F18 Alzheimer's pet scan benefits

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The Dementia Caregiver's Little Book of Hope [Kindle Edition]

Lippincott Williams & Wilkins 

Today's state-of-the-art in diagnosing Alzheimer's is the F18 PET Scan. See how it changed one man's life. Learn how 87% of patients who received an F18 scan made at least one change in their treatment plan.

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Until recently, the hardest part in diagnosing Alzheimer's was the difficulty in "seeing" what was going on in the brain. F18 PET scans changed all that, allowing doctors to "see" how much Alzheimer's plaque, if any, appeared in the brain. 

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When the first F18 tests hit the market, they cost a few thousand dollars and were available from only one source. Since then, there has been a rush of activity on the part of pharmaceutical companies to bring better and less expensive F18 tests to market. 

The first F18 test to detect brain amyloid deposits (also known as Alzheimer's plaques)was approved by the FDA in 2012. It was called Florbetapir F18 (renamed AMYViD™).

F18 tests approved by the FDA include:

Generic Name	Brand Name
Flutemetamol F18	Vizamyl™
Florbetaben F18	Neuraceq™
Florbetapir F18	AMYViD™

A Closer Look at Florbetapir F18

Seeing the amount of Alzheimer's plaque provides doctors with useful information on treatment and further testing for patients with cognitive impairment, according to the study published online by the journal Alzheimer Disease & Associated Disorders. The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

Positron emission tomography (PET) scans "light up" the florbetapir F18 biomarker to show amyloid plaques in the brain — a characteristic feature of Alzheimer's disease (AD). 

"Amyloid imaging results altered physicians' diagnostic thinking, intended testing and management of patients undergoing evaluation for cognitive decline," according to the study by Dr. Mark Mintun of Avid Pharmaceuticals, Philadelphia, and colleagues.

Is It Alzheimer's? Florbetapir Provides Evidence

The researchers designed a "real-world" study to determine how florbetapir would affect clinical management of patients with cognitive impairment. While a florbetapir PET scan showing amyloid plaques doesn't prove that AD is present, it provides a previously unavailable piece of evidence to support the diagnosis.

The study included 229 patients seen by neurologists or other specialists for evaluation of cognitive decline or impairment of uncertain etiology. Before the florbetapir PET scan, doctors provided a provisional diagnosis, an estimate of their diagnostic confidence, and their plans for further testing and treatment. The goal was to assess the value of florbetapir PET in making the final diagnosis and in providing doctors with useful information for clinical decision making.

The florbetapir PET scans showed amyloid deposits in 113 out of 229 patients. The information provided led doctors to change their diagnosis in 55 percent of cases. 

When the provisional diagnosis was AD, imaging results led to a change in diagnosis in 37 percent of cases. When the pre-scan diagnosis was either “indeterminate” or another cause of dementia, the diagnosis changed in over 60 percent of cases. In either direction, the scans increased the physicians' ratings of diagnostic confidence by about 20 percent.

Impact on Treatment and Testing Decisions

Florbetapir PET also provided useful information for treatment decision-making: in 87 percent of patients, the results contributed to at least one change in the treatment plan. The main impact was in deciding whether or not to use medications that are helpful in AD. The scan results also affected decisions on further testing—in many cases, physicians dropped plans to perform additional brain imaging studies or neuropsychological tests.

Alzheimer disease is the most common cause of dementia, but the diagnosis can be challenging to make. The only definitive way to diagnose AD is by autopsy examination of the brain after death. Up to 20 percent of patients diagnosed with AD turn out not to have had AD on autopsy, while up to 40 percent of patients diagnosed with other causes of dementia have evidence of AD at autopsy.

Florbetapir PET is the first FDA-approved imaging that can estimate amyloid deposits in the brain of a living patient. Previous studies have shown that the scans are accurate in identifying patients later shown to have AD at autopsy.

The new results show that florbetapir PET scans can have a significant effect in "real world" clinical evaluation of patients with cognitive impairment. By strengthening the case for or against a diagnosis of AD, this test can have a significant impact on patient management—particularly related to the use of AD medications and the need for further testing. Additional studies will be needed to confirm whether "clinical care that includes amyloid imaging will translate into better outcomes" for patients with cognitive impairment and possible AD.

Researchers move closer to delaying dementia

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UQ News

Scientists at UQ's Queensland Brain Institute are one step closer to developing new therapies for treating dementia.



