FAQs About Dementia, memory loss and Alzheimer's DiseaseBy Michael Mullan MD, PhD.
Although nothing in this document is meant to replace the attention of a well trained professional in the diagnosis and treatment of dementia, memory loss or Alzheimer's Disease, it is meant as a helpful guide to frequently asked questions that many friends and family members have asked me over the years.Question: what is the difference between dementia and Alzheimer's Disease?
To be described as having dementia you have the have three things amiss:
1) Loss of memory
2) Loss of some other mental faculty such as the normal use of language - word finding problems or repetitiveness are examples (there are many others - see below)
3) Problems 1) and 2) are sufficiently severe to interfere with normal activities of daily living such as dressing washing attending to finances or successfully navigating to shops.
So dementia is a general term that just describes the state of the subject but it does not describe the cause.
Alzheimer's Disease is a specific type of dementia but there are many many other forms of dementia. Alzheimer's Disease has certain characteristics which distinguish it from other types of dementia and will be discussed in more detail below. Question: What is Alzheimer's Disease?Alzheimer's Disease is named after a German psychiatrist that first described it in a relatively young woman in 1907. However, nowadays we are most accustomed to the much more common late onset form of the disease ie when the disease occurs in those over 65 years of age. Alzheimer's Disease is known as a neurodegenerative disease which means that as the disease progresses the brain is gradually destroyed but that is in the relatively late stages of the disease. In the earlier stages not so much damage had been done to the brain and in the very early stages it is difficult to see any changes on brain scans. But what is actually happening in the brains of people with Alzheimer's Disease? Well it depends on the stage. In the very early stages there is an accumulation of a small protein called amyloid. Amyloid is a normal constituent of the brain and we all make it throughout our lives but we are able to clear it from our brains into the blood stream where it is broken down by the liver. For reasons which are not completely clear in some brains amyloid begins to accumulate and forms insoluble clumps called plaques. The accumulation of amyloid results in a lot of inflammation in the brain and over a long period this leads to destruction of neurons. As the neurons are being placed under stress from the toxic effects of the amyloid they start to lose their normal structures and start to accumulate another protein called tau. Tau has a normal function in transporting chemicals inside the neurons so when it is disrupted so are important functions of the neuron. When tau accumulates it forms structures called tangles. When neurons start to malfunction we lose our memories or the use of language, orientation and other mental faculties. So the underlying cause of all the clinical symptoms in Alzheimer's Disease is the damage caused by amyloid plaques and the tau tangles. This process takes place over many years perhaps as long as twenty in many cases. During the early stages of amyloid accumulation and even tangle formation there may be no symptoms. People have been found to have a lot of amyloid in their brains with no clinical symptoms. But generally speaking when amyloid persists for many years the other changes described here begin to take place with the inevitable decline in mental functioning.To learn more about Dr. Michael Mullan's research please visit Roskamp Institute website or about Dr. Michael Mullan webpage
Binding of Nicotine and Anatabine in the Receptor Pocket
Roskamp Institute recently made three presentations, thirteen posters and a press conference at the Society for Neuroscience 2012 convention in New Orleans, the largest annual neurology related conference in the world. The Institute demonstrated, in support of previous research, anatabine’s anti-inflammatory properties. Building on these findings show that anatabine could be beneficial to control inflammation in the treatment of Alzheimer’s disease, traumatic brain injury, multiple sclerosis and other autoimmune disorders.
Dr. Michael Mullan, president and CEO the Roskamp Institute noted that; “Both traumatic brain injury (TBI) and multiple sclerosis (MS) have in common massive brain inflammation. The reason anatabine looks so promising in both these conditions is likely because, as we have previously shown, it is a potent anti-inflammatory agent. Although anatabine’s anti-inflammatory activity may have different roles in each of these conditions the net result is to reduce the clinical and neuropathological consequences.”
