Glossary of terms
A
Aß*56: an
amyloid-beta protein different from that
involved in plaques; shown to be directly involved in
memory loss.
Protein identified as
cause of memory loss
acetylcholine:
is what is known as a neurotransmitter -- a chemical produced by
brain cells which transmits information within the brain.
Acetylcholine is vital for memory, attention and thought.
Acetylcholine-producing cells are among the first to die in
Alzheimer's disease. Parkinson's disease, dementia due to multiple
strokes, multiple sclerosis and schizophrenia, are all, like
Alzheimer’s, associated with lower levels of acetylcholine in the
brain.
Apples fight memory
loss ;
Research clarifies how
Alzheimer's medicines work
acetylcholinesterase (AChE): an enzyme which breaks down acetylcholine
ACT: see alpha1-antichymotrypsin
ADDLs: see amyloid ß-derived diffusible ligands
Adenosine Triphosphate (ATP): an important cellular chemical that bonds at nerve terminals for normal neural communication; produced in the mitochondria. see mitochondrial dysfunction
advanced
glycation endproducts: through some chemical process not yet
well understood,
proteins can be permanently and irreversibly
modified; these modified proteins then interact with other chemicals
to form a variety of compounds known as advanced glycation
endproducts.Advanced glycation endproducts have been implicated in
numerous diseases including diabetes, cancer, atherosclerosis, and
Alzheimer’s disease.
A nicotine by-product implicated in Alzheimer’s
AF267B: new drug compound that
successfully reduced plaques and
tangles in the
hippocampus
in mice.
New drug reduces
plaque and tangles in Alzheimer's mice
alpha1-antichymotrypsin (ACT): is a
serin protease inhibitor. Production of ACT increases in brains with
Alzheimer's disease, and this strongly increases the build-up of amyloid
proteins. How it does this is not yet known.
Increased production of protein alpha1-antichymotrypsin found to
strongly increase plaque deposits
Alzhemed:
an experimental drug now in human clinical trials for
treatment of mild-to-moderate Alzheimer's, Alzhemed works by binding
with
amyloid beta to prevent
plaque formation.
New type of
Alzheimer's drug on trial
amyloid ß-derived diffusible ligands
(ADDLs): tiny toxic proteins only discovered
a few years ago, they attack specific synapses rather than the neurons
themselves. The synapses attacked are those where there is a gene linked to
memory that is normally expressed, thus disrupting the normal expression of the
gene. ADDLs are a form of
amyloid beta, but differ from
plaques in that they are very much smaller, are soluble and diffuse between
brain cells until they find vulnerable synapses. They are found in much higher
quantities in the brains of those with Alzheimer's, and it is theorized that
they accumulate at the beginning of Alzheimer's disease and block memory
function. The process is predicted to be reversible, because the ADDLs disrupt
communication between cells rather than destroying the cells.
Support for view of Alzheimer's as form of diabetes;
Why chances of
Alzheimer's increase with age;
Findings show how
toxic proteins rob Alzheimer's patients of memory
; New toxic protein
found
amyloid beta
peptides:
peptides derived from amyloid
precursor protein, these fragments of amyloid beta are the main
protein component of plaques, and probably a major cause for the
their toxicity. They are thought to bind to a receptor in the brain,
blocking the signals needed for learning and memory. The peptides
come in two forms: A-beta 42 and A-beta 40. A subunit of
gamma-secretase, the protein
CD147, is now thought to regulate the
production of A-beta 42. Amyloid beta peptides routinely circulate
in the human bloodstream, where they are harmless. Early beta
amyloid accumulation within neurons is the trigger for the onset of
memory decline in Alzheimer's.
