ALZHEIMER’S DISEASE
 
   

Alzheimer’s Disease

This section was compiled by Frank M. Painter, D.C.
Send all comments or additions to:
  Frankp@chiro.org

If there are terms in these articles you don't understand, you can get a definition from the Merriam Webster Medical Dictionary. If you want information about a specific disease, you can access the Merck Manual. You can also search Pub Med for more abstracts on this, or any other health topic.

Jump to:    Alzheimer’s Research                  The Nutritional Approach

 
   

Alzheimer’s Research
 
   

Neurodegenerative Diseases and Esssential Fatty Acids
A Chiro.Org article collection

This collection details research demonstrating the protective effects of omega-3 fatty acids on cognitive decline.

Transcriptional Effects of ApoE4: Relevance to Alzheimer's Disease
Molecular Neurobiology 2018 (Jun);   55 (6):   5243–5254 ~ FULL TEXT

The major genetic risk factor for sporadic Alzheimer's disease (AD) is the lipid binding and transporting carrier protein apolipoprotein E, epsilon 4 allele (ApoE4). One of the unsolved mysteries of AD is how the presence of ApoE4 elicits this age-associated, currently incurable neurodegenerative disease. Recently, we showed that ApoE4 acts as a transcription factor and binds to the promoters of genes involved in a range of processes linked to aging and AD disease pathogenesis. These findings point to novel therapeutic strategies for AD and aging, resulting in an extension of human healthspan, the disease-free and functional period of life. Here, we review the effects and implications of the putative transcriptional role of ApoE4 and propose a model of Alzheimer's disease that focuses on the transcriptional nature of ApoE4 and its downstream effects, with the aim that this knowledge will help to define the role ApoE4 plays as a risk factor for AD, aging, and other processes such as inflammation and cardiovascular disease.

Clinical Lifestyle Medicine Strategies for Preventing and Reversing Memory Loss in Alzheimer's
American J Lifestyle Medicine 2018 (May 11);   12 (5):   391–395 ~ FULL TEXT

Alzheimer's disease (AD) is the most common form of dementia and currently affects over 5 million Americans and 30 million individuals worldwide. Unfortunately, the current approach to treating AD provides nothing more than a marginal, unsustained, symptomatic effect, with little or no effect on disease progression itself. To attain effective improvements in AD, one must determine risk factors, address the underlying causes, and focus on a combination of functional and lifestyle medicine strategies that provide a comprehensive, programmatic, and network-based approach that is sufficient to achieve epigenetic transformation and neurologic healing through its multiple and necessary synergistic components. Rather than normalizing metabolic parameters, the focus is on optimization of each metabolic parameter. Papers published by research neurologist, Dr Dale Bredesen have documented that symptoms of mild cognitive impairment and early AD may often be reversed within 6 months after initiating a comprehensive, functional and lifestyle medicine-focused program.

Evidence for Brain Glucose Dysregulation in Alzheimer's disease
Alzheimers Dement. 2018 (Mar);   14 (3):   318–329 ~ FULL TEXT

To the best of our knowledge, this report is the first to measure brain tissue glucose concentrations and assess glycolytic flux to demonstrate their relationships with both severity of AD pathology and the expression of AD symptoms. Including brain tissue samples from “asymptomatic Alzheimer’s disease (ASYMAD)” individuals who represent an intermediate group in the gradation of neuropathology from controls to AD patients in the absence of cognitive impairment during life allowed us to relate measures of brain glucose concentration and glycolytic flux to incremental levels of AD pathology and symptom expression. Equally importantly, by measuring glucose concentrations in brain regions both vulnerable to distinct pathological features of AD, that is, MFG (amyloid deposition) and ITG (tau accumulation) as well as in a region relatively resistant to AD pathology, that is, cerebellum [34], we were able to determine whether the observed alterations in brain glucose concentrations and abnormalities in glycolysis were related to defining pathological processes.

