oxidative damage found to be present in early Alzheimer's disease. This early mild cognitive impairment is the time for treatment to delay disease progression. As this study points out, most studies up to this point have been done on individuals with late Alzheimer's disease. This show that oxidative damage plays a prominent role in disease development. This study found oxidative damage through several markers: lipid peroxides,isoprostanes, 8-hydroxy-2-deoxyguanosine...
Combination of DHA, EPA, choline, phospholipids, Folate, B12, B6, vitamin C and E, and selenium improves memory and cognitive function in those with mild Alzheimer's disease.
Androgen deprivation therapy appears to increase Alzheimer's disease risk. In this study, the men on ADT the longest was found to be associated with increased diagnosis of Alzheimer's disease.
small study, but well designed that showed that huperzine A supplementation improved executive function in Alzheimer's patients. Huperzine A is an acetylcholinesterase inhibitor.
Review of 6 trials on 454 patients found Huperzine A improved cognition and executive function with no serious adverse events in patients with Alzheimer's disease. Yet, their conclusion is, "...inadequate evidence to make any recommendation..." Does it improve executive cognitive function? Yes. Does in have serious side effects? No. And we are waiting on...?
vitamin C inhibits acetylcholinesterase. This will increase acetylcholine and thus can play a role in Alzheimer's disease. People with Alzheimers disease have low levels of Vitamin C. Vitamin C shown to improve memory in Alzheimer's mouse model.
Long-chain polyunsaturated fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are highly enriched in neuronal synaptosomal plasma membranes and vesicles
The predominant CNS polyunsaturated fatty acid is DHA
effective supplementation and/or increased ingestion of dietary sources rich in EPA and DHA, such as cold-water fish species and fish oil, may help improve a multitude of neuronal functions, including long-term potentiation and cognition.
multiple preclinical studies have suggested that DHA and/or EPA supplementation may have potential benefit through a multitude of diverse, but complementary mechanisms
pre-injury dietary supplementation with fish oil effectively reduces post-traumatic elevations in protein oxidation
The benefits of pre-traumatic DHA supplementation have not only been independently confirmed,[150] but DHA supplementation has been shown to significantly reduce the number of swollen, disconnected and injured axons when administered following traumatic brain injury.
DHA has provided neuroprotection in experimental models of both focal and diffuse traumatic brain injury
potential mechanisms of neuroprotection, in addition to DHA and EPA's well-established anti-oxidant and anti-inflammatory properties
Despite abundant laboratory evidence supporting its neuroprotective effects in experimental models, the role of dietary DHA and/or EPA supplementation in human neurological diseases remains uncertain
Several population-based, observational studies have suggested that increased dietary fish and/or omega-3 polyunsaturated fatty acid consumption may reduce risk for ischemic stroke in several populations
Randomized control trials have also demonstrated significant reductions in ischemic stroke recurrence,[217] relative risk for ischemic stroke,[2] and reduced incidence of both symptomatic vasospasm and mortality following subarachnoid hemorrhage
Clinical trials in Alzheimer's disease have also been largely ineffective
The clinical evidence thus far appears equivocal
curcumin has gained much attention from Western researchers for its potential therapeutic benefits in large part due to its potent anti-oxidant[128,194,236] and anti-inflammatory properties
Curcumin is highly lipophilic and crosses the blood-brain barrier enabling it to exert a multitude of different established neuroprotective effects
in the context of TBI, a series of preclinical studies have suggested that pre-traumatic and post-traumatic curcumin supplementation may bolster the brain's resilience to injury and serve as a valuable therapeutic option
Curcumin may confer significant neuroprotection because of its ability to act on multiple deleterious post-traumatic, molecular cascades
studies demonstrated that both pre- and post-traumatic curcumin administration resulted in a significant reduction of neuroinflammation via inhibition of the pro-inflammatory molecules interleukin 1β and nuclear factor kappa B (NFκB)
no human studies have been conducted with respect to the effects of curcumin administration on the treatment of TBI, subarachnoid or intracranial hemorrhage, epilepsy or stroke
studies have demonstrated that resveratrol treatment reduces brain edema and lesion volume, as well as improves neurobehavioral functional performance following TBI
green tea consumption or supplementation with its derivatives may bolster cognitive function acutely and may slow cognitive decline
At least one population based study, though, did demonstrate that increased green tea consumption was associated with a reduced risk for Parkinson's disease independent of total caffeine intake
a randomized, placebo-controlled trial demonstrated that administration of green tea extract and L-theanine, over 16 weeks of treatment, improved indices of memory and brain theta wave activity on electroencephalography, suggesting greater cognitive alertness
Other animal studies have also demonstrated that theanine, another important component of green tea extract, exerts a multitude of neuroprotective benefits in experimental models of ischemic stroke,[63,97] Alzheimer's disease,[109] and Parkinson's disease