Inhaled
anesthetics might increase the risk of Alzheimer's ;
New way to target Alzheimer's disease
; New early
diagnostic test trialed
; Brain activity,
drugs could affect Alzheimer's progression ;
Finding an
Alzheimer's switch
; Beta amyloid
accumulation shown to be trigger for onset of Alzheimer's
;Scientists
begin to unravel cause of blocked memory in Alzheimer's
amyloid deposits: see beta-amyloid plaques
amyloid plaques: see beta-amyloid plaques
amyloid precursor protein
(APP): is found in many tissues besides brain, but
its functions are largely unknown. It is anchored across the cell
membrane, so part of it is inside and part of it is outside the
cell.
Enzymes
called secretases snip it apart into three
protein fragments, two of which are released
outside the cell and one inside. One of those which is found outside
the cell is made of
amyloid beta peptides. It's speculated
that the creation of amyloid plaque is a byproduct of a
misregulation in normal APP processing. Mutation in the APP is
thought to be involved in early-onset Alzheimer's;
the APP gene is located on chromosome 21, at 21q21.
Paradoxical finding may shed new light on memory loss
; New genetic cause of
Alzheimer's disease ;
Brain activity, drugs could affect Alzheimer's progression ;
Evidence that
Alzheimer's protein switches on genes
amyloid beta protein
cascade: the process by which
APP is clipped by the
beta form of secretase, then
further clipped by
gamma secretase, resulting in
amyloid beta peptides.
Finding an Alzheimer's switch
anthocyanins: perhaps the most
important of the visible plant pigments, responsible for the reds,
purples, and blues you see in plants, they have strong antioxidant
properties; found in fruit such as blackberries, raspberries,
blueberries, etc, and vegetables such as red cabbage.
Blackcurrants may protect against Alzheimer's
apolipoprotein E
(APoE): is a protein whose main
responsibility is transporting cholesterol out of the cell. Too much
of this protein results in an increase in the level of free
cholesterol in the cells. An allele of the gene responsible for this
protein has been identified as a major genetic risk factor for
Alzheimer's (see APOE).
Neurons can produce
apolipoprotein E
; Link between APOE
and memory neurotransmitter
apolipoprotein-E
gene (APOE): the e4 allele of the
apolipoprotein E gene has been identified as a major genetic
risk factor for Alzheimer's. There are three versions (alleles) of
the APOE gene; the most common is e3, present in over half the
population. Those who inherit one copy of the e4 allele are at
higher risk of developing type 2 Alzheimer's, a late-onset form;
those who inherit two copies are at greater risk. Most people with
familial hypercholesterolemia have 2 copies of the e4 allele. One
study suggests having the e4 allele is particularly risky in
combination with a small head size. Similarly, calorie and fat
intake appear to increase the risk of developing Alzheimer's in
those with the allele. An Australian study has more recently
identified the -491A allele as another risk factor. The same study
found that people with these alleles were more likely to complain of
memory difficulties. APOE is located on chromosome 19. A gene on
chromosome 10 has also recently been identified as significantly
increasing the risk of Alzheimer's when found in combination with
APOE e4.
Smokers are more likely to develop dementia;
More on why high
cholesterol might increase your risk of Alzheimer’s ;
Donezepil slows
brain deterioration for some on road to Alzheimer's ;
Link between APOE and
memory neurotransmitter
; Alzheimer's has
higher genetic risk than thought ;
High calorie consumption associated with higher risk of Alzheimer’s
in those genetically disposed to Alzheimer’s ;
New genetic risk factor for susceptibility to Alzheimer's disease
APP: see amyloid precursor protein
Arc: a protein
involved in memory
New light on how
amyloid beta accumulation leads to long-term memory loss
Aricept: the brand name for the generic drug donepezil
ATP: see Adenosine Triphosphate
B
beta-amyloid plaques: are
considered one of the hallmarks of Alzheimer's disease. The plaques
are hard, insoluble aggregations of various
peptides and proteins,
chiefly and most important amyloid-beta
peptides. Recent research suggests plaques attach primarily to
blood vessels, damaging them.
New light on why
plaques form
beta-secretase:
one of three forms of secretase, it and
gamma-secretase are implicated in the formation
of plaques.
