches to identify patterns of molecular damage in postmortem brain samples. We show that alterations in DNAme are associated with accelerated biological aging, AD, and the APOE e4 genotype, which is a major risk factor for AD. We also demonstrate that these associations are present in the PFC but not cerebellum -- in line with the current understanding of AD progression in the brain. Finally, we perform whole-exome sequencing and protein mass spectrometry on the same brain samples to test our hypothesis as to whether AD-associated alterations of DNAme are linked with the accumulation of somatic mutations that affect the structural and binding properties of protein epigenetic regulators.

scholarly journals Memory Decline in Peri- and Post-menopausal Women: The Potential of Mind–Body Medicine to Improve Cognitive Performance

2014 ◽  
Vol 9 ◽  
pp. IMI.S15682 ◽  
Author(s):  
Jim R. Sliwinski ◽  
Aimee K. Johnson ◽  
Gary R. Elkins
Keyword(s):  
Cognitive Decline ◽  
Cognitive Performance ◽  
Hot Flashes ◽  
Integrative Approach ◽  
Future Research ◽  
Memory Decline ◽  
Estrogen Production ◽  
Menopausal Women ◽  
Mind Body Medicine ◽  
Post Menopausal

Cognitive decline is a frequent complaint during the menopause transition and among post-menopausal women. Changes in memory correspond with diminished estrogen production. Further, many peri- and post-menopausal women report sleep concerns, depression, and hot flashes, and these factors may contribute to cognitive decline. Hormone therapy can increase estrogen but is contraindicated for many women. Mind–body medicine has been shown to have beneficial effects on sleep, mood, and hot flashes, among post-menopausal women. Further, mind–body medicine holds potential in addressing symptoms of cognitive decline post-menopause. This study proposes an initial framework for how mind–body interventions may improve cognitive performance and inform future research seeking to identify the common and specific factors associated with mind–body medicine for addressing memory decline in peri- and post-menopausal women. It is our hope that this article will eventually lead to a more holistic and integrative approach to the treatment of cognitive deficits in peri- and post-menopausal women.

Estimates of age-related memory decline are inflated by unrecognized Alzheimer's disease

2018 ◽  
Vol 70 ◽  
pp. 170-179 ◽  
Author(s):  
Karra D. Harrington ◽  
Adrian Schembri ◽  
Yen Ying Lim ◽  
Christa Dang ◽  
David Ames ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Memory Decline ◽  
Age Related

“Brain-Specific” Nutrients: A Memory Cure?

2002 ◽  
Vol 3 (1) ◽  
pp. 12-38 ◽  
Author(s):  
Mark A. McDaniel ◽  
Steven F. Maier ◽  
Gilles O. Einstein
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Animal Studies ◽  
Memory Decline ◽  
Memory Tests ◽  
Positive Effects ◽  
Age Related ◽  
Per Se ◽  
The Brain

