Sunset Overlooking the Laguna Beach Bette Davis House

Vascular Dementia vs. Alzheimer's

Vascular Conditions

Neurobiol Aging 2000 Mar-Apr;21(2):357-61
Vascular abnormalities: the insidious pathogenesis of Alzheimer's disease*.
Shi J, Perry G, Smith MA, Friedland RP
Laboratory of Neurogeriatrics, Department of Neurology, Case Western Reserve University, 44106, Cleveland, OH, USA.

Alzheimer's disease (AD) and cerebrovascular dementia (CVD) are two major causes of senile dementia in elderly individuals. Mounting evidence from epidemiological, clinical, and neuropathological studies suggests that there is considerable overlap between AD and CVD with respect to risk factors, prevalence, and pathological changes. Although our lack of understanding on the important contribution of vascular disturbance to pathogenesis of AD has further hindered our understanding of AD, data on the roles of cerebrovascular diseases and systemic vascular diseases in AD need to be carefully analyzed to avoid misinterpretation. Here, we review studies on the cerebral vasculature, cardiac vasculature, and apoE that lead us to contend that vascular abnormalities are likely an important mechanism underlying dementia. Because early and aggressive intervention is available to prevent and treat a number of vascular diseases, therapies that attenuate vascular risk factors could be valuable in preventing and treating AD.

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J Neurol 2000 Feb;247(2):81-7
Vascular risk factors in dementia.
Schmidt R, Schmidt H, Fazekas F
Department of Neurology, Karl-Franzens University Graz, Austria. reinhold.schmidt@kfunigraz.ac.at

This review describes differing profiles of vascular risk factors in different types of dementia. Although vascular risk factors are related to various types of strokes, their independent effect on the occurrence of poststroke dementia appears to be small. Various risk factors have been identified for microangiopathy-related cerebral abnormalities, such as white matter changes and lacunae, which are the core lesions for the development of a vascular dementia syndrome without stroke symptoms. Most consistently, arterial hypertension and diabetes mellitus have been found to be associated with such brain abnormalities. Diastolic blood pressure seems to be of particular importance as recent investigations demonstrate that this factor is related to the course of multiple lacunar strokes and the progression of white matter disease. Epidemiological studies report that various vascular risk factors including arterial hypertension, diabetes mellitus, and atrial fibrillation may also be associated with Alzheimer's disease. There is also evidence of a direct relationship between Alzheimer's disease and general atherosclerosis. Further investigations are needed to determine whether these associations are due to the weakness of diagnostic criteria, or whether vascular risk factors indeed modulate the clinical expression of primary degenerative dementia. Common susceptibility genes leading to shared risk factors may be one of the reasons for a higher coincidence of Alzheimer's disease and vascular dementia than can be expected by chance. A modulatory effect of vascular risk factors in the development of primary degenerative dementia may extend treatment options.
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Ann N Y Acad Sci 1999;893:113-25
The blood-brain barrier and cerebrovascular pathology in Alzheimer's disease.
Kalaria RN
Institute for Health of the Elderly, Newcastle General Hospital, Newcastle upon Tyne, United Kingdom. r.n.kalaria@ncl.ac.uk

The pathology of Alzheimer's disease (AD) is not limited to amyloid plaques and neurofibrillary tangles. Recent evidence suggests that more than 30% of AD cases exhibit cerebrovascular pathology, which involves the cellular elements that represent the blood-brain barrier. Certain vascular lesions such as microvascular degeneration affecting the cerebral endothelium, cerebral amyloid angiopathy and periventricular white matter lesions are evident in virtually all cases of AD. Furthermore, clinical studies have demonstrated blood-brain barrier dysfunction in AD patients who exhibit peripheral vascular abnormalities such as hypertension, cardiovascular disease and diabetes. Whether these vascular lesions along with perivascular denervation are coincidental or causal in the pathogenetic processes of AD remains to be defined. In this chapter, I review biochemical and morphological evidence in context with the variable but distinct cerebrovascular pathology described in AD. I also consider genetic influences such as apolipoprotein E in relation to cerebrovascular lesions that may shed light on the pathophysiology of the cerebral vasculature. The compelling vascular pathology associated with AD suggests that transient and focal breach of the blood-brain barrier occurs in late onset AD and may involve an interaction of several factors, which include perivascular mediators as well as peripheral circulation derived factors that perturb the endothelium. These vascular abnormalities are likely to worsen cognitive disability in AD.