Gene targeting
prevents memory loss in Alzheimer's disease model
Enzyme found
essential for nerve cells to form amyloid plaques
C
CD147: is a
protein, a subunit of
gamma-secretase. Only recently discovered, it
is thought to regulate the production of the toxic
beta-amyloid peptides. CD147 is expressed
in many tissues and has many functions, including a neural function:
when the CD147 gene is deleted in mice, the result is defective
nervous system development, loss of working memory, spatial learning
deficits, and disorientation.
Finding an
Alzheimer's switch
ceramides: are a group of lipid-signaling molecules implicated in programmed cell death. Ceramide can stimulate growth or bring about cell death; which of these occurs is determined by contextual factors. Ceramide content is significantly increased in skeletal muscle in insulin-resistant obese humans. Ceramides have been implicated in ischemic stroke and Parkinson's. Ceramide content is high in the white matter of those with Alzheimer's, peaking at the stage of very mild dementia.
choline acetyltransferase (ChAT): synthesizes acetylcholine in neurons and other cells. Decreases in ChAT activity are associated with a number of diseases, including Alzheimer's. Interestingly, older people with mild cognitive impairment have been found to have higher levels of ChAT; it's suggested that this reflects the brain's attempt to maintain normal function as neurons die.
cholinesterase
inhibitors: are drugs that slow the breakdown of
acetylcholine
(see donepezil;
rivastigmine; galantamine).
Research clarifies how Alzheimer's medicines work
Clioquinol:
an experimental drug that binds zinc and copper, shown to lower the
levels of beta amyloid. A small-scale
clinical trial had some success in slowing cognitive decline in
patients with moderate-to-severe Alzheimer's.
Clioquinol
slowed progression of cognitive decline in Alzheimer's patients
corticotropin-releasing
factor: a neuropeptide released in the brain in response to
stress, linked to increased levels of brain cell communication and
implicated in increases in amyloid beta
production. Different receptors - CRF1 AND CRF2 - have been
respectively implicated in worsening and protecting the effects of
stress on
tau protein.
Why stress
increases Alzheimer's risk
cytokines: small proteins that regulate immunity and inflammation
D
DAF-16: a
protein
that helps slow down the accumulation of
amyloid-beta
by clumping extra amyloid together in a way that makes it less
toxic.
Why chances of
Alzheimer's increase with age
donepezil:
donepezil hydrochloride is a
cholinesterase inhibitor, marketed as
Aricept
Aricept
E
early-onset
Alzheimer's: is characterized by symptoms appearing before
age 65; it is thankfully rare (some 6-8% of Alzheimer's cases are
early-onset). Early-onset Alzheimer's has a much stronger genetic
basis that late-onset Alzheimer's, and is therefore also known as
familial Alzheimer's. Three genes have been implicated, on
chromosomes 1, 14 and 21 (see presenilins).
Any one of these will almost certainly lead to early-onset
Alzheimer's. Early-onset Alzheimer's can begin as early as the 30s
or 40s but that is exceedingly rare; more usually it begins in the
50s.
Two-fold role of
Alzheimer’s genes?
EGCG: see epigallocatechin-3-gallate
enzymes: are a type of protein; they are responsible for catalyzing the chemical reactions in a living cell -- that is, they accelerate the rates of reactions.
epigallocatechin-3-gallate:
a major antioxidant in green tea; decreased production of
beta-amyloid in
genetically engineered mice.
Green tea ingredient
prevents Alzheimer's-like brain damage in mice
Exelon: the brand name for the generic drug rivastigmine
F
familial Alzheimer's: see early-onset Alzheimer's
FDDNP: a
molecular marker that tracks the progression of Alzheimer’s in PET
scans more effectively than other markers
Compound shows
promise for early detection of Alzheimer's disease
folate: is a
water-soluble B vitamin occurring naturally in food, especially
green leafy vegetables, citrus fruits and juices, whole wheat bread
and dry beans. Folic acid is a synthetic form of folate. Low levels
of folate are associated with high levels of
homocysteine.