We review the experimental evaluations of several widely marketed nonprescription compounds claimed to be memory enhancers and treatments for age-related memory decline. We generally limit our review to double-blind placebo-controlled studies. The compounds examined are phos-phatidylserine (PS), phosphatidylcholine (PC), citicoline, piracetam, vinpocetine, acetyl-L-carnitine (ALC), and antiox-idants (particularly vitamin E). In animals, PS has been shown to attenuate many neuronal effects of aging, and to restore normal memory on a variety of tasks. Preliminary findings with humans, though, are limited. For older adults with probable Alzheimer's disease, a single study failed to demonstrate positive effects of PS on memory performance. For older adults with moderate cognitive impairment, PS has produced consistently modest increases in recall of word lists. Positive effects have not been as consistently reported for other memory tests. There is one report of consistent benefits across a number of memory tests for a subset of normal adults who performed more poorly than their peers at baseline. The choline compounds PC and citicoline are thought to promote synthesis and transmission of neurotransmitters important to memory. PC has not proven effective for improving memory in patients with probable Alzheimer's disease. The issue remains open for older adults without serious degenerative neural disease. Research on citicoline is practically nonexistent, but one study reported a robust improvement in story recall for a small sample of normally aging older adults who scored lower than their peers in baseline testing. Animal studies suggest that piracetam may improve neuronal efficiency, facilitate activity in neurotransmitter systems, and combat the age-related decrease in receptors on the neuronal membrane. However, for patients with probable Alzheimer's disease, as well as for adults with age-associated memory impairment, there is no clear-cut support for a mnemonic benefit of piracetam. Vinpocetine increases blood circulation and metabolism in the brain. Animal studies have shown that vinpocetine can reduce the loss of neurons due to decreased blood flow. In three studies of older adults with memory problems associated with poor brain circulation or dementia-related disease, vinpocetine produced significantly more improvement than a placebo in performance on global cognitive tests reflecting attention, concentration, and memory. Effects on episodic memory per se have been tested minimally, if at all. ALC participates in cellular energy production, a process especially important in neurons, and in removal of toxic accumulation of fatty acids. Animal studies show that ALC reverses the age-related decline in the number of neuron membrane receptors. Studies of patients with probable Alzheimer's disease have reported nominal advantages over a range of memory tests for ALC-treated patients relative to placebo groups. Significant differences have been reported rarely, however. Whether ALC would have mnemonic benefits for aging adults without brain disease is untested as far as we know. Antioxidants help neutralize tissue-damaging free radicals, which become more prevalent as organisms age. It is hypothesized that increasing antioxidant levels in the organism might retard or reverse the damaging effects of free radicals on neurons. Thus far, however, studies have found that vitamin E does not significantly slow down memory decline for Alzheimer's patients and does not produce significant memory benefits among early Parkinson's patients. Neither did a combination of vitamins E and C significantly improve college students' performance on several cognitive tasks. In sum, for most of the “brain-specific” nutrients we review, some mildly suggestive effects have been found in preliminary controlled studies using standard psychometric memory assessments or more general tests designed to reveal cognitive impairment. We suggest that future evaluations of the possible memory benefits of these supplements might fruitfully focus on memory processes rather than on memory tests per se.

fMRI analysis of the hippocampal subregions in age-related memory decline and Alzheimer's disease

NeuroImage ◽  
1998 ◽  
Vol 7 (4) ◽  
pp. S850
Author(s):  
Scott A. Small ◽  
Gerard M. Perera ◽  
Robert DeLaPaz ◽  
Yaakov Stern
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Memory Decline ◽  
Age Related ◽  
Fmri Analysis

scholarly journals A REVIEW ON “NEW TREATMENT STRATEGIES FOR ALZHEIMER’S DISEASE AS NEURODEGENERATIVE DISEASE AND ITS RISK FACTOR CAUSE, SYMPTOMS, AND TREATMENT AT WORLDWIDE”

2016 ◽  
Vol 9 (9) ◽  
pp. 16
Author(s):  
Rohit Jaysing Bhor
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Working Memory ◽  
Risk Factor ◽  
Social Life ◽  
Disease Risk ◽  
Treatment Strategies ◽  
Disease Diagnosis ◽  
Age Related ◽  
Antidementia Drugs

ABSTRACTAlzheimer’s disease (AD) is a dynamic and irreversible neurodegenerative illness and relates to the most widely recognized reason for dementiaaround the world. AD is a dynamic and lethal cerebrum ailment. Alzheimer’s obliterates mind cells, bringing on memory issue or misfortune and issueswith speculation and conduct sufficiently serious to influence work, long lasting leisure activities or social life. Alzheimer’s illness is quickly becomingworldwide, but there is no cure for it. Now, accessible medications just give symptomatic help and do not mediate in infection prepare adequatelyenough to avert or cure it. Various late studies have reported that working memory does not appear to demonstrate regular age-related deficienciesin solid more established grown-ups when enthusiastic data are included. Indeed, contingent upon the capacity included, patients might demonstratean enthusiastic advantage in their working memory execution. Moreover, this advantage is not generally obviously one-sided (e.g., toward negativeor positive data). We decipher this intricate example of results as an outcome of the cooperation between numerous components including theseriousness of AD, the nature of emotional jolts, and sort of working memory errand. Clinical advantages of the accessible pharmacological treatmentfor AD with antidementia drugs (to be specific cholinesterase inhibitors and Memantine) are obvious. In an unexpected way, learns about the transientcapacity to encode and effectively control enthusiastic data in dementia of Alzheimer’s sort are few and have yielded blended results.Keywords: Alzheimer’s disease, Risk factor for Alzheimer’s disease, Diagnosis, Classification of Anti-Alzheimer’s drug.

scholarly journals Diagnosis of Alzheimer’s Disease with [18F]PET in Mild and Asymptomatic Stages

