Alan MacDonald discuses with the Lyme Disease Research Database founder his research looking into a connection between Alzheimer’s and Lyme disease.
October 26, 2009
October 23, 2009
Manipulating Brain Inflammation May Help Clear Brain Of Amyloid Plaques, Researchers Say
In a surprising reversal of long-standing scientific belief, researchers have discovered that inflammation in the brain is not the trigger that leads to buildup of amyloid deposits and development of Alzheimer’s disease. (Source: ScienceDaily Headlines)
Apathy is a prominent neuropsychiatric feature of radiological white-matter changes in patients with dementia
The objective was to study the relationships between WMCs on MRI/CT and neuropsychiatric symptoms and vascular factors in patients with cognitive impairment. One hundred and seventy-six patients with Alzheimer’s disease, vascular dementia, mixed dementia, and mild cognitive impairment were included. All patients underwent a standardized examination including medical history, clinical examinations, laboratory tests and brain imaging (CT or MRI). The identification and severity degree of WMCs was assessed blindly to clinical findings, using a semi-quantitative scale. For statistical analyses, patients were grouped based on absence or presence of WMCs. Significant variables in bivariate analyses were included as predictors in stepwise multiple logistic regression analyses.updated hourly from thousands of authoritative health and news sources./p/div
October 17, 2009
Olive oil compound linked to Alzheimer’s
CHICAGO, Oct. 17 (UPI) — A compound in olive oil targets and blocks toxic proteins that damage brain cells and cause memory loss in Alzheimer’s disease victims, U.S. researchers said.
The compound, oleocanthal, alters the structures of the proteins, ADDLs, said William L. Klein of Northwestern University and Paul A.S. Breslin of Monell Chemical Senses Center.
“Binding of ADDLs is thought to be a crucial first step in the initiation of Alzheimer’s disease,” Klein said in a statement. “Oleocanthal alters ADDL structure in a way that deters the protein from binding to synapses that allow the nervous system to connect.”
ADDLs bind within the synapses of the brains of Alzheimer’s patients and are believed directly to disrupt nerve cell function, eventually leading to memory loss, cell death and global disruption of brain function, the researchers said.
Klein and colleagues identified ADDLs in 1998, leading to a major shift in thinking about the causes, progression and treatment of Alzheimer’s disease. ADDLs are structurally different from the amyloid plaques that accumulate in brains of Alzheimer’s patients.
Future studies are needed to identify more precisely how oleocanthal changes ADDL composition. Such insights could provide discovery pathways related to disease prevention and treatment, the researchers said.
The findings are published in the journal Toxicology and Applied Pharmacology.
March 14, 2008
Cannabis Based Treatments Could Improve Memory Loss
This week at a symposium of cannabis experts hosted by the Royal Pharmaceutical Society of Great Britain (RPSGB) where the scientists from Israel and Spain said that a compound present in cannabis significantly slows memory problems caused by Alzheimer’s disease.
Ten years ago the RPSGB launched its protocols to demonstrate the therapeutic effectiveness of cannabis which led to Government-funded trials in Britain to explore the benefits for patients with multiple sclerosis and in the treatment of severe pain.
Professor Tony Moffat, chairman of the Symposium says progress has been made in the last ten years but more research is needed as there is considerable interest in the medical benefits of cannabis and related compounds for a range of conditions including arthritis, multiple sclerosis and neurological pain.
Alzheimer’s disease is the commonest form of dementia, which affects an estimated 24.3 million people worldwide. Most of us reading this blog is well aware that most cases of Alzheimers are actually Lyme Disease..
February 20, 2006
Plaques of Alzheimer’s disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete
Elsevier Health Journal
Alan B. MacDonald
St. Catherine of Siena Medical Center, Department of Pathology, 50 Rte 25 A, Smithtown, NY 11787, USA
Received 20 February 2006; accepted 23 February 2006
Summary Here is hypothesized a truly revolutionary notion that rounded cystic forms of Borrelia burgdorferi are the
root cause of the rounded structures called plaques in the Alzheimer brain. Rounded ‘‘plaques’ in high density in brain
tissue are emblematic of Alzheimer’s disease (AD). Plaques may be conceptualized as rounded ‘‘pock mark-like’’ areas
of brain tissue injury. In this century, in brain tissue of AD, plaques are Amyloid Plaques according to the most up to date
textbooks. In the last century, however, Dr. Alois Alzheimer did not require amyloid as the pathogenesis for either the
disease or for the origin of its plaques. Surely, amyloid is an event in AD, but it may not be the primal cause of AD. Indeed
in plaques, amyloid is regularly represented by the ‘‘congophilic core’’ structure which is so named because the waxy
amyloid material binds the congo red stain and is congophilic. However an accepted subset of plaques in AD is devoid of a
congophilic amyloid core region (these plaques ‘‘cotton wool’’ type plaques, lack a central congophilic core structure).
Furthermore, there is ‘‘plaque diversity’’ in Alzheimer’s; small, medium and large plaques parallel variable cystic
diameters for Borrelia burgdorferi. Perturbations of AD plaque structure (i.e. young plaques devoid of a central core
and older plaques with or without a central core structure) offer room for an alternate pathway for explanation of
ontogeny of the plaque structures. If amyloid is not required to initiate all of the possible plaques in Alzheimer’s, is it
possible that amyloid just a by product of a more fundamental primal path to dementia? If a byproduct status is assigned
to amyloid in the realm of plaque formation, then is amyloid also an epiphenomenon rather than a primary pathogenesis
for Alzheimer’s disease. In the ‘‘anatomy is destiny’’ model, cysts of borrelia are always round. Why then not accept
roundness as a fundamental ‘‘structure determines function’’ argument for the answer to the mystery of why Alzheimer
plaques are always round? Parataxis causality, a concept borrowed from philosophy, is the error that comes from linking
two events, which occur contemporaneously or in close proximity to one another with a cause and effect relationship.
Parataxis tells us that what appears to be cause and effect in the couplet ‘‘amyloid plaque’’ merely by a proximity
relationship may be ‘‘spurious causality’’ which is a cognitive dead end.