QBI's Dr Jana Vukovic said the work was aimed at understanding the molecular mechanism that may impair learning and memory in the aging population.


“Aging slows the production of new nerve cells, reducing the brain's ability to form new memories,” said Dr Vokovic, who performed the work in the laboratory of Professor Perry Bartlett, the Director of QBI at The University of Queensland.


"But our research shows for the first time that the brain cells usually responsible for mediating immunity, microglia, have an inhibitory effect on memory during aging.


“Furthermore, they have shown that a molecule produced by nerve cells, fractalkine, can reverse this process and stimulate stem cells to produce new neurons.”


The discovery, published in The Journal of Neuroscience today, came after QBI scientists observed that the increased production of new neurons in mice that were actively running was due to the release of fractalkine in the hippocampus – the brain structure responsible for specific types of learning and memory.

Professor Bartlett said it had been known for some time that exercise increased the production of new nerve cells in the hippocampus in young and even aged mice.

“But this study found that it is fractalkine that appears to be specifically mediating this effect by making the microglia produce factors that activate the stem cells that produce new nerve cells,” he said.

“Once the cells are activated they divide and produce new cells, which underpin the animal's ability to learn and form memories.



"This means that fractalkine may form the basis for the development of future therapies.

“The discovery is especially exciting because we have found that older animals suffering cognitive decline showed significantly lower levels of fractalkine.

“We are seeking ways of increasing fractalkine levels in patients with cognitive decline, and hoping this may be a new frontline therapy in treating dementia.”


Dr Vukovic said that until relatively recently, it was thought the adult brain was incapable of generating new neurons.

“But work from Professor Bartlett's laboratory over the past 20 years has demonstrated that the brains of adult animals, including humans, retain the ability to make new nerve cells,” she said.


“The challenge is to find out how to stimulate this production in the aged animal and human where production has slowed.”

The latest work was a significant step toward achieving this goal, she said.


The article published today is titled Microglia modulate hippocampal neural precursor activity in response to exercise and aging. Its authors are Jana Vukovic, Michael J. Colditz, Daniel G. Blackmore, Marc J. Ruitenberg, Perry F. Bartlett

Dementia therapy-patch or pill (part 2)

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Family Practice News

The NMDA (N-methyl-d-aspartate) receptor antagonist memantine is also approved for patients with mild to moderate Alzheimer’s, with optimal dosing titration to 10 mg b.i.d. "Side effects are quite rare, but can include somnolence, headache, and dizziness," said Dr. Cummings, who is also chair of neurotherapeutics at the Cleveland Clinic’s Neurological Institute. "Most patients, by the time they reach mid-disease, are on both a cholinesterase inhibitor and memantine."

Other treatment options include the medical foods CerefolinNAC and Axona, which are generally recognized as safe by the Food and Drug Administration and are available by prescription. "No demonstration of clinical benefit is required for these agents," Dr. Cummings said. "The data set supporting medical foods is not as robust as the data set supporting cholinesterase inhibitors."

CerefolinNAC is a combination of vitamin B6, vitamin B12, and folate that Dr. Cummings uses for hyperhomocysteinemia. "I know that high levels of homocysteine are correlated with cognitive impairment, so I try to reduce that by giving CerefolinNAC," he said. "However, there are no data which prove that lowering will necessarily improve the prognosis of the patient. What you are doing is piecing together various types of data to support that use, but it’s not as strong as a double-blind, placebo-controlled trial showing a direct benefit."

Axona is a proprietary formulation of medium-chain triglycerides that increase plasma concentrations of ketone bodies. "This is considered an energy source for neurons," Dr. Cummings said.

Dr. Cummings disclosed that he has provided consultation to the following pharmaceutical companies: Abbott, Acadia, Adamas, Anavex, Astellas, Avanir, Bayer, BMS, Eisai, EnVivo, ExonHit, Janssen, Forest, Genentech, GSK, Lundbeck, Merck, Neurokos, Novartis, Otsuka, Pfizer, Prana, QR Pharma, Sanofi-Aventis, and Takeda.

Clinical Description Of Dementia

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eHow
A clinical description of dementia has to do with the examination and treatment of patients with dementia. In order to understand how to examine and treat people who have dementia, you must have a basic understanding of the group of symptoms that causes a progressive loss of memory and other intellectual operations.