2009 ◽  
Vol 21 (1-2) ◽  
pp. 101-115 ◽  
Author(s):  
Alexander Drzezga
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Early Diagnosis ◽  
Fdg Pet ◽  
Neuronal Damage ◽  
Treatment Strategies ◽  
Specific Method ◽  
Diagnostic Challenge ◽  
Age Related ◽  
18F Fdg

With longer life expectancy, dementia based on the age-related Alzheimers’ disease (AD) has turned into one of the most prevalent disorders of older age, representing a serious medical and socio-economic issue. There has been growing interest in early diagnosis of this disease, particularly regarding the initiation of new treatment strategies ahead of the onset of irreversible neuronal damage. It is accepted that the pathologic changes underlying AD appear in the brain years to decades before the symptomatic stages. Consequently, clinical measures of cognitive impairment, as used for definition of dementia, will not allow early diagnosis of AD-pathology in the mild or asymptomatic stages. Thus, a need for complementary sensitive biomarkers is apparent. Brain imaging markers are among the most promising candidates for this diagnostic challenge. Particularly, [18F]FDG PET as a marker of regional neuronal function has been demonstrated to represent a most sensitive and specific method for early identification of AD-pathology and thus for prediction of dementia of the Alzheimer type (DAT), even in the mild and asymptomatic stages. Currently, systematic data of comparable quality are hardly available for any other imaging procedure. The purpose of this article is to describe the typical findings of [18F]FDG PET in different stages of AD and to demonstrate its value for early and reliable diagnosis of Alzheimer's disease, particularly ahead of the stage of dementia of the Alzheimer’s type.

Collaborative Memory Interventions for Age-Related and Alzheimer’s Disease-Related Memory Decline

2018 ◽  
Author(s):  
Helena M. Blumen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Healthy Aging ◽  
Therapeutic Potential ◽  
Neural Systems ◽  
Memory Decline ◽  
Collaborative Memory ◽  
Age Related ◽  
Collaborative Recall ◽  
Individual Memory

This chapter discusses the potential for using collaboration as a tool to compensate for age-related and Alzheimer’s disease (AD) related memory decline. Recent research suggest that collaborating with others during recall improves later individual memory, but such post-collaborative recall benefits must be confirmed in AD, and transitional stages of AD such as amnestic mild cognitive impairment (aMCI). Identifying the neural systems that operate during collaboration is also essential for determining the therapeutic value of collaborative recall in these populations. Examining post-collaborative recall benefits, and identifying the neural systems associated with collaborative recall, in healthy aging, AD, and aMCI will be methodologically challenging and necessitate interdisciplinary expertise—but is vital for determining the therapeutic potential of collaborative recall in these populations.

scholarly journals Protofibrils of Amyloid-β are Important Targets of a Disease-Modifying Approach for Alzheimer’s Disease

2020 ◽  
Vol 21 (3) ◽  
pp. 952 ◽  
Author(s):  
Kenjiro Ono ◽  
Mayumi Tsuji
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Damage ◽  
Membrane Integrity ◽  
Reactive Oxygen Species Generation ◽  
Amyloid Β ◽  
Plaque Burden ◽  
Amyloid Β Protein ◽  
Age Related ◽  
Culture Models

Worldwide, Alzheimer’s disease (AD) is the most common age-related neurodegenerative disease and is characterized by unique pathological hallmarks in the brain, including plaques composed of amyloid β-protein (Aβ) and neurofibrillary tangles of tau protein. Genetic studies, biochemical data, and animal models have suggested that Aβ is responsible for the pathogenesis of AD (i.e., the amyloid hypothesis). Indeed, Aβ molecules tend to aggregate, forming oligomers, protofibrils, and mature fibrils. However, while these Aβ species form amyloid plaques of the type implicated in AD neurodegeneration, recent clinical trials designed to reduce the production of Aβ and/or the plaque burden have not demonstrated clinical efficacy. In addition, recent studies using synthetic Aβ peptides, cell culture models, Arctic transgenic mice, and human samples of AD brain tissues have suggested that the pre-fibrillar forms of Aβ, particularly Aβ protofibrils, may be the most critical species, compared with extracellular fibrillar forms. We recently reported that protofibrils of Aβ1-42 disturbed membrane integrity by inducing reactive oxygen species generation and lipid peroxidation, resulting in decreased membrane fluidity, intracellular calcium dysregulation, depolarization, and synaptic toxicity. Therefore, the therapeutic reduction of protofibrils may prevent the progression of AD by ameliorating neuronal damage and cognitive dysfunction through multiple mechanisms.

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