Folic acid possibly a key factor in preventing Alzheimer's disease
Fos: a
protein
involved in memory
New light on how
amyloid beta accumulation leads to long-term memory loss
frontotemporal dementia:
an umbrella term for a group of disorders characeterized by atrophy
in parts of the frontal and temporal lobes; often mistaken for
Alzheimer's, although it tends to occur earlier and affects
personality more than memory initially.
see frontotemporal dementia news
Fyn: an
enzyme
located at the synapses, where it regulates the activity of several
memory-related proteins; increases in Fyn
activity significantly increase the susceptibility of
hippocampal
granule cells to amyloid beta-induced
depletion of memory proteins.
New light on how
amyloid beta accumulation leads to long-term memory loss
G
GAB2:
GRB-associated binding protein 2 - a
protein over-expressed in neurons containing
tangles.
New Alzheimer's gene
HSF-1: a
protein
that normally breaks apart amyloid and
disposes of it.
Why chances of
Alzheimer's increase with age
iNOS: an enzyme
that triggers the production of nitric oxide. Although normally
turned on during infection and needed to help immune cells destroy
invading pathogens, it is not normally found in the brain, where it
may cause cellular damage that destroys neurons. It's found in the
brain lesions of Alzheimer’s patients, where it appears to worsen
the damage.
Gas-blockers might
slow down Alzheimer's disease
interleukin-1:
is a protein that is increased in the brains of Alzheimer's
patients, producing excessive immune activation and inflammation. A
rise in
acetylcholine reduces the production of
interleukin-1.
Anti-inflammatory function of Alzheimer's drugs revealed
galanin: is a
neuropeptide
that has been implicated in Alzheimer's, as well as depression and
eating disorders. Considerably more than usual is produced in the
early stages of Alzheimer’s, possibly as a response to the
deterioration of brain cells. While this might help initially, as
the disease progresses, the overexpression of galanin may become its
own problem, contributing to cognitive decline.
Overproduction of the brain chemical galanin might contribute to
cognitive decline
galantamine:
a cholinesterase inhibitor, marketed as
Reminyl
Reminyl
gamma-secretase:
is one of the two secretases implicated in
plaque formation. Gamma-secretase makes the
final cut in the APP, and it does so within the
cell membrane, using the thickness of the membrane as a guide for
where to cut. Membranes expand or contract depending on the lipid
content of the cell, and so, therefore, does the length of the cut
product. When the cleavage goes wrong, plaques result.
Gamma-secretase is divided into several subunits, which have
recently been discovered to act separately on different tissues (see
CD147).
Potential new drug target identified
; Progress toward a more targeted treatment of Alzheimer's disease
gene therapy: a technique for correcting defective genes; in Alzheimer's research this is generally achieved through surgical placement of genetically modified tissue directly into the brain. see http://www.ornl.gov/sci/techresources/Human_Genome/medicine/genetherapy.shtml for more information on gene therapy
genetically engineered mice: mice that are genetically engineered to develop an Alzheimer's-like disease by the introduction of transgenes. Mice ordinarily do not develop symptoms of the disease. see http://www.mni.mcgill.ca/nm/1999f/en/transgenes.html for a description of how this achieved
glia: the support cells in the brain; the brain contains ten times as many glia as neurons, who do most of the information processing.
H
homocysteine:
is an amino acid. Elevated levels of homocysteine are associated with a greatly
increased risk for coronary heart disease, stroke, vascular dementia, and
Alzheimer's disease. Levels of homocysteine in the blood are strongly influenced
by diet -- high levels are particularly associated with deficiencies in vitamin
B12 and
folate -- lifestyle factors such as smoking,
and genetic factors.
Folic acid
supplementation may improve cognitive performance ;
Diet rich in foods
with Vitamin E may reduce Alzheimer’s disease risk
; High
homocysteine levels may double Alzheimer's risk ;
High homocysteine levels are associated with decreased memory capability after
age 60
I
insulysin: an enzyme that degrades
insulin, now found to also degrade
amyloid beta peptides. Lowered insulysin
activity has been found to raise amyloid beta peptide levels in the
brain. It is suggested that low levels of insulysin can therefore be
considered a risk factor for Alzheimer's.