Definition

The Diagnostic and Statistical Manual of Mental Disorders (DSM) defines dementia as the decline in many intellectual functions of a patient. The difficulties that a patient with dementia may have include problems with language, planning and judgment, simple calculations, muscular movement as well as memory loss. Dementia is not caused by aging; this syndrome has a multitude of causes. It is caused by brain diseases, infections, injuries tumors, consequences of mental illness and other disorders. As you age, your risk for developing dementia increases. Patients may develop dementia for over 40 different reasons. Some of the causes are reversible. Reversible dementia may be seen with depression, decreased levels of thyroid hormone or vitamin B deficiencies.
.Types & Causes

Primary dementias are characterized by damage that causes brain tissue to waste away. These include Alzheimer's disease, frontotemporal lobe dementia and Pick's disease. Multi-infarct dementia is also called vascular dementia. This dementia is caused by blood clots or bleeds in the small blood vessels of the brain. The clots or bleeding cuts off the blood supply to the brain. The brain cells get damaged and may die. Lewy body dementia is caused by the development of Lewy bodies in the brain, which interrupt the transmission of nerve impulses in the brain. Alcoholism or exposure to heavy metals may cause brain damage, leading to dementia. Infectious diseases like HIV and other viruses may destroy brain cells, resulting in dementia. Abnormalities in the structure of the brain, such as hydrocephalus, tumors or subdural hematomas can cause dementia to develop.
.Symptoms

The fourth edition of the DSM talks about certain symptoms that a patient must have to be diagnosed with dementia. One symptom is a moderate decline in a patient's memory. This applies to learning new information and recalling information previously learned. Also the patient must have at least one other mental impairment. It could be problems with expressing or understanding language, an inability to perform movements well known to him like tying his shoes, inability to recognize familiar objects, problems understanding abstract concepts or displaying good judgment. These difficulties must be bad enough to interfere with normal daily life. There may also be personality changes. People with dementia may become paranoid, have delusions, mood swings, anxiety or frequent bouts of anger.
.Examination

The examination to determine if a patient has dementia is long, complicated and has many parts. The first step is for the doctor to take a full history, including a discussion with the family. Next the patient takes a mental status examination (MSE), which evaluates a patient's ability to follow instructions, recall information, communicate in general, perform simple tasks, as well as getting a sense of a patient’s emotional state. A neurological examination is also done. This exam includes an evaluation of a patient's reflexes and cranial nerves. Blood and urine samples are tested to rule out treatable causes of dementia.

A patient, suspected of having dementia may be given a computed tomography (CT) scan, magnetic resonance imaging (MRI) or a positron-emission tomography (PET) scan. These tests allow the doctor to see if different portions of the brain are abnormal.

.Treatment read all of Clinical Description of Dementia

"It was like a vacuum cleaner had removed the plaques."

Alzheimer's and Dementia Weekly

New Haven, Conn. — Blocking a common immune system response cleared up plaques associated with Alzheimer’s Disease and enabled treated mice to recover some lost memory, Yale University researchers reported in the journal Nature Medicine.

Researchers hope the new approach may one day overcome one of the biggest obstacles to development of new dementia medications – the difficulty in finding drugs that can safely cross the blood-brain barrier.

The results of the research surprised the scientists working in the lab of Richard Flavell, senior author of the...read the whole story

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Boston Docs Study Promising New Alzheimer's Drug

BOSTON (WBZ) ―

Alzheimer's May Affect Patients' Memory Earlier (2/19/2009)
Massachusetts researchers are looking for patients to test a promising new Alzheimer's drug. Experts believe it could be the first drug to actually slow down the disease.

Irene Courchesne was diagnosed with early symptoms of Alzheimer's three years ago. "Things started to get really funny," Irene said. "I couldn't remember. I used to have to go to court and I couldn't get my stuff correct."

That's why Irene decided to take part in a new clinical trial being done at the Boston University School of Medicine.

Researchers at B.U. are testing a promising new drug which they believe can actually slow down the progression of Alzheimer's, instead of just temporarily treating the symptoms like current treatments.

Dr. Robert Stern, co-director of the Alzheimer's disease Clinical and Research Program at the B.U. School of Medicine explains, "This new drug has as its goal the ability to suck out the amyloid proteins from the brain which we think is the cause of Alzheimer's and will dramatically alter the course of Alzheimer's disease."

Irene Courchesne, who enrolled in the study in December, says she started to notice....read the whole article

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