Scientists at Roskamp Institute in Sarasota, Florida have conducted research with results that suggest anatabine may benefit people who have autoimmune disorders such as multiple sclerosis. Experiments were conducted using well established protocols in mice with pathologies typical of multiple sclerosis. Among the data recorded was the amount of inflammation on the spinal cord of control and anatabine treated mice during the acute phase of the disease. Results show a 86% effective rate in controlling inflammation and recovery from posterior hindlimb paralysis versus 34% in the placebo control population. Conclusions are that production of pro-inflammatory cytokines seem to be regulated with the administering of anatabine treated mice over the control which leads to greater recover from the paralysis condition. This study warrants further study especially associate with the chronic phase of multiple sclerosis and other autoimmune disorders.
According to the Centers for Disease Control, 80,000 people in the United States suffer long-term disability from a traumatic brain injury (TBI) annually. Roskamp Institute scientists conducted a research study of TBI and control mice by administering anatabine to measure its effectiveness for recovery from injury using scientific accepted methods. TBI mice treated with a placebo and the sham (untreated) mice recovered at a similar rate with deteriorated motor and cognitive functions. The anatabine treated mice however had a significant recovery the researchers believe, by inhibiting inflation and reducing amyloid production. To quote the published research paper; “Anatabine treatment appeared to completely prevent the loss of spatial memory retention following severe TBI. Further study of this promising treatment is warranted and will include treatment in a mild closed head injury model as well as long term outcome from injury. Dietary supplementation for reducing secondary injury after TBI offers an easy path to clinical application and simplifies the administration of the therapeutic.” This pathological information warrant further studies with ongoing research in exploring other models of TBI using anatabine.
Research study findings by Roskamp Institute were presented at Neuroscience 2012 about the impact of anatabine in treating Alzheimer’s disease (AD). AD is a neurodegenerative disorder that causes problems with memory and behavior due to the increasing death of nerve cells in the brain. Most scientists, supported by research done at Roskamp Institute, agree that excessive amyloid plaque buildup (Abeta peptides) and neurofibrillary tangles (twisted protein fibers named tau) are directly related to the brain nerve cell loss. Data from the study using a well-known mouse model of AD shows that anatabine treated mice have a significant reduction in the accumulation of plaque in the brain as compared to the control population. Scientists believe this occurs because anatabine reduces or regulates human neuronal like protein BACE-1 (the rate limiting enzyme responsible for Abeta production). Cognitive tests of an ongoing investigation of anatabine treated mice show greater cerebral functions and improved abilities as compared to the non-treated sample. Data from the study also show anatabine’s anti-inflammatory results. Anatabine reduces neuroinflammation and STAT3 phosphorylation in the brain of transgenic AD mice. Additional research is warranted based upon results of this study regarding the potential benefit of anatabine in the treatment of Alzheimer’s disease.
The Roskamp Institute, located in Tampa, was one of few memory clinics across the United States that participated in a study that tested the effect of NSAIDs on the cognitive ability of patients suffering from Alzheimer’s disease (AD). The NSAIDs, non-steroidal anti-inflammatory drugs used to decrease inflammation, did not improve the cognitive functions of the Alzheimer’s patients. The Roskamp Institute registered over 400 seniors of at least 70 years of age. Each was required to have at least one relative with AD-like dementia. Two-third of the patients received either Naproxen or Celecoxib, and the remaining received a sugar pill. All were checked on and given memory tests annually for five years. The results showed that Naproxen may be a factor in impairing the memory and other mental functions, but further study is needed to verify if the results are consistent or if they were due to the fact that the patients who did not test as well were already suffering from early stages of dementia. The results for this study, as part of the Alzheimer’s Disease Anti-Inflammatory Prevention Trial (ADAPT), were published in Archives of Neurology
For more information about this study, please visit http://www.ncbi.nlm.nih.gov/pubmed/18474729
August 3, 2012
Alzheimer’s disease (AD) characterized by two main features in the brain, an extracellular accumulation of beta-amyloid peptide (Aβ) into plaques and an intracellular buildup of neurofibrillary tangles made of a protein called tau. In addition, it has also been found that the brains of AD patients are continuously present in inflammatory states.
The neurofibrillary tangles are results of an accumulation in neuronal cells of tau protein that has been hyper-phosphorylated and self-assembled into a new form. The buildup of Aβ is a likely cause for the formation of the neurofibrillary tangles in Alzheimer’s patients.