Insulin-degrading enzyme may affect risk of Alzheimer’s disease
L
low density lipoprotein receptor-related
protein (LRP-1): is a protein
that rapidly shuttles
beta amyloid out of the brain and across
the blood-brain barrier to the body, where it breaks down into harmless waste
products. Mouse studies have revealed that a decrease in LRP-1 is normal with
aging.
Accumulation of plaque may occur because of a decrease in the
molecule involved in removing it
LRP-1: see low density lipoprotein receptor-related protein
M1 receptors: receptors for the
neurotransmitter
acetylcholine implicated in recent
research as having an important role in modulating the
plaques and tangles
characteristic of Alzheimer’s.
New drug reduces
plaque and tangles in Alzheimer's mice
M
MCI-A: mild cognitive impairment,
amnesic subtype; patients with this disorder show memory impairments
but not other cognitive impairments (e.g., in reasoning).
Post-mortem brain
studies reveal features of mild cognitive impairment ;
Two pathways lead
to Alzheimer's disease
MCI-MCD: mild cognitive impairment,
multiple cognitive domain subtype; patients with this disorder show
mild impairments in cognitive tasks such as judgment or language,
and mild or no memory loss.
Post-mortem brain
studies reveal features of mild cognitive impairment ;
Two pathways lead
to Alzheimer's disease
memantine: is in a different class than other approved
Alzheimer's drugs, which are all
cholinesterase inhibitors; memantine, marketed as Namenda, is an
NMDA (N-methyl-D-aspartate)
receptor antagonist.
Memantine
memapsin 2:
an enzyme responsible for producing
beta-amyloid
Designer
chemical offers Alzheimer's hope
methionine: is an amino acid found in beta-amyloid; suggested as being the source of the toxic free radicals produced by amyloid-beta peptides
micro-molecular aggregates: tiny
clumps made up of several amyloid beta
molecules; implicated in Alzheimer's development
Study links
Alzheimer's disease to abnormal cell division
mitochondrial
dysfunction: mitochondria have been termed the cell's "power
plants"; dysfunction in them contributes to a wide range of human
diseases, including neurodegenerative diseases, ischaemic stroke and
heart attack, diabetes and the cumulative degeneration associated
with ageing. Mitochondrial dysfunction is well-documented in
Alzheimer's; it's thought that by decreasing the supply of
ATP, synapses and synaptic function might be lost.
More light on apoE4
and Alzheimer’s ;
How Alzheimer's impacts important brain cell function
MW01-5-188WH: an
orally administered compound specifically targeted to suppress brain cell
inflammation and neuron loss associated with Alzheimer's disease
New compound
stops brain cell degeneration in Alzheimer's disease
myelin: the fatty insulation coating the brain's internal wiring,
critical for speedy communication between neurons. Myelin breakdown has been
implicated in Alzheimer's disease, and is worse in those with the
ApoE gene.
Breakdown of myelin
implicated in Alzheimer's
; Key genetic risk
for Alzheimer's linked to myelin breakdown
N
neurofibrillary
tangles: are tangled bundles of fibers
inside neurons. Like
plaques, they are considered one of the
hallmarks of Alzheimer's disease, although they also occur in other
neurological disorders. Tangles mainly consist of tau
protein. By disrupting the structure of the neuron and disabling
the transport of nutrients, tangles cause neurons to die. Plaques
can induce tangles, but that is only one way in which tangles can
form. Nicotine is, apparently, another.
Abnormal cell
division possible precursor of Alzheimer's
NSAID: nonsteroidal anti-inflammatory
drug (examples: ibuprofen and naproxen). Some of these have been
found to lower levels of Abeta-42.