Reversal of Cognitive Decline in Alzheimer's Disease
Aging (Albany NY). 2016 (Jun);   8 (6):   1250–1258 ~ FULL TEXT

Alzheimer's disease is one of the most significant healthcare problems nationally and globally. Recently, the first description of the reversal of cognitive decline in patients with early Alzheimer's disease or its precursors, MCI (mild cognitive impairment) and SCI (subjective cognitive impairment), was published. [1] The therapeutic approach used was programmatic and personalized rather than monotherapeutic and invariant, and was dubbed metabolic enhancement for neurodegeneration (MEND). Patients who had had to discontinue work were able to return to work, and those struggling at work were able to improve their performance. The patients, their spouses, and their co-workers all reported clear improvements. Here we report the results from quantitative MRI and neuropsychological testing in ten patients with cognitive decline, nine ApoE4+ (five homozygous and four heterozygous) and one ApoE4–, who were treated with the MEND protocol for 5-24 months. The magnitude of the improvement is unprecedented, providing additional objective evidence that this programmatic approach to cognitive decline is highly effective. These results have far-reaching implications for the treatment of Alzheimer's disease, MCI, and SCI; for personalized programs that may enhance pharmaceutical efficacy; and for personal identification of ApoE genotype.

Enhancement of SAPP as a Therapeutic Strategy for Alzheimer’s and
Other Neurodegenerative Diseases

J Alzheimers & Neurodegenerative Diseases 2015 (Aug 3);   1 (1):   33–44 ~ FULL TEXT

Soluble, secreted Amyloid Precursor Protein-? (sAPP?), a product of ?-secretase (ADAM10) cleavage of Full Length-APP (FL-APP), is a trophic factor critical for synaptic complexity and maintenance. As cleavage at the ?-site of APP precludes the ?-site cleavage that is the first step in Amyloid ? (A?) production, enhancing sAPP? production may not only support and restore neuronal health, but may also decrease the generation of anti-trophic A?. Over-production or reduced clearance of A? is a hallmark of Alzheimer’s Disease (AD), and recent findings suggest it also plays a role in other neurodegenerative diseases and neurological conditions, such as Amyotrophic Lateral Sclerosis (ALS), Cerebral Amyloid Angiopathy (CAA), and Traumatic Brain Injury (TBI). Yet decades of focus on A?-lowering strategies alone including passive and active immunotherapy and ?-secretase and BACE1 (BACE) inhibition have yet to yield positive clinical results. Clinical trials of several BACE inhibitors are underway in AD patients, and although there is optimism about this strategy, there are also concerns about mechanism-based side-effects of these drugs. A truly effective therapy would not only slow the degenerative process underlying onset and progression of the disease, it should also restore healthy neuronal function. It is very likely this will comprise combination therapy utilizing more than one drug or intervention. Molecules that enhance sAPP? may be a safe, effective component of a multi-modal therapeutic approach to AD and other neurodegenerative diseases, and have the potential to increase neuronal health by providing trophic support and disrupting neurodegenerative mechanisms.

Metabolic Profiling Distinguishes Three Subtypes of Alzheimer's disease
Aging (Albany NY). 2015 (Aug);   7 (8):   595–600 ~ FULL TEXT

In summary, metabolic profiling of patients with cognitive decline, as described previously [5], reveals three readily distinguishable subtypes of Alzheimer's disease: inflammatory, non-inflammatory, and cortical. The distinctive features, presentation, lack of association with ApoE4, and marked hypozincemia, together suggest that the cortical subtype of Alzheimer's disease is a fundamentally different disease than the other two subtypes. This subtype deserves further genetic, epigenetic, and metabolomic studies.

Dynamic Self-guiding Analysis of Alzheimer's disease
Oncotarget 2015 (Jun 10);   6 (16):   14092–14122 ~ FULL TEXT

As constituents of a continuously remodeling tissue, neurons may undergo localized, transient, reversible, EMT-like, organizational transitions in response to a variety of physiological and non-physiological stimuli, such as growth factors, hormones, neuronal/brain stimulation/activity, learning, diet, physical activity, sleep, drugs, alcohol, smoking, hypoxia, and inflammation. In all likelihood, reversible organizational transitions occur continuously on multiple scales of space and time in synapses, neurites, neurons, and neuronal networks to enable neuronal plasticity, learning, memory, and cognition. They are expected to occur continuously throughout life throughout the body, with an especially high frequency and/or extent during developmental stages, active learning, regeneration, sleep-wake cycles, and in the regions of high neuronal plasticity/restructuring. However, when the (APP-associated?) signaling/metabolic network that controls these transitions is dysregulated, neurons/neurites/synapses may become locked in cancer-like, pro-secretion, pro-inflammatory modes/phenotypes, which are unable to support stable tissue architecture, thus leading to a progressive impairment of synaptic and neuronal functions, the accumulation and deposition of A-beta and neurofibrillary tangles, and impaired learning, progressive loss of memory, and cognitive decline. Similar to tumorigenesis, AD pathogenesis is expected to progress slowly and imperceptibly over time, accelerating non-linearly in the elderly and/or during the last stages of the disease, as an avalanche