Theanine, like EGCG, contains multiple mechanisms of neuroprotective action including protection from excitotoxic injury[97] and inhibition of inflammation
potent anti-oxidant EGCG which is capable of crossing the blood-nerve and blood-brain barrier,
Epigallocatechin-3-gallate also displays neuroprotective properties
More recent research has suggested that vitamin D supplementation and the prevention of vitamin D deficiency may serve valuable roles in the treatment of TBI and may represents an important and necessary neuroprotective adjuvant for post-TBI progesterone therapy
Progesterone is one of the few agents to demonstrate significant reductions in mortality following TBI in human patients in preliminary trials
in vitro and in vivo studies have suggested that vitamin D supplementation with progesterone administration may significantly enhance neuroprotection
Vitamin D deficiency may increase inflammatory damage and behavioral impairment following experimental injury and attenuate the protective effects of post-traumatic progesterone treatment.[37]
emerging evidence has suggested that daily intravenous administration of vitamin E following TBI significantly decreases mortality and improves patient outcomes
high dose vitamin C administration following injury stabilized or reduced peri-lesional edema and infarction in the majority of patients receiving post-injury treatment
it has been speculated that combined vitamin C and E therapy may potentiate CNS anti-oxidation and act synergistically with regards to neuroprotection
one prospective human study has found that combined intake of vitamin C and E displays significant treatment interaction and reduces the risk of stroke
Pycnogenol has demonstrated the ability to slow or reduce the pathological processes associated with Alzheimer's disease
Pcynogenol administration, in a clinical study of elderly patients, led to improved cognition and reductions in markers of lipid peroxidase
One other point of consideration is that in neurodegenerative disease states like Alzheimer's disease and Parkinson's disease, where there are high levels of reactive oxygen species generation, vitamin E can tend to become oxidized itself. For maximal effectiveness and to maintain its anti-oxidant capacity, vitamin E must be given in conjunction with other anti-oxidants like vitamin C or flavonoids
These various factors might account for the null effects of alpha-tocopherol supplementation in patients with MCI and Alzheimer's disease
preliminary results obtained in a pediatric population have suggested that post-traumatic oral creatine administration (0.4 g/kg) given within four hours of traumatic brain injury and then daily thereafter, may improve both acute and long-term outcomes
Acutely, post-traumatic creatine administration seemed to reduce duration of post-traumatic amnesia, length of time spent in the intensive care unit, and duration of intubation
At three and six months post-injury, subjects in the creatine treatment group demonstrated improvement on indices of self care, communication abilities, locomotion, sociability, personality or behavior and cognitive function when compared to untreated controls
patients in the creatine-treatment group were less likely to experience headaches, dizziness and fatigue over six months of follow-up
CNS creatine is derived from both its local biosynthesis from the essential amino acids methionine, glycine and arginine
Studies of patients with CNS creatine deficiency and/or murine models with genetic ablation of creatine kinase have consistently demonstrated significant neurological impairment in the absence of proper creatine, phosphocreatine, or creatine kinase function; thus highlighting its functional importance
chronic dosing may partially reverse neurological impairments in human CNS creatine deficiency syndromes
Several studies have suggested that creatine supplementation may also reduce oxidative DNA damage and brain glutamate levels in Huntington disease patients
Another study highlighted that creatine supplementation marginally improved indices of mood and reduced the need for increased dopaminergic therapy in patients with Parkinson's disease
Proof of concept study in Alzheimer's model finds high fat diet improves brain cholinergic synapses, targeting directly the neurotransmission deficits in Alzheimer's disease
Can Alzheimer's be prevented? New study suggests that nutrition, exercise, and healthy weight are key to Alzheimer's prevention. A decrease in amyloid plaques and tau tangles were noted in normal BMI individuals, those with greater physical activity and those on a mediterranean diet.
Study of memantine finds effect on insulin is the same in the brain as in the pancreas. In essence, Alzheimer's disease, is in part, a diabetes of the brain disease.
Ketone bodies have been shown to benefit the mitochondria in the brains of those with Alzheimer's disease. This ketosis can be achieved through low carb/protein, high fat diet.
SAMe helps to correct disordered homocysteine metabolism due to B- vitamin deficiency found in Alzheimer's disease. SAMe show to reduce amyloid production, improve memory, decrease Tau, and reduced plaque formation. Now, this was in a mice model, but SAMe as a methyl donor can benefit clients with dementia with minimal side effects.
SAMe shown to be neuroprotective by increasing SOD activity, increasing glutathione production and decreasing homocysteine levels in Alzheimer's even in the presence of vitamin B deficiency.
microglial and inflammatory response in Alzheimer's disease. Agonists of PPAR-gamma inhibit this action. This has important implications in reducing the local inflammatory response found in the brains of those with Alzheimers and other neuordegenerative disease.