Anti-inflammatories
O
olanzapine: an antipsychotic
drug commonly used with people with dementia; there have been
concerns about its safety because of an increased risk of stroke
Drugs used to treat Alzheimer's in nursing homes are worsening
sufferers' illness
P
p25: is a
protein whose overproduction is thought to
lead to beta amyloid plaques,
neurofibrillary tangles, and neuron loss. It
is a fragment of another protein, p35, and can be formed when a
stroke or some other unknown event breaks the p35. P25 alters the
behavior of an
enzyme, Cdk5, causing it to kill neurons.
p25 only good in small
doses
; Why stroke and
hypertension may increase risk of Alzheimer's
p75NTR: a
receptor that in the body binds
neurotrophins. There is some evidence that in Alzheimer's, some
of the neurons that die express the p75NTR binding site, indicating
they may be dying because neurotrophins are binding to them.
Potential new
treatment strategy for Alzheimer's
PAK: p21-activated kinase -- a type of enzyme
PAK enzyme signaling pathways: a
critical part of the machinery that controls the connections between
neurons; defects are implicated in both mental retardation and
Alzheimer's
Study links
Alzheimer's and Down’s syndrome
peptide: a compound of two or more amino acids linked by a peptide bond. Peptides differ from proteins by their size; peptides are shorter. Proteins can be broken down into peptides (this occurs during digestion).
peroxisome-proliferator activated receptor
(PPAR): receptors in the brain that controls
insulin responses; stimulation of these has been found to reduce
neurodegeneration of brain cells and preserve learning and memory in
rats with induced Alzheimer's disease, raising the possibility that
patients in the very early stages of Alzheimer’s might be treatable.
PPAR alpha and PPAR gamma were effective in reducing amyloid gene
expression, while PPAR delta had the most benefit for reducing
oxidative stress and improving learning and memory. PPAR gamma is
already FDA approved as a treatment for Type 2 diabetes.
Insulin receptor
stops progression of Alzheimer's
PIB: see Pittsburgh Compound B
Pin1
(prolyl isomerase): an enzyme that helps
prevent tangles and
plaques.
Pin1 enzyme key in
preventing onset of Alzheimer's disease
Pittsburgh Compound B:
a compound that, through PET scanning, enables researchers to
see the amyloid plaque deposits in the brains of Alzheimer’s
sufferers.
Study validates Pittsburgh Compound-B in identifying
Alzheimer's disease toxins ; Brain scans show
early Alzheimer's disease in people with memory problems
;
New
technique allows sight of amyloid plaque in living brains
plaques: see beta-amyloid plaques
polyphenols:
antioxidant chemicals that may help reduce the risk of Alzheimer's.
Most exist primarily in the skins of fruits and vegetables and are
particularly abundant in teas, juices and wines.
Juices may reduce
Alzheimer's disease risk
PPAR: see peroxisome-proliferator activated receptor
presenilins:
are related genes implicated in early-onset
Alzheimer's. Presenilin 1 (PS1) is found on chromosome 14, and
PS2 on chromosome 1. Presenilins are involved in the production of
amyloid peptides, but exactly how
mutations in the genes cause Alzheimer's is not yet understood.
Mouse studies have found that deletion of these genes causes memory
loss and gradual death of nerve cells in the mouse brain,
demonstrating that the protein products of these genes are essential
for normal learning, memory and nerve cell survival.
Two-fold role of
Alzheimer’s genes? ;
Inactivation of Alzheimer's genes in mice causes dementia and brain
degeneration
proteases: are enzymes that decompose peptide bonds, leading to the disassembly of proteins.
proteins: are essential to living organisms; they are long chains of amino acids linked together by peptide bonds. Enzymes, hormones, and antibodies are all types of protein.
Q
quetiapine: is an anti-psychotic
drug commonly used in nursing homes to treat agitation and related
symptoms in people with Alzheimers' disease. Although regarded as
one of the safer of the antipsychotic drugs available, recent
research suggests it actually worsens patients' illness,
significantly speeding up their rate of cognitive decline.
Drugs used to treat Alzheimer's in nursing homes are worsening
sufferers' illness
R
RAGE: receptor for
advanced glycation end products. They are
peptides that routinely circulate in the bloodstream, where
they help attract waste products and remove them. When they
attract beta amyloid, however, they
can combine to form a complex capable of generating an immune
response. Considerably more antibodies to RAGE are found in
people with Alzheimer’s disease.
Antibody detection
in Alzheimer's may improve diagnosis, treatment
Reminyl: the brand name for the generic drug galantamine.
resveratrol:
a natural compound occurring in abundance in grapes, berries and
peanuts. It has been found to lower levels of
amyloid-beta peptides in
cell cultures. The highest concentration has been reported in wines
prepared from Pinot Noir grapes.
Cabernet sauvignon
red wine reduces the risk of Alzheimer's disease ;
Compound in wine reduces levels of Alzheimer's disease-causing
peptides ;
Dietary
supplement helps Alzheimer’s
risperidone: an antipsychotic drug
commonly used with people with dementia; there have been concerns
about its safety because of an increased risk of stroke
Drugs used to treat Alzheimer's in nursing homes are worsening
sufferers' illness
rivastigmine:
rivastigmine tartrate is a
cholinesterase inhibitor, marketed as
Exelon
Exelon
Rolipram: an experimental drug
being tested for its effectiveness in moderate-to-severe
Alzheimer's. Rolipram is a phosphodiesterase 4 inhibitor, able to
modify gene expression, making brain synapses more resistant to the
insult caused by the accumulation of
amyloid-beta.
Rolipram - a
potential new treatment
S
secretase: is a protease. There are three known forms: alpha, beta, and gamma. They process APP.
serin protease inhibitor (serpin): normally prevents proteases from digesting proteins.
serpin: see serin protease inhibitor
SGS742: an experimental drug now in
human clinical trials; SGS742 works by blocking certain chemicals
that interfere with memory formation, thus enabling better
acquisition and retention of new information.
New memory drug works best in combination with older drug
sporadic Alzheimer's: is the more common form of Alzheimer's; unlike the rare early-onset form of Alzheimer's, it is not strongly familial, although there are genes that increase vulnerability to the disease (see APOE gene).
statins: are a class of
cholesterol-lowering drug. The jury is still out on whether these
drugs have any effect on Alzheimer's.
Statins
synaptic proteins: are
proteins involved in brain cell
communications. They are decreased in the brains of Alzheimer's,
especially in the
frontal cortex.
The loss seems to occur early in the disease process, and may be
caused by
mitochondrial dysfunction.
How Alzheimer's impacts important brain cell function
T
tau proteins: are
proteins that form part of a structure
called a microtubule, which helps transport nutrients and other
important substances from one part of the nerve cell to another. In
Alzheimer's disease, however, the tau protein is abnormal and the
microtubule structures collapse, causing neuron death.
Reduction of tau
protein protects against Alzheimer’s
; Abnormal cell
division possible precursor of Alzheimer's
transgenes: genes from one organism that have been incorporated into another organism.
U
ubiquitin
C-terminal hydrolase L1: an enzyme that helps neurons rid
themselves of excess or aberrant proteins; part of a network that
controls a memory molecule called CREB, which is inhibited by
amyloid beta proteins in people with Alzheimer's. Uch-L1 is found at
reduced levels in the Alzheimer's brain.
Brain enzyme
treatment for Alzheimer's
Uch-L1: see ubiquitin C-terminal hydrolase L1
V
vascular
dementia: dementia caused by poor blood flow, produced by a
single, localized stroke, or series of strokes. It's the second most
common type of dementia, after Alzheimer's, accounting for up to a
third of diagnosed dementia cases.
Vascular dementia
W
WIN-55212-2: a synthetic compound
similar to marijuana, found to reduce inflammation in older rats and
improve their memories.
Marijuana may
slow progression of Alzheimer's disease
Now available as a downloadable ebook!