Reversal of Cognitive Decline: A Novel Therapeutic Program
Aging (Albany NY). 2014 (Sep);   6 (9):   707–717 ~ FULL TEXT

This report describes a novel, comprehensive, and personalized therapeutic program that is based on the underlying pathogenesis of Alzheimer's disease, and which involves multiple modalities designed to achieve metabolic enhancement for neurodegeneration (MEND). The first 10 patients who have utilized this program include patients with memory loss associated with Alzheimer's disease (AD), amnestic mild cognitive impairment (aMCI), or subjective cognitive impairment (SCI). Nine of the 10 displayed subjective or objective improvement in cognition beginning within 3-6 months, with the one failure being a patient with very late stage AD. Six of the patients had had to discontinue working or were struggling with their jobs at the time of presentation, and all were able to return to work or continue working with improved performance. Improvements have been sustained, and at this time the longest patient follow-up is two and one-half years from initial treatment, with sustained and marked improvement. These results suggest that a larger, more extensive trial of this therapeutic program is warranted. The results also suggest that, at least early in the course, cognitive decline may be driven in large part by metabolic processes. Furthermore, given the failure of monotherapeutics in AD to date, the results raise the possibility that such a therapeutic system may be useful as a platform on which drugs that would fail as monotherapeutics may succeed as key components of a therapeutic system

Neuroprotective Sirtuin Ratio Reversed by ApoE4
Aging (Albany NY). 2014 (Sep);   6 (9):   707–717 ~ FULL TEXT

The canonical pathogenesis of Alzheimer's disease links the expression of apolipoprotein E ε4 allele (ApoE) to amyloid precursor protein (APP) processing and Aβ peptide accumulation by a set of mechanisms that is incompletely defined. The development of a simple system that focuses not on a single variable but on multiple factors and pathways would be valuable both for dissecting the underlying mechanisms and for identifying candidate therapeutics. Here we show that, although both ApoE3 and ApoE4 associate with APP with nanomolar affinities, only ApoE4 significantly

(i)   reduces the ratio of soluble amyloid precursor protein alpha (sAPPα) to Aβ;

(ii)   reduces Sirtuin T1 (SirT1) expression, resulting in markedly differing ratios of neuroprotective SirT1 to neurotoxic SirT2;

(iii)   triggers Tau phosphorylation and APP phosphorylation; and

(iv)   induces programmed cell death.

We describe a subset of drug candidates that interferes with the APP-ApoE interaction and returns the parameters noted above to normal. Our data support the hypothesis that neuronal connectivity, as reflected in the ratios of critical mediators such as sAPPα:Aβ, SirT1:SirT2, APP:phosphorylated (p)-APP, and Tau:p-Tau, is programmatically altered by ApoE4 and offer a simple system for the identification of program mediators and therapeutic candidates.

Next Generation Therapeutics for Alzheimer's disease
EMBO Mol Med. 2013 (Jun);   5 (6):   795–798 ~ FULL TEXT

However, if the optimal therapeutic approach to AD does indeed turn out to involve a multi-component cocktail, an obvious consideration relates to the development and approval processes required for a cocktail approach: in the case of HIV treatment, each of the cocktail's constituents exerts a significant, albeit modest, effect on HIV infection. However, considering the numerous mechanisms identified as underlying AD pathogenesis, it is conceivable that many more than three different therapeutic agents will be required for optimal treatment of AD. Of even greater concern is the possibility that none of the components of the optimal therapeutic cocktail will turn out to exert a significant therapeutic effect when administered alone. How, then, would the optimal combination be identified, and ultimately approved for clinical use? Significant modernization of the current translational approach, clinical trial methodology and approval process may be required to render the optimization and approval of such a therapeutic cocktail feasible.

Nutrient Biomarker Patterns, Cognitive Function, and MRI Measures of Brain Aging
Neurology. 2012 (Jan 24);   78 (4):   241–249 ~ FULL TEXT

Research investigators at the Department of Neurology of the Oregon Health & Science University reveal that higher blood levels of omega-3 fatty acids, vitamin B, vitamin C, vitamin D and vitamin E are associated with better mental functioning in the elderly.
You may want to review this New York Times review of this study.