Inflammation in the brain also has a possible link to the accumulation of Aβ. The Roskamp Institute has found that the binding of CD40 ligand (CD40L) to its receptor CD40 is harmful for AD. This proved to be true in a transgenic mouse model for AD TG2576, as prohibiting the binding of CD40-CD40L lessened Aβ buildup and the neuroinflammation.
In a study published in Brian Research, the Roskamp Institute reported findings that indicated that a decrease in the hyper-phosphorylation of the tau protein is not related to the accumulation of Aβ. A CD40 or CD40L deficiency in the mouse model for AD Tg2576 also decreased the hyper-phosphorylation of the tau protein, which implies that the CD40-CD40L pathway has a direct impact on tau phosphorylation.
These studies and findings indicate that the CD40-CD40L pathway has a direct effect on the two main characteristics of AD, which increases the possibility for it to be targeted in future therapeutic solutions.
For more information and updates on Alzheimer’s disease, please visit
August 3, 2012
Alzheimer’s disease (AD) is recognized by the buildup of the protein amyloid beta (Aβ), but many researchers have also found an increase of the molecule CD40L in the brains of Alzheimer’s patients. A research group at the Roskamp Institute, headed by Dr. Michael Mullan, found that the stimulation of CD40L increases the levels of Aβ in the cellular models of AD and the stimulation of CD40L of cells that are needed for the defense of the nervous system results in increases of cytokines (pro-inflammatory molecules). GM-SCF, the granulocyte macrophage colony stimulation factor, is a cytokine that is a part of the brain’s inflammation responses. Many previous studies have linked Alzheimer’s disease with increases in levels of pro-inflammatory cytokines. Through their study, which was published in the journal, Cytokine, the Roskamp researchers’ results have indicated that GM-SCF “operates downstream of CD40/CD40L interaction and that GM-CSF modulates Aβ production” (Volmar et al., in press).
For the publication of this study, please visit http://www.ncbi.nlm.nih.gov/pubmed/18434187.
For more information and updates on Alzheimer’s disease, please visit
Dementia robs individuals of their memory, mental function, and social interaction skills. Alzheimer’s disease (AD) is a form of dementia that is easily distinguishable from the others. This neurodegenerative disease includes early signs that are consistent with each patient and involves the loss of short term memory. Recently presented information will evaporate after a short period of time for Alzheimer’s patients.
Individuals in the early stages of AD will have a hard time retaining any fresh information presented to them. Forgetting what they talked about on the phone only a few minutes ago or arriving at the grocery store with no recollection of what they planned on purchasing are just simple examples of how AD can impact the daily routine of an individual’s life.
In today’s society, technology is a leading source of knowledge. Computers, televisions, radios, and phones are regularly used to distribute ideas and provide the latest updates about the happenings around the world. Because of this, Alzheimer’s disease patients are at a disadvantage since they lack the ability to store these current events in their memory. An individual’s incapability to remember any updates about current events, such as the presidential election or the Olympics, can be an early sign of the disease and should serve as a trigger for visiting a memory disorder clinic for an evaluation.
The Roskamp Institute, with one location in Sarasota, Florida and one in Tampa, Florida, offers full evaluations for Alzheimer’s disease and other causes of memory loss.
For the original article, please visit http://www.roskampinstitute.us/articles/archives/39.
For more information and updates on Alzheimer’s disease, please visit
August 2, 2012
The search for signs in the human body that can be effective in screening and preventing Alzheimer’s disease (AD) is never ending. In a recently published on the online issue of Neurology
, the medical journal of the American Academy of Neurology, on July 18th, researchers from Mayo Clinic, John Hopkins University School of Medicine, and Columbia University share their findings of about the series of serum ceramides that are possibility linked with the development of AD. Previous studies have associated serum ceramides with memory impairment and volume loss in the hippocampus. This cohort study involved two types of fatty molecules, sphingomyelins and ceramides. Ceramides are involved in the production of the precursors of amyloid, which can form into insoluble plaques in the brain and lead to AD. The participants were 99 women in the Women’s Health and Aging Study II, and all were without dementia and within the age range of 70 to 79. Their blood was tested, and levels of sphingomyelins and ceramides were measured. They were split into three groups, high, middle, and low, based on the levels of ceramides in their blood. All 99 were registered to be in a prospective study and checked on for up to six visits over nine years. The results showed that 27 of the 99 participants had developed incident dementia, and of the 27, two-thirds received a diagnosis of probable AD. In relation to the level of ceramides found in their blood, those in the high group were ten times at risk for AD than those in the low group, while those in the middle group were eight times more at risk.
These results are significant, as they are consistent with previous research and could possibly provide an economical, convenient, and accurate biomarker for AD. Further studies will need to be conducted with a larger and more diverse study group to confirm these findings.
Keywords: Alzheimer’s disease; serum ceramides; biomarker
Sources: http://www.neurology.org/content/early/2012/07/18/WNL.0b013e318264e3e2.excerpt http://www.neurology.org/content/early/2012/07/18/WNL.0b013e318264e380.abstract
July 25, 2012
Recent studies in at this month’s Alzheimer’s Association International Conference in Vancouver, Canada has shown that the way a person walks is linked to cognitive function. That is, the speed and style by which a person walks correlates with cognitive changes that may eventually lead to the development of Alzheimer’s disease (AD). Signs of cognitive failure include walking at a slower pace, and fluctuated or uncontrolled walking. Usual studies of AD involve patients who do not move, but the thinking capabilities of the human brain have a strong relationship with its movement skills. While research for the link between walking and mental function has been going on for the past decade, it has been recently taken into new heights because these studies have revealed more specifics about the relationship. For example, the variation and pace in walking is linked with a person’s ability to plan and organize, while rhythm is associated with the speed by which information is processed. The decline in cognitive functions has a parallel relationship with a decrease in walking speed. Newer studies have been incorporated more detailed and advanced approaches than previous research in terms of measuring changes in gait, such as making the participants multitask or having them use electronic walkways. These studies may lead to a new method in which symptoms of AD can be detected earlier on, as to prevent the development of the disease. It also reinforces the idea that dementia can be delayed with an activity that should be common to humankind, exercise.
For further details on these studies and on Alzheimer’s disease, please visit:
Keywords: Alzheimer’s disease; walking; exercise; cognitive functions
July 24, 2012
Preliminary results of the treatment of a mouse model of Multiple Sclerosis with Anatabine. Roskamp Institute scientists Dr. Michael Mullan and Dr. Daniel Paris used a standard model of MS (multiple sclerosis) to assess the effects of anatabine in this disease characterized by very high levels of inflammation in the brain. The mouse model known as EAE (experimental autoimmune enchephalomyelitis) is characterized by high levels of circulating antibodies to the fatty sheaths that surround nerve fibers. The model is induced by vaccinating mice with myelin which induces an autoimmune reaction. As a consequence there is a devastating inflammatory process in the brain which has the effect of destroying neurons and causing progressive paralysis. In this regard the disease model looks very similar to that which occurs in human MS. Treatment with anatabine resulted in a dramatic reduction in the rate of paralysis of hind limbs.
Dr. John L. Faessel
ON THE MARKET
Commentary and InsightsReport from the Harvard Club Meeting
Dr. Mullan and the Roskamp Institute have conducted research relating to the company's anatabine compound for a number of years. Dr. Mullan first spoke to and thoroughly reprised with the supporting graphs the research that the Roskamp Institute has performed, essentially what he presented last June at a Roskamp Institute meeting. Mullan again played the videos that showed standard
Alzheimer's-afflicted mice beginning not only to remember again, but becoming able to add critical new information to the cognitive equation and, thus, to change behavior so as even to improve their lot after the administration of anatabine. That's impossible for a "demented" mouse. A split screen video depicted for comparison a mouse fully impaired with the disease. He went on to say that CRP* levels also fell 50% in these test animals, indicating less inflammation. Dr. Mullan called the research "profound." For more details of the articles please visit: http://seekingalpha.com/instablog/576542-dr-john-faessel/618891-report-from-the-harvard-club-meeting-re-cigx-snowballing-progress