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Neurobiol Aging 2000 Mar-Apr;21(2):321-30
The role of cerebral ischemia in Alzheimer's disease.
Kalaria RN
Wolfson Research Centre, Institute for Health of the Elderly, Newcastle General Hospital, Westgate Road, NE4 6BE, Newcastle upon Tyne, United Kingdom.

The Alzheimer type of dementia and stroke are known to increase at comparable rates with age. Recent advances suggest that vascular risk factors linked to cerebrovascular disease and stroke in the elderly significantly increase the risk of developing Alzheimer's disease (AD). These include atherosclerosis, atrial fibrillation, coronary artery disease, hypertension, and diabetes mellitus. Moreover, review of various autopsy series shows that 60-90% of AD cases exhibit variable cerebrovascular pathology. Although some vascular lesions such as cerebral amyloid angiopathy, endothelial degeneration, and periventricular white matter lesions are evident in most cases of AD, a third will exhibit cerebral infarction. Despite the interpretation of pathological evidence, longitudinal clinical studies suggest that the co-existence of stroke and AD occurs more than by chance alone. Strokes known to occur in patients with Alzheimer syndrome and most frequently in the oldest old substantially worsen cognitive decline and outcome, implicating some interaction between the disorders. Nevertheless, the nature of a true relationship between the two disorders seems little explored. What predisposes to strokes in underlying cognitive decline or AD? Is it possible that cerebral ischemia is a causal factor for AD? I examined several vascular factors and the vascular pathophysiology implicated in stroke and AD, and propose that cerebral ischemia or oligemia may promote Alzheimer type of changes in the aging brain. Irrespective of the ultimate pathogenetic mechanism, these approaches implicate that management of peripheral vascular disease is important in the treatment or prevention of Alzheimer's disease or mixed dementia.

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Eur J Neurol 2000 Mar;7(2):159-69
An efficacy and safety analysis of Exelon in Alzheimer's disease patients with concurrent vascular risk factors.
Kumar V, Anand R, Messina J, Hartman R, Veach J
Florida Institute of Neurosciences and Clinical Research, 530 S. Nokomis Avenue, Suite 14, Venice, FL 34284, USA.

We evaluated the efficacy and safety of the centrally acting cholinesterase inhibitor, rivastigmine tartrate, for patients with mild to moderately severe Alzheimer's disease (AD) with or without concurrent vascular risk factors (VRF). Patients (45-90 years of age) were randomized to placebo (n = 235), low-dose rivastigmine (1-4 mg/day, n = 233), or high-dose rivastigmine (6-12 mg/day, n = 231) for 26 weeks. Efficacy measures included the Alzheimer's Disease Assessment Scale-Cognitive subscale (ADAS-Cog), the Clinician's Interview Based Impression of Change (CIBIC-Plus), the Progressive Deterioration Scale (PDS), the Global Deterioration Scale (GDS), and the Mini-Mental State Examination (MMSE). For efficacy and safety analysis, patients were categorized by baseline Modified Hachinski Ischemic Score (MHIS) for the determination of VRF (MHIS > 0: presence of VRF; MHIS = 0: absence of VRF). As early as 12 weeks, the mean change from the baseline ADAS-Cog score was significantly different for those patients treated with high-dose rivastigmine compared with placebo controls in both MHIS categories. However, the treatment difference between high-dose rivastigmine and placebo at each time-point was larger for patients with MHIS > 0. The proportion of responders was significantly greater in the high-dose rivastigmine group for each level of improvement. No differences were noted between treatment groups regarding safety evaluations. Rivastigmine is effective in both categories of patients, and those with VRF experience greater clinical benefit (cognition, activities of daily living, and disease severity).

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Neurobiol Aging 2000 Mar-Apr;21(2):331-42
Critically attained threshold of cerebral hypoperfusion: the CATCH hypothesis of Alzheimer's pathogenesis.
de la Torre JC
Department of Neurosciences (MTF-0624), University of California, San Diego, 9500 Gilman Drive, 92093-0624, La Jolla, CA, USA.