Novel Mediators of Amyloid Precursor Protein Signaling
Journal of Neuroscience 2009 (Dec 16);   29 (50):   15703–15712 ~ FULL TEXT

Multiple recent reports implicate amyloid precursor protein (APP) signaling in the pathogenesis of Alzheimer's disease, but the APP-dependent signaling network involved has not been defined. Here, we report a novel consensus sequence for interaction with the PDZ-1 and PDZ-2 domains of the APP-interacting proteins Mint1, Mint2, and Mint3 (X11alpha, X11beta, and X11gamma), and multiple novel interactors for these proteins, with the finding that transcriptional coactivators are highly represented among these interactors. Furthermore, we show that Mint3 interaction with a set of the transcriptional coactivators leads to nuclear localization and transactivation, whereas interaction of the same set with Mint1 or Mint2 prevents nuclear localization and transactivation. These results define new mediators of the signal transduction network mediated by APP.

Neurodegeneration in Alzheimer's disease: Caspases and Synaptic Element Interdependence
Molecular Neurodegeneration 2009 (Jun 26);   4:   27 ~ FULL TEXT

We present here a model for Alzheimer's disease that is based not on chemically and physically-mediated toxic effects of Aβ, but on imbalanced signal transduction. The model suggests that the imbalance lies in the ratio of the signals that mediate synaptic maintenance, neurite extension, and cell survival vs. those that mediate synaptic reorganization, neurite retraction, and programmed cell death – essentially, memory retention vs. forgetting and memory reorganization. This model suggests that Aβ has a physiological function as a neuromodulatory peptide, and at least in some cases that it functions as an anti-trophin – competing, for example, with netrin-1 for binding to APP. Whether it has analogous functions related to its described interactions with other receptors, such as PrP, p75NTR, and RAGE, remains to be determined. This model also proposes that synaptic element interdependence is a critical factor in synaptic maintenance vs. reorganization, with associated effects on memory retention vs. loss. Both pre-synaptic and post-synaptic elements exert trophic and anti-trophic influences on each other, and the balance determines whether synaptic maintenance or reorganization will occur. The molecular details of the model are summarized in Figure 4.

Netrin-1 Interacts with Amyloid Precursor Protein and Regulates Amyloid-beta Production
Cell Death Differ. 2009 (May);   16 (5):   655–663 ~ FULL TEXT

The beta-amyloid precursor protein (APP) is an orphan transmembrane receptor whose physiological role is largely unknown. APP is cleaved by proteases generating amyloid-beta (Abeta) peptide, the main component of the amyloid plaques that are associated with Alzheimer's disease. Here, we show that APP binds netrin-1, a multifunctional guidance and trophic factor. Netrin-1 binding modulates APP signaling triggering APP intracellular domain (AICD)-dependent gene transcription. Furthermore, netrin-1 binding suppresses Abeta peptide production in brain slices from Alzheimer model transgenic mice. In this mouse model, decreased netrin-1 expression is associated with increased Abeta concentration, thus supporting netrin-1 as a key regulator of Abeta production. Finally, we show that netrin-1 brain administration in Alzheimer model transgenic mice may be associated with an amelioration of the Alzheimer's phenotype.

Reversal of Alzheimer's-like Pathology and Behavior in Human APP
Transgenic Mice by Mutation of Asp664

Proc Natl Acad Sci U S A. 2006 (May 2);   103 (18):   7130–7135 ~ FULL TEXT

The deficits characteristic of Alzheimer's disease (AD) are believed to result, at least in part, from the neurotoxic effects of beta-amyloid peptides, a set of 39-43 amino acid fragments derived proteolytically from beta-amyloid precursor protein (APP). APP also is cleaved intracytoplasmically at Asp-664 to generate a second cytotoxic peptide, APP-C31, but whether this C-terminal processing of APP plays a role in the pathogenesis of AD is unknown. Therefore, we compared elements of the Alzheimer's phenotype in transgenic mice modeling AD with vs. without a functional Asp-664 caspase cleavage site.

Surprisingly, whereas beta-amyloid production and plaque formation were unaltered, synaptic loss, astrogliosis, dentate gyral atrophy, increased neuronal precursor proliferation, and behavioral abnormalities were completely prevented by a mutation at Asp-664. These results suggest that Asp-664 plays a critical role in the generation of Alzheimer-related pathophysiological and behavioral changes in human APP transgenic mice, possibly as a cleavage site or via protein-protein interactions.

Misfolded Proteins, Endoplasmic Reticulum Stress and Neurodegeneration
Curr Opin Cell Biol. 2004 (Dec);   16 (6):   653–662 ~ FULL TEXT

The ER is very sensitive to changes in its environment, and such changes may lead to disruption of its normal homeostasis. A variety of environmental insults, as well as genetic diseases associated with the accumulation of misfolded proteins, can all affect the ER structure, function and integrity, leading to ER stress and contributing to the pathogenesis of different disease states. Prolonged stress leads to organelle damage and dysfunction, and ultimately triggers PCD. The accumulation of misfolded proteins seen in various neurodegenerative diseases leads to an ER stress response, irrespective of whether the misfolded proteins build up within the ER or outside the ER. Further insights into the pathways triggered by misfolded proteins, ER stress responses and cell death programs should facilitate the development of new therapeutic strategies for neurodegenerative disorders and other disorders that feature misfolded proteins.

Amyloid Beta Protein Toxicity Mediated by the Formation of Amyloid-beta Protein Precursor Complexes
Annals of Neurology 2003 (Dec);   54 (6):   781–789

The amyloid-beta protein precursor, a type 1 transmembrane protein, gives rise to the amyloid beta-protein, a neurotoxic peptide postulated to be involved in the pathogenesis of Alzheimer's disease. Here, we show that soluble amyloid beta protein accelerates amyloid precursor protein complex formation, a process that contributes to neuronal cell death. The mechanism of cell death involves the recruitment of caspase-8 to the complex, followed by intracytoplasmic caspase cleavage of amyloid precursor protein. In vivo, the levels of soluble amyloid beta protein correlated with caspase-cleaved fragments of the amyloid precursor protein in brains of Alzheimer's disease subjects. These findings suggest that soluble amyloid beta protein-induced multimerization of the amyloid precursor protein may be another mechanism by which amyloid beta protein contributes to synapse loss and neuronal cell death seen in Alzheimer's disease.

 
   

The Nutritional Approach
 
   

Brain Atrophy in Cognitively Impaired Elderly: The Importance of Long-chain ω-3 Fatty Acids
and B Vitamin Status in a Randomized Controlled Trial

American J Clinical Nutrition 2015 (Jul);   102 (1):   215–221 ~ FULL TEXT

The beneficial effect of B vitamin treatment on brain atrophy was observed only in subjects with high plasma ω-3 fatty acids. It is also suggested that the beneficial effect of ω-3 fatty acids on brain atrophy may be confined to subjects with good B vitamin status. The results highlight the importance of identifying subgroups likely to benefit in clinical trials. This trial was registered at www.controlled-trials.com as ISRCTN94410159.

Effect of Vitamin E and Memantine on Functional Decline in Alzheimer Disease:
The TEAM-AD VA Cooperative Randomized Trial

JAMA. 2014 (Jan 1);   311 (1):   33–44 ~ FULL TEXT

We found that a dosage of 2000 IU/d of alpha tocopherol was effective in slowing the functional decline of mild to moderate AD and was also effective in reducing caregiver time in assisting patients. Neither memantine nor the combination of alpha tocopherol and memantine showed clinical benefit in patients with mild to moderate AD. These findings suggest that alpha tocopherol is beneficial in mild to moderate AD by slowing functional decline and decreasing caregiver burden.

Preventing Alzheimer's Disease-related Gray Matter Atrophy by B-vitamin Treatment
Proc Natl Acad Sci U S A. 2013 (Jun 4);   110 (23):   9523–9528 ~ FULL TEXT

A combination of B vitamins was found to slow brain loss in areas of the brain associated with Alzheimer's disease. This same combination of vitamins has also been shown previously to slow cognitive decline.

Omega-3 Fatty Acids Enhance Phagocytosis of Alzheimer's Disease-Related Amyloid-ß42
by Human Microglia and Decrease Inflammatory Markers