This review discusses the experimental and clinical data which indicate that chronic cerebral hypoperfusion can affect metabolic, anatomic, and cognitive function adversely. In aged but not young animals, chronic brain hypoperfusion results in regional pre- and post-synaptic changes, protein synthesis abnormalities, energy metabolic dysregulation, reduced glucose utilization, cholinergic receptor loss, and visuo-spatial memory deficits. Additionally, aging animals that are kept for prolonged periods of time after chronic brain hypoperfusion, also develop brain capillary degeneration in CA1 hippocampus and neuronal damage extending from the hippocampal region to the temporo-parietal cortex where neurodegenerative tissue atrophy eventually forms. All these pathologic events occur in rodents in the absence of senile plaques and neurofibrillary tangles. Alzheimer brains reveal similar biochemical and structural changes as those experimentally induced in aging animals. Moreover, regional cerebral hypoperfusion is one of the earlier (if not the earliest) clinical manifestations in both the sporadic and familial forms of Alzheimer's disease. In addition, therapy that improves or increases cerebral perfusion is generally of some benefit to Alzheimer patients. Conversely, a variety of disorders with different etiologies that impair or diminish cerebral perfusion are reported to be risk factors for this dementia. These findings have prompted us to propose the concept that advanced aging in the presence of a vascular risk factor can converge to create a critically attained threshold of cerebral hypoperfusion (CATCH) that triggers regional brain microcirculatory disturbances and impairs optimal delivery of energy substrates needed for normal brain cell function. The outcome of this defect generates a chain of events leading to the progressive evolution of brain metabolic, cognitive and tissue pathology that characterize Alzheimer's disease. The possible role of CATCH in familial and early onset Alzheimer's disease is briefly discussed from a theoretical vantagepoint. The growing and most recent evidence in support of the CATCH concept is the focus of this review.

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Neurobiol Aging 2000 Mar-Apr;21(2):215-24
Are cerebrovascular factors involved in Alzheimer's disease?
Kudo T, Imaizumi K, Tanimukai H, Katayama T, Sato N, Nakamura Y, Tanaka T, Kashiwagi Y, Jinno Y, Tohyama M, Takeda M
Department of Clinical Neuroscience, Psychiatry, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, 565-0871, Osaka, Japan.

Recent epidemiological studies have shown that vascular risk factors may be involved in Alzheimer's disease (AD) as well as dementia in general. To investigate the relation between a vascular disorder and AD pathology, current criteria are defective because most depend on exclusion of a cerebrovascular disorder. Epidemiological studies have indicated the possibilities that arteriosclerosis, abnormal blood pressure, diabetes mellitus and smoking may be related to the pathogenesis of AD. As for the mechanism that vascular disorders influence AD, it is presumed that amyloid deposition may be caused by a vascular disorder. Alternatively, a vascular event may cause progression of subclinical AD to a clinical stage. Insulin resistance and apolipoprotein E may also be involved in these mechanisms. Our studies show that ischemia-induced the Alzheimer-associated gene presenilin 1 (PS1) and endoplasmic reticulum-stress, generated from a vascular disorder, may unmask clinical AD symptoms caused by presenilin mutation, suggesting that a vascular factor might be involved in the onset of familial AD.

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Neurobiol Aging 2000 Mar-Apr;21(2):153-60
Vascular risk factors for Alzheimer's disease: An epidemiologic perspective.
Breteler MM
Department of Epidemiology and Biostatistics, Erasmus Medical Center Rotterdam, PO Box 1738, 3000 DR, Rotterdam, The Netherlands.

Vascular disease and Alzheimer's disease are both common disorders, in particular among elderly subjects. Therefore, it can be expected that the joint occurrence of these two disorders is not a rare phenomenon. In recent years, evidence is increasing that the two may be more closely linked than just by chance. Epidemiological studies have suggested that risk factors for vascular disease and stroke are associated with cognitive impairment and Alzheimer's disease, and that the presence of cerebrovascular disease intensifies the presence and severity of the clinical symptoms of Alzheimer's disease. In this paper, current knowledge on the relation between vascular risk factors and risk indicators and Alzheimer's disease will be reviewed.

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Alzheimer Dis Assoc Disord 1999 Oct-Dec;13 Suppl 3:S106-14
Vascular factors and Alzheimer disease.
Skoog I, Kalaria RN, Breteler MM
Institute of Clinical Neuroscience, Section of Psychiatry, Sahlgrenska University Hospital, Goteborg, Sweden.

Vascular risk factors are normally associated with cerebrovascular disease, which may lead to vascular dementia (VaD). Several recent studies suggest that there is increased risk of developing Alzheimer disease when exposed to these same vascular risk factors. In addition to old age, hypertension, peripheral arterial disease, certain types of cardiovascular disorders, diabetes mellitus, and smoking are now considered risk factors for late-onset Alzheimer disease. In this review, we examine several vascular factors and peripheral vascular pathophysiology implicated in Alzheimer disease and suggest certain mechanisms that might promote the association of vascular factors and late-onset Alzheimer disease. We support the implication that prevention or management of peripheral vascular disease may prevent or delay the onset of Alzheimer disease or mixed dementia.

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Aust N Z J Psychiatry 1999 Dec;33(6):809-13
Vascular risk factors and Alzheimer's disease.
Stewart R, Prince M, Mann A
Section of Old Age Psychiatry, Institute of Psychiatry, London, United Kingdom.

OBJECTIVE: We aim to summarise the recent and accumulating epidemiological research which suggests that cardiovascular disease and vascular risk factors play an important role as risk factors for Alzheimer's disease (AD) in later life. METHOD: The epidemiological literature is summarised in considering the evidence for such an association, focusing on optimally designed population-based studies. Potential mechanisms of association are considered, drawing on relevant findings from neuroscience. RESULTS: Cardiovascular disease and vascular risk disorders appear to be important factors in the aetiology of AD. However, there is a paucity of prospective studies with an adequate duration of follow-up to investigate the apparent age- and time-dependent nature of these associations. CONCLUSIONS: Vascular disorders represent potentially preventable risk factors with an important population impact due to their high prevalence in developed countries. The concept of AD and vascular dementia as clearly distinguishable disorders clinically or aetiologically is becoming increasingly tenuous. A better understanding of the relationship between AD and vascular disorders will depend on a more flexible diagnostic and conceptual framework.

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Lancet 1999 Sep 11;354(9182):919-20
Cerebrovascular disease and threshold for dementia in the early stages of Alzheimer's disease.
Esiri MM, Nagy Z, Smith MZ, Barnetson L, Smith AD

Cerebrovascular disease and Alzheimer's disease commonly occur together in the elderly and each may contribute to dementia. Here we present evidence that cerebrovascular disease significantly worsens cognitive performance in the earliest stages of Alzheimer's disease.

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Marilyn

Photosensitive Epilepsy

Many thanks to Professors G Harding (Aston University, England) and S Seri for providing the information on which the following is based.

Introduction

It is often assumed that everybody with epilepsy is photosensitive, but only around five per cent of people with epilepsy are. Photosensitive epilepsy is the name given to a form of epilepsy in which seizures are triggered by flickering or flashing light.

Both natural and artificial light sources can cause flickering which might be a problem for people with photosensitive epilepsy. For example, sunlight reflected off wet surfaces or through leaves of trees, flashing lights in discos and the flickering of faulty fluorescent lighting may also trigger seizures. However the commonest trigger for people with photosensitive epilepsy appears to be television.

Most people with photosensitive epilepsy are sensitive to flickering around 16-25Hz, although some people may be sensitive to rates as low as 3Hz and as high as 60Hz.

People with photosensitive epilepsy usually develop the condition before the age of 20, with it being most common between the ages of nine and 15. More females than males seem to have photosensitive epilepsy. There is also evidence of a genetic factor in this condition.

Various types of seizure may be triggered by flickering light, but a tonic-clonic seizure is certainly the most frequent type induced by television, sometimes beginning with myoclonic jerking (brief jerking of the limbs).

More specific information about photosensitive epilepsy can be obtained from Epilepsy Action by using the Email Helpline or if you live in the UK, by phoning the freephone Helpline on 0808 800 5050

Information updated 28 October 2005
Information update
http://www.hardingfpa.tv/index.html

Hippocampus

The Hippocampus

The hippocampus is a horseshoe shaped region of the subcortical brain. As part of the limbic system, located in the temporal lobe, it has a role in emotion and sexuality. It also contains "place" cells that construct mental maps of position, and with the parahippocampal gyrus, is implicated in the learning and remembering of space (spatial orientation). Studies with monkeys show that damage to the hippocampus results in the inability to navigate through familiar areas.

From Michio Kaku's book "Visions" (How Science will Revolutionize the 21st Century): "The hippocampus helps construct a three dimensional "mental map" of our surroundings, and is crucial for our ability to move around in the real world.

"Memories are probably first processed and kept in the hippocampus for several weeks, before they are transferred to the cerebral cortex for permanent storage. This may explain why people with brain damage to their hippocampal region retain previous memories of faces and places, which are stored in the cortex, but have difficulty forming new short-term memories.

"The hippocampus of the mouse brain contains about a million large nerve cells, called "place cells," which enable mice to record where they are located in space. These place cells consolidate their memory via the protein kinase.

Scientists at MIT and Columbia University independently announced in 1996 that they could change memory in mice by altering a gene that codes for kinase...In both studies the mice appeared perfectly normal, but were severely impaired in their ability to find their way around..."

Damage to the hippocampal region results in a failure to remember spatial layouts or landmarks. This may be one reason why people with Alzheimer's disease become progressively unable to navigate in space despite normal vision. In a 4 year study of 405 elderly volunteers, de Leon and coworkers found that probable cases of Alzheimer's disease often emerge in people who start out with a small hippocampus and mild memory problems. Hippocampal volume declined from 20 to 50 percent in victims of Alzheimers compared to healthy elderly controls.

Stroke patients who experience navigation problems inevitably manifest brain damage in an area just below (and connected to) the hippocampus, a region called the parahippocampal gyri. This area is crucial to the storage and recall of spatial information. After stroke damage to the parahippocampus, patients develop topographical disorientation. They lose the ability to learn new routes or to travel familiar routes.

There may be a connection between children with navigational disabilities, stroke patients, and victims of Alzheimer's disease. It may be that the blood supply to the hippocampus and parahippocampus is vulnerable, ie. more easily damaged by infarction, more prone to damage faster when oxygen (and/or nutrients) is reduced. (speculation on my part).

A study in the July, 1997 issue of the magazine Science indicates that semantic memory (memory of context-free facts) and episodic memory (memory of context-rich events) take place in separate areas of the brain. The hippocampus regulates episodic memory, but plays a very small role in the remembering of factual information. (study done by a research team at University College London Medical School).

Another study at Dartmouth College by psychologists Golob and Taube (reported in the July 8, 1997 issue of the Proceedings of the National Academy of Sciences), suggests that "Despite the hippocampus' powerful influence on episodic memory, other brain areas may independently gather and retrieve information that animals use to orient themselves in a new setting."

The hippocampus seems to be a major hub through which all new experiences must pass on their way to forming a new memory. When the region is damaged, patients become prisoners of the past. Yet they can learn new skills like golf or bridge. They improve their skills each time they play golf or bridge for example, all the while thinking that this is the first time they have ever tried the game. This suggests that skill development is its own kind of memory, governed by another brain region.

Patients with damage to the basal ganglia display exactly the opposite: they can practice a skill like playing the piano hundreds of times, retaining clear memories of every previous lesson, yet make absolutely no progress with the skill.

Many patients with hippocampal damage remember things from before an injury, but not since. A patient studied at Rutgers University convulses in agony every time he hears that his father has died, yet he awakes each morning fresh thinking that his father is alive.

notes:

The hippocampus is a center for short term memory. It weighs the importance of episodic acts and decides which should be kept as memories. Therefore it has an important role in learning.

Brain scan evidence shows that healthy people experience a drop in hippocampal volume of about 15 percent as they age.

The hippocampus appears to shrink in people who have been exposed to severe trauma; like sexual abuse cases or combat victims.

Since the hippocampus is a center for event memory, does this suggest a connection with the visual movement center, area 5 (?) of the visual cortex? I am assuming that an event primarily involves movement recall.

It receives input from auditory as well as visual tracts

The hippocampus is sometimes removed in epilepsy surgery causing a loss of the ability to form new long term memories. Problems in the thalamus can result in the inability to retrieve memories.

Damage to the hippocampus disrupts recent memory, but leaves remote (already learned?) memory intact.

Researchers think there may be at least five memory systems operating in parallel.

The hippocampus allows for rapid learning of new items.

According to Jeff Hawkins in the book On Intelligence: The hippocampus is the "uppermost" level of the neocortex.

The hippocampus creates longterm memories (which are then stored in the neocortext).

People working on the hippocampus and its relation to spatial orientation
:

Richard Morris: University of Edinbourgh

Jack Loomis: psychologist at the University of California at Santa Barbara

University of Pennsylvania Hospital is also involved in research

Endocrinologist Michael M. Cohen at Applied Medical Research (AMR) in Fairfax, Virginia

Immunologist Walter Pierprole (?) of the Biancalana-Masera Foundation for the aged in Italy

Beta- Amyloid gets piggy back ride to brain.

Main Entry: be·ta–am·y·loid
Variant: also β–amyloid /-'am-&-"loid/
Function: noun
: an amyloid that is derived from a larger precursor protein and is a component of the neurofibrillary tangles and plaques characteristic of Alzheimer's disease called also amyloid beta-protein, beta-amyloid protein

Molecular "Piggyback Ride" Carries Alzheimer's Protein Into Brain, URMC News Next Article
Excerpts: The new findings center on amyloid beta, a tiny protein molecule that accumulates over time to form tell-tale plaques in the brain tissue of Alzheimer's patients. While various cells within the brain itself produce amyloid beta, that amount may be just the tip of the iceberg. Mounting evidence suggests that the bulk of amyloid beta is produced in cells throughout the body and gets circulated in the blood. The new study reveals for the first time how the protein gets from the blood into the brain, thwarting the brain's elaborate filtration mechanism that normally keeps away toxins. (...) "For more than a decade we've known that this protein wreaks havoc in the brains of Alzheimer's patients, but we haven't known how it gets there or how to prevent it from getting there. This study answers both of those basic questions, and opens an entirely new avenue for the treatment of Alzheimer's disease," said lead author Berislav Zlokovic, M.D., Ph.D., of the University of Rochester Medical Center.(...) The blood-brain barrier blocks the passage of toxins while allowing the flow of oxygen, sugar, and other nutrients to brain cells. In the current study, Zlokovic and his colleagues found that amyloid beta protein molecules cannot flow through the blood-brain barrier unaided. Rather, they get through by riding piggyback on a much larger molecule, called RAGE, which is nontoxic and moves unfettered across the blood-brain barrier. Normally, RAGE is produced in small amounts by the cells that form the blood-brain barrier. But in mice that were genetically engineered to develop Alzheimer's disease, Zlokovic found that RAGE was produced in huge amounts - eight times normal - and ferried an avalanche of amyloid beta into the brain.

Tricking the Brain for Stroke Survivor

I have read an article written by a young Neurologist.
While working with stroke patients, he discovered that by having them exercise the functioning side of the body in front of a mirror, the brain perceives it as the stroke side that is performing. Go get em tiger.

mk

Forgetting Doesn't Mean Alzheimer's.

It is important to remember the diagnostic criteria,because sometimes people are wrongly labeled as having Dementia or Alzheimer's disease.

Forgetting something does not mean a person is developing any kind of dementia. There are many reasons for memory lapses and momentary confusion.
Anyone may forget something, especially when sick, stressed, mildly depressed, tired, distracted, or trying to remember too much. Alzheimer's disease, and dementia in general, are not a part of aging.

Reversible Causes of Dementia-like Symptoms.

HYPOTHERMIA - Low body terperature
.
HYPERTHERMIA - High body termerature
.
DEHYDRATION - Not enough fluid in the body
.
NUTRITIONAL DEFICITS - Inadequate diet
.
SENSORY PROBLEMS - Sight and hearing decline normally with age.Vision and hearing impairments can result in behaviors that are symptomatic of dementia by blocking or distorting the person's perception of environmental and interpersonal cues. Eyeglasses (prescription accuracy, fit, and cleanliness) and hearing aids (batteries, cleanliness and fit) should be checked
.
ENVIRONMENTAL SITUATIONS - Four common environmental situations that can cause dementia-like symptoms are: relocation, rapid changes in the environment, loss of familiar objects and faces in the environment, and lack in the environment of orienting information such as clocks and calendars.

ALTERED PHYSIOLOGY - This term refers to changes in normal body functions, such as a full bladder, constipation, pain or immobility.

ANEMIA - The oxygen carrying capacity of the blood is reduced.

CHRONIC DISEASES - The brain needs oxygen to function. The kidneys and liver clear the waste products from the blood, the lungs supply oxygen to the blood, and the heart and blood vessels transport the oxygen to the brain. Problems in any of these systems can cause dementia-like symptoms.

DRUGS - Drugs can cause dementia-like symtoms because of side effects and interactions with each other or with alcohol. Moreover, drugs can take longer to work, and remain in the body longer for the elderly than for young people.

DEPRESSION - Depression is the most common emotional disorder of the elderly and serious depression can mimic dementia.

Remember, these conditions and problems are reversible and can unnecessarily reduce the functioning of anyone, including a person with Alzheimer's disease.

The Brain and the Effects of Alzheimer's Disease

Neurons

It has been estimated that the brain has over 100 billion brain cells, a large proportion of which are nerve cells, called neurons. The functions of neurons are to process, send and receive information. A neuron is made up of a cell body (with its nucleus) dendrites (which receive messages from other neurons) and an axon (which sends messages to other neurons). Neurons are highly interconnected, forming the message pathways we need to think and function.




The Brain

The brain is composed of many different structures that work independently and together to supervise the rest of the body. If we think of the body as a large company, the brain is the board of directors.


The Brain Stem

The brain stem is located at the point where the brain and spinal cord are connected. It is important among the brain structures involved in basic physical survival, and participates in the regulation of consciousness. It also signals other brain areas to "get ready" for incoming information. In people with Alzheimer's disease, the brain stem continues to function normally at least until the advanced stages of the disease.

The Cerebellum

The Cerebellum is a large structure attached to the back of the brain stem. It helps maintain and adjust posture and balance, as well as coordinate and refine movement. The cerebellum is not highly affected by Alzheimer's disease.

The Cerebrum

The Cerebrum makes up about 85% of the weight of the human brain. Within the cerebrum are many structures that play a acritical role in normal living.

Cerebral Hemispheres: The brain is divided into two halves called hemispheres. Each hemisphere controls the opposite side of the body. while each hemisphere has some uniquely special features, they normally work together, constantly sending messages back-and-forth. Alzheimer's disease effects both hemispheres.

The Cerebral Cortex: The cerebral hemispheres are covered with an intricately folded layer of nerve cells called the cortex. The cortex is about an eighth to a quarter of and inch thick. Among other functions, the cortex makes possible all our higher mental abilities, such as thinking, speaking, and remembering. If the brain is considered the board of directors of our body, the cortex is the chairman of the board. The cortex is one of the brain structures that is greatly affected by Alzheimer's disease.

Lobes of the Cerebrum: Each cerebral hemisphere is divided into four parts: the frontal lobe the parietal lobe, the temporal lobe and the occipital lobe.

The Frontal lobes: The frontal lobe of each hemisphere is located behind the forehead. The frontal lobes oversee much of what the rest of the brain is doing and are important in our ability to plan, make judgments, and carry out purposeful behavior. The frontal lobes are connected with other brain systems which control alertness and emotion.

Alzheimer's disease causes damage to the frontal lobes that results in distinct changes in behavior.

1. Inability to plan or carry out complex action or comprehend a complex idea.
For example, the completion of a sequence of steps may be difficult or impossible for a person with of Alzheimer's disease, even though the individual may be capable of performing each step by itself.

2. Inability to change behavior. Damage to the frontal lobes may also cause an individual to be less able to change a current behavior when a new one is required. He may make more mistakes and may be harder to get along with when placed in a new situation.

3. Inability to focus attention. When the frontal lobes are damaged, individuals may lose the ability to focus their attention, becoming easily distracted and drifting from one task to another without completing any of them.

4. Emotional aspects of frontal lobe damage. Because the frontal lobes are highly interconnected to other brain areas which are important in the control of emotion, people with Alzheimer's disease experience many emotional problems. Apathy, irritibility and suspiciousness are all common features of the disease. Also people with frontal lobe damage may be unable to inhibit or control the expression of urges that are socially inappropriate, such as sexual urges, anger, and hostility. They may also laugh or cry inappropriately.

The Temporal Lobes: The temporal lobes, located behind the temples, interpret the sounds from the environment, both language and non-language. Alzheimer's disease also causes significant damage to these lobes.

Left Temporal Lobe: The left temporal lobe is especially important to communication. Damage to the left temporal lobe may cause loss of ability to understand language in written or oral form. It can also cause difficulty in understanding and remembering lists of words, sentences or complex verbal material. The ability to acquire new verbal learning may be dramatically diminished. Finally, damage to the left temporal lobe may leave the individual unable to perform simple addition and subtraction.

Right Temporal Lobe: The right temporal lobe is specialized for recognition and interpretation of non-language sounds, including environmental sounds, music and rhythm. When the right temporal lobe is damaged, individuals may not be able to recognize what a sound is or what it means.

The right temporal lobe is also important for organizing what we see into meaningful patterns and for remembering things that we see. Individuals with right temporal damage are likely to have spatial disorientation and difficulty recognizing complex visual stimuli. They may also have problems making fine visual discrimination, such as being able to detect the edges of a place mat on a table cloth.

Summary: The temporal lobes are prominently affected by Alzheimer's disease, which is a primary reason communication, memory, and visual-perceptual problems occur.

The Parietal Lobes: The parietal lobes are located above the temporal lobes and behind the frontal lobes. It is in the parietal lobes that sensory information for the enviroment is analyzed. The parietal lobes help us keep track of the placement of our bodies, and how we are positioned in space.

1. Constructional disorders: When damage occurs to the parietal lobes, constructional disorders may occur. Constuctional disorders include difficulty drawing a picture of a clock or assembling a coffee pot correctly.

2. Association cortex: The function of the temporal and parietal lobes includes an area that is called the association cortex, which is significantly affected by Alzheimer's disease. Damage to the association cortex is primarily responsible for impairment of conceptual knowledge and the ability to make inferences.

The Occipital Lobes: The occipital lobes are situated at the back of each hemisphere and are primarily involved in visual perception and association. Of the four lobes, this one is least affected by Alzheimer's disease.

Hippocampus

The hippocampus plays a major role in emotion, behavior, the ability to reason, and the selective storage and retrieval of information. It is responsible for transferring new information to long term memory. A principal basis for problems with reasoning and memory in Alzheimer's disease is damage to the hippocampus.

A Deterioration Scale For Stages of Alzheimers

No Cognitive Decline
Level 1

No subjective complaints of memory deficit. No memory deficit evident on clinical interview.

Very Mild Forgetfulness
Level 2

Subjective complaints of memory deficit, most frequently in following areas,
Forgetting where one has placed familiar objects, forgetting names one formerly knew well. No objective evidence of memory deficit on clinical interview. No subjective deficits in employment or social situations. Appropriate concern with respect to symptomatology.

Mild (Early Confusional)
Level 3

Earliest clear-cut deficits. Manifestations in more than one of the following areas: Patient may have gotten lost when traveling to an unfamiliar location: co-workers become aware of patient’s relatively poor performance: word and name finding deficit becomes evident to intimates: patient : Patient may read passages in a book and retain relatively little material: Patient may demonstrate decreased facility in remembering names upon introduction to new people: Patient may have lost or misplaced an object of value:, Concentration deficit may be evident in clinical testing. Objective evidence of memory deficit obtained only with an intensive interview. Decreased performance in demanding employment and social settings. Denial begins to become manifest in patient. Mild to moderate anxiety accompanies symptoms.

Moderate (Late Confusional)
Level 4

Clear-cut deficit on careful clinical interview. Deficit manifest in following areas: Decreased knowledge of current and recent events: May exhibit some deficit in memory of one’s personal history: Concentration deficit elicited on serial sub-tractions: Decreased ability to travel, handle finances, etc.
Frequently no deficit in following areas: Orientation to time and person: Recognition of familiar persons and faces: Ability to travel to familiar locations. Inability to perform complex tasks. Denial is dominant defense mechanism. Flattening of affect and withdrawal from challenging situations occur.

Moderately severe (Early Dementia)
Level 5

Patient can no longer survive without some assistance. Patient is unable during interview to recall a major relevant aspect of their current lives: e.g., an address or telephone number of many years, the names of close family members (such as grandchildren): The name of the high school or college from which they graduated. Frequently some disorientation to time (date, day of week, season etc.) or to place. An educated person may have difficulty counting back from 40 by 4’s or from 20 by 2’s.
Persons at this stage retain knowledge of many major facts regarding themselves and others. They invariably know their own names and generally know their spouses’ and children’s names. They require no assistance with toileting and eating, but may have some difficulty choosing proper clothing to wear.

Severe (Middle Dementia)
Level 6

May occasionally forgets the name of the spouse upon whom they are entirely dependent for survival. Will be largely unaware of all recent events and experiences in their lives. Retain some knowledge of their past life, but this is very sketchy. Generally unaware of their surroundings, the year, the season, etc. Diurnal rhythm frequently disturbed. (Daytime). Will require some assistance with activities of daily living, e.g., may become incontinent, will require travel assistance but occasionally will Almost always recall their own name. Frequently continue to be able to distinguish familiar from unfamiliar persons in their environment Personality and emotional changes occur. These are quite variable and include: Delusional behavior, e.g., patients may accuse their spouse of being an imposter, may talk to imaginary figures in the environment, or to their own reflection in the mirror. Obsessive symptoms: e.g., person may continually repeat simple cleaning activities. Anxiety symptoms: Agitation and even previously non-existent violent behavior may occur. Cognitive abulla: i.e., loss of willpower because and individual cannot carry a thought long enough to determine a purposeful course of action

Very severe (Late Dementia)
Level 7

All verbal abilities are lost. Frequently there is no speech at all, only grunting. Incontinent of urine: Requires assistance toileting and feeding. Lose basic psychomotor skills, e.g., ability to walk. The brain appears to no longer be able to tell the body what to do. Generalized and cortical neurologic signs and symptoms are frequently present. The disease ends with death.