J Alzheimers Dis. 2013 (May 21);   35 (4):   697–713 ~ FULL TEXT

The use of supplements with omega-3 fatty acids (FAs) such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) is widespread due to proposed beneficial effects on the nervous and cardiovascular systems. Many effects of omega-3 FAs are believed to be caused by down-regulation and resolution of inflammation. Alzheimer's disease (AD) is associated with inflammation mediated by microglia and astrocytes, and omega-3 FAs have been proposed as potential treatments for AD. The focus of the present study is on the effects of DHA and EPA on microglial phagocytosis of the AD pathogen amyloid-ß, on secreted and cellular markers of immune activity, and on production of brain-derived neurotrophic factor (BDNF). Human CHME3 microglial cells were exposed to DHA or EPA, with or without the presence of Aß42. Phagocytosis of Aß42 was analyzed by flow cytometry in conjunction with immunocytochemistry using antibodies to cellular proteins. Secreted proteins were analyzed by ELISA. Both DHA and EPA were found to stimulate microglial phagocytosis of Aß42. Phagocytosis of Aß42 was performed by microglia with a predominance of M2 markers. EPA increased the levels of BDNF in the culture medium. The levels of TNF-alpha were decreased by DHA. Both DHA and EPA decreased the pro-inflammatory M1 markers CD40 and CD86, and DHA had a stimulatory effect on the anti-inflammatory M2 marker CD206. DHA and EPA can be beneficial in AD by enhancing removal of Aß42, increasing neurotrophin production, decreasing pro-inflammatory cytokine production, and by inducing a shift in phenotype away from pro-inflammatory M1 activation.

Cognitive Function After Supplementation With B Vitamins and Long-chain
Omega-3 Fatty Acids: Ancillary Findings From the SU.FOL.OM3 Randomized Trial

Am J Clin Nutr. 2011 (Jul);   94 (1):   278–286 ~ FULL TEXT

This study investigated the effects of supplementation on cognition in a high-risk population. In subjects with prior stroke, B vitamins plus omega-3 fatty acids were associated with a higher score on the temporal orientation cognition task vs those assigned to placebo. Effects may be group specific and may be useful in interventions aimed at preventing cognitive decline in high-risk individuals

Homocysteine-lowering by B Vitamins Slows the Rate of Accelerated Brain Atrophy
in Mild Cognitive Impairment: A Randomized Controlled Trial

PLoS One. 2010 (Sep 8);   5 (9):   e12244 ~ FULL TEXT

The Oxford Project to Investigate Memory and Ageing (OPTIMA) investigated the effect of B-vitamin supplementation on various parameters of brain aging and associated cognitive function. The treatment group was given daily supplementation of the following B vitamins: folic acid (800 mcg), vitamin B12 (500 mcg) and vitamin B6 (20 mg). The main outcome measured was change in rate of whole brain atrophy on MRI investigation after 24 months of supplementation compared to the placebo group. Study results showed that the group taking the B-vitamin cocktail experienced a 30–percent slower rate of brain atrophy, on average, and in some cases patients experienced reductions as high as 53 percent. Greater rates of atrophy were associated with lower cognitive test scores. In the control group, the the rate of atrophy was directly associated with elevated homocysteine levels.

Trace Elements and Cognitive Impairment: An Elderly Cohort Study
Archives of Gerontology and Geriatrics 2004;   (9):   393–402 ~ FULL TEXT

Dementia is one of the most pressing public health problems with social and economic implication. The form called cognitive impairment non-dementia (CIND)represents a subclinical phase of dementia. Different studies have shown a possible effect of micro- and macro-nutrients on cognitive function. Trace elements, being involved in metabolic processes and redox reactions in the central nervous system (CNS), could influence the cognitive functions. This study evaluated the presence of an eventual correlation between serum trace element concentrations and cognitive function in a group of subjects with CIND and manifest dementia (Alzheimer dementia = AD, and vascular dementia = VaD), and compared them with a control group. Thirty -five patients were enrolled in this study. Each patient underwent a clinical and biochemical examination. We also performed a neuropsychological and functional assessment (the Milan overall dementia assessment = MODA, activities of daily living = ADL, and instrumental activities of daily living = IADL), and a computerized tomographic (CT) cerebral scan. Patients were than divided in 4 groups according to the obtained diagnosis (Controls, CIND, AD, VaD).

The presence of any acute or chronic conditions, affecting cognitive functions, was considered as exclusion criteria. A blood sample was collected to determine iron (Fe), zinc (Zn), manganese (Mn), selenium (Se), cobalt (Co), chromium (Cr), copper (Cu), molybdenum (Mo) and aluminium (Al) serum concentrations (chromatographic, spectrophotometric methods). In our cohort we found a positive correlation between cognitive function, expressed as the MODA score, and Se, Cr, Co and Fe serum levels, while a negative correlation was observed between MODA score, Cu and Al serum levels. Moreover, some statistically significant differences in Se, Cr, Co, Cu and Al concentrations were found among the groups. According to these results, we may suppose that Se, Cr and Co protect cognitive function, Cu influences the evolution of cognitive impairment, while Al contributes to the pathogenesis